---
_id: '9094'
abstract:
- lang: eng
text: Dendritic cells (DCs) are crucial for the priming of naive T cells and the
initiation of adaptive immunity. Priming is initiated at a heterologous cell–cell
contact, the immunological synapse (IS). While it is established that F-actin
dynamics regulates signaling at the T cell side of the contact, little is known
about the cytoskeletal contribution on the DC side. Here, we show that the DC
actin cytoskeleton is decisive for the formation of a multifocal synaptic structure,
which correlates with T cell priming efficiency. DC actin at the IS appears in
transient foci that are dynamized by the WAVE regulatory complex (WRC). The absence
of the WRC in DCs leads to stabilized contacts with T cells, caused by an increase
in ICAM1-integrin–mediated cell–cell adhesion. This results in lower numbers of
activated and proliferating T cells, demonstrating an important role for DC actin
in the regulation of immune synapse functionality.
article_number: e202006081
article_processing_charge: No
article_type: original
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: LM
full_name: Altenburger, LM
last_name: Altenburger
- first_name: R
full_name: Hauschild, R
last_name: Hauschild
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: K
full_name: Rottner, K
last_name: Rottner
- first_name: Stradal
full_name: TEB, Stradal
last_name: TEB
- first_name: A
full_name: Diz-Muñoz, A
last_name: Diz-Muñoz
- first_name: JV
full_name: Stein, JV
last_name: Stein
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Leithner AF, Altenburger L, Hauschild R, et al. Dendritic cell actin dynamics
control contact duration and priming efficiency at the immunological synapse.
Journal of Cell Biology. 2021;220(4). doi:10.1083/jcb.202006081
apa: Leithner, A. F., Altenburger, L., Hauschild, R., Assen, F. P., Rottner, K.,
TEB, S., … Sixt, M. K. (2021). Dendritic cell actin dynamics control contact duration
and priming efficiency at the immunological synapse. Journal of Cell Biology.
Rockefeller University Press. https://doi.org/10.1083/jcb.202006081
chicago: Leithner, Alexander F, LM Altenburger, R Hauschild, Frank P Assen, K Rottner,
Stradal TEB, A Diz-Muñoz, JV Stein, and Michael K Sixt. “Dendritic Cell Actin
Dynamics Control Contact Duration and Priming Efficiency at the Immunological
Synapse.” Journal of Cell Biology. Rockefeller University Press, 2021.
https://doi.org/10.1083/jcb.202006081.
ieee: A. F. Leithner et al., “Dendritic cell actin dynamics control contact
duration and priming efficiency at the immunological synapse,” Journal of Cell
Biology, vol. 220, no. 4. Rockefeller University Press, 2021.
ista: Leithner AF, Altenburger L, Hauschild R, Assen FP, Rottner K, TEB S, Diz-Muñoz
A, Stein J, Sixt MK. 2021. Dendritic cell actin dynamics control contact duration
and priming efficiency at the immunological synapse. Journal of Cell Biology.
220(4), e202006081.
mla: Leithner, Alexander F., et al. “Dendritic Cell Actin Dynamics Control Contact
Duration and Priming Efficiency at the Immunological Synapse.” Journal of Cell
Biology, vol. 220, no. 4, e202006081, Rockefeller University Press, 2021,
doi:10.1083/jcb.202006081.
short: A.F. Leithner, L. Altenburger, R. Hauschild, F.P. Assen, K. Rottner, S. TEB,
A. Diz-Muñoz, J. Stein, M.K. Sixt, Journal of Cell Biology 220 (2021).
date_created: 2021-02-05T10:08:04Z
date_published: 2021-04-05T00:00:00Z
date_updated: 2023-09-05T13:57:53Z
day: '05'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1083/jcb.202006081
external_id:
isi:
- '000626365700001'
pmid:
- '33533935'
file:
- access_level: open_access
checksum: 843ebc153847c8626e13c9c5ce71d533
content_type: application/pdf
creator: dernst
date_created: 2022-05-12T14:16:21Z
date_updated: 2022-05-12T14:16:21Z
file_id: '11367'
file_name: 2021_JournCellBiology_Leithner.pdf
file_size: 5102328
relation: main_file
success: 1
file_date_updated: 2022-05-12T14:16:21Z
has_accepted_license: '1'
intvolume: ' 220'
isi: 1
issue: '4'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-sa/4.0/
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dendritic cell actin dynamics control contact duration and priming efficiency
at the immunological synapse
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 220
year: '2021'
...
---
_id: '9429'
abstract:
- lang: eng
text: De novo loss of function mutations in the ubiquitin ligase-encoding gene Cullin3
lead to autism spectrum disorder (ASD). In mouse, constitutive haploinsufficiency
leads to motor coordination deficits as well as ASD-relevant social and cognitive
impairments. However, induction of Cul3 haploinsufficiency later in life does
not lead to ASD-relevant behaviors, pointing to an important role of Cul3 during
a critical developmental window. Here we show that Cul3 is essential to regulate
neuronal migration and, therefore, constitutive Cul3 heterozygous mutant mice
display cortical lamination abnormalities. At the molecular level, we found that
Cul3 controls neuronal migration by tightly regulating the amount of Plastin3
(Pls3), a previously unrecognized player of neural migration. Furthermore, we
found that Pls3 cell-autonomously regulates cell migration by regulating actin
cytoskeleton organization, and its levels are inversely proportional to neural
migration speed. Finally, we provide evidence that cellular phenotypes associated
with autism-linked gene haploinsufficiency can be rescued by transcriptional activation
of the intact allele in vitro, offering a proof of concept for a potential therapeutic
approach for ASDs.
acknowledged_ssus:
- _id: PreCl
acknowledgement: We thank A. Coll Manzano, F. Freeman, M. Ladron de Guevara, and A.
Ç. Yahya for technical assistance, S. Deixler, A. Lepold, and A. Schlerka for the
management of our animal colony, as well as M. Schunn and the Preclinical Facility
team for technical assistance. We thank K. Heesom and her team at the University
of Bristol Proteomics Facility for the proteomics sample preparation, data generation,
and analysis support. We thank Y. B. Simon for kindly providing the plasmid for
lentiviral labeling. Further, we thank M. Sixt for his advice regarding cell migration
and the fruitful discussions. This work was supported by the ISTPlus postdoctoral
fellowship (Grant Agreement No. 754411) to B.B., by the European Union’s Horizon
2020 research and innovation program (ERC) grant 715508 (REVERSEAUTISM), and by
the Austrian Science Fund (FWF) to G.N. (DK W1232-B24 and SFB F7807-B) and to J.G.D
(I3600-B27).
article_number: '3058'
article_processing_charge: No
article_type: original
author:
- first_name: Jasmin
full_name: Morandell, Jasmin
id: 4739D480-F248-11E8-B48F-1D18A9856A87
last_name: Morandell
- first_name: Lena A
full_name: Schwarz, Lena A
id: 29A8453C-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Bernadette
full_name: Basilico, Bernadette
id: 36035796-5ACA-11E9-A75E-7AF2E5697425
last_name: Basilico
orcid: 0000-0003-1843-3173
- first_name: Saren
full_name: Tasciyan, Saren
id: 4323B49C-F248-11E8-B48F-1D18A9856A87
last_name: Tasciyan
orcid: 0000-0003-1671-393X
- first_name: Georgi A
full_name: Dimchev, Georgi A
id: 38C393BE-F248-11E8-B48F-1D18A9856A87
last_name: Dimchev
orcid: 0000-0001-8370-6161
- first_name: Armel
full_name: Nicolas, Armel
id: 2A103192-F248-11E8-B48F-1D18A9856A87
last_name: Nicolas
- first_name: Christoph M
full_name: Sommer, Christoph M
id: 4DF26D8C-F248-11E8-B48F-1D18A9856A87
last_name: Sommer
orcid: 0000-0003-1216-9105
- first_name: Caroline
full_name: Kreuzinger, Caroline
id: 382077BA-F248-11E8-B48F-1D18A9856A87
last_name: Kreuzinger
- first_name: Christoph
full_name: Dotter, Christoph
id: 4C66542E-F248-11E8-B48F-1D18A9856A87
last_name: Dotter
orcid: 0000-0002-9033-9096
- first_name: Lisa
full_name: Knaus, Lisa
id: 3B2ABCF4-F248-11E8-B48F-1D18A9856A87
last_name: Knaus
- first_name: Zoe
full_name: Dobler, Zoe
id: D23090A2-9057-11EA-883A-A8396FC7A38F
last_name: Dobler
- first_name: Emanuele
full_name: Cacci, Emanuele
last_name: Cacci
- first_name: Florian KM
full_name: Schur, Florian KM
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
- first_name: Johann G
full_name: Danzl, Johann G
id: 42EFD3B6-F248-11E8-B48F-1D18A9856A87
last_name: Danzl
orcid: 0000-0001-8559-3973
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
citation:
ama: Morandell J, Schwarz LA, Basilico B, et al. Cul3 regulates cytoskeleton protein
homeostasis and cell migration during a critical window of brain development.
Nature Communications. 2021;12(1). doi:10.1038/s41467-021-23123-x
apa: Morandell, J., Schwarz, L. A., Basilico, B., Tasciyan, S., Dimchev, G. A.,
Nicolas, A., … Novarino, G. (2021). Cul3 regulates cytoskeleton protein homeostasis
and cell migration during a critical window of brain development. Nature Communications.
Springer Nature. https://doi.org/10.1038/s41467-021-23123-x
chicago: Morandell, Jasmin, Lena A Schwarz, Bernadette Basilico, Saren Tasciyan,
Georgi A Dimchev, Armel Nicolas, Christoph M Sommer, et al. “Cul3 Regulates Cytoskeleton
Protein Homeostasis and Cell Migration during a Critical Window of Brain Development.”
Nature Communications. Springer Nature, 2021. https://doi.org/10.1038/s41467-021-23123-x.
ieee: J. Morandell et al., “Cul3 regulates cytoskeleton protein homeostasis
and cell migration during a critical window of brain development,” Nature Communications,
vol. 12, no. 1. Springer Nature, 2021.
ista: Morandell J, Schwarz LA, Basilico B, Tasciyan S, Dimchev GA, Nicolas A, Sommer
CM, Kreuzinger C, Dotter C, Knaus L, Dobler Z, Cacci E, Schur FK, Danzl JG, Novarino
G. 2021. Cul3 regulates cytoskeleton protein homeostasis and cell migration during
a critical window of brain development. Nature Communications. 12(1), 3058.
mla: Morandell, Jasmin, et al. “Cul3 Regulates Cytoskeleton Protein Homeostasis
and Cell Migration during a Critical Window of Brain Development.” Nature Communications,
vol. 12, no. 1, 3058, Springer Nature, 2021, doi:10.1038/s41467-021-23123-x.
short: J. Morandell, L.A. Schwarz, B. Basilico, S. Tasciyan, G.A. Dimchev, A. Nicolas,
C.M. Sommer, C. Kreuzinger, C. Dotter, L. Knaus, Z. Dobler, E. Cacci, F.K. Schur,
J.G. Danzl, G. Novarino, Nature Communications 12 (2021).
date_created: 2021-05-28T11:49:46Z
date_published: 2021-05-24T00:00:00Z
date_updated: 2024-03-28T23:30:23Z
day: '24'
ddc:
- '572'
department:
- _id: GaNo
- _id: JoDa
- _id: FlSc
- _id: MiSi
- _id: LifeSc
- _id: Bio
doi: 10.1038/s41467-021-23123-x
ec_funded: 1
external_id:
isi:
- '000658769900010'
file:
- access_level: open_access
checksum: 337e0f7959c35ec959984cacdcb472ba
content_type: application/pdf
creator: kschuh
date_created: 2021-05-28T12:39:43Z
date_updated: 2021-05-28T12:39:43Z
file_id: '9430'
file_name: 2021_NatureCommunications_Morandell.pdf
file_size: 9358599
relation: main_file
success: 1
file_date_updated: 2021-05-28T12:39:43Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
issue: '1'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 25444568-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '715508'
name: Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo
and in vitro Models
- _id: 2548AE96-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W1232-B24
name: Molecular Drug Targets
- _id: 05A0D778-7A3F-11EA-A408-12923DDC885E
grant_number: F07807
name: Neural stem cells in autism and epilepsy
- _id: 265CB4D0-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I03600
name: Optical control of synaptic function via adhesion molecules
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: press_release
url: https://ist.ac.at/en/news/defective-gene-slows-down-brain-cells/
record:
- id: '7800'
relation: earlier_version
status: public
- id: '12401'
relation: dissertation_contains
status: public
status: public
title: Cul3 regulates cytoskeleton protein homeostasis and cell migration during a
critical window of brain development
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '10307'
abstract:
- lang: eng
text: Bacteria-host interactions represent a continuous trade-off between benefit
and risk. Thus, the host immune response is faced with a non-trivial problem –
accommodate beneficial commensals and remove harmful pathogens. This is especially
difficult as molecular patterns, such as lipopolysaccharide or specific surface
organelles such as pili, are conserved in both, commensal and pathogenic bacteria.
Type 1 pili, tightly regulated by phase variation, are considered an important
virulence factor of pathogenic bacteria as they facilitate invasion into host
cells. While invasion represents a de facto passive mechanism for pathogens to
escape the host immune response, we demonstrate a fundamental role of type 1 pili
as active modulators of the innate and adaptive immune response.
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
- _id: PreCl
- _id: EM-Fac
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
citation:
ama: Tomasek K. Pathogenic Escherichia coli hijack the host immune response. 2021.
doi:10.15479/at:ista:10307
apa: Tomasek, K. (2021). Pathogenic Escherichia coli hijack the host immune response.
Institute of Science and Technology Austria. https://doi.org/10.15479/at:ista:10307
chicago: Tomasek, Kathrin. “Pathogenic Escherichia Coli Hijack the Host Immune Response.”
Institute of Science and Technology Austria, 2021. https://doi.org/10.15479/at:ista:10307.
ieee: K. Tomasek, “Pathogenic Escherichia coli hijack the host immune response,”
Institute of Science and Technology Austria, 2021.
ista: Tomasek K. 2021. Pathogenic Escherichia coli hijack the host immune response.
Institute of Science and Technology Austria.
mla: Tomasek, Kathrin. Pathogenic Escherichia Coli Hijack the Host Immune Response.
Institute of Science and Technology Austria, 2021, doi:10.15479/at:ista:10307.
short: K. Tomasek, Pathogenic Escherichia Coli Hijack the Host Immune Response,
Institute of Science and Technology Austria, 2021.
date_created: 2021-11-18T15:05:06Z
date_published: 2021-11-18T00:00:00Z
date_updated: 2023-09-07T13:34:38Z
day: '18'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: MiSi
- _id: CaGu
- _id: GradSch
doi: 10.15479/at:ista:10307
file:
- access_level: open_access
checksum: b39c9e0ef18d0484d537a67551effd02
content_type: application/pdf
creator: ktomasek
date_created: 2021-11-18T15:07:31Z
date_updated: 2022-12-20T23:30:05Z
embargo: 2022-11-18
file_id: '10308'
file_name: ThesisTomasekKathrin.pdf
file_size: 13266088
relation: main_file
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checksum: c0c440ee9e5ef1102a518a4f9f023e7c
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: ktomasek
date_created: 2021-11-18T15:07:46Z
date_updated: 2022-12-20T23:30:05Z
embargo_to: open_access
file_id: '10309'
file_name: ThesisTomasekKathrin.docx
file_size: 7539509
relation: source_file
file_date_updated: 2022-12-20T23:30:05Z
has_accepted_license: '1'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: '73'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '10316'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-4561-241X
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
title: Pathogenic Escherichia coli hijack the host immune response
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2021'
...
---
_id: '10316'
abstract:
- lang: eng
text: A key attribute of persistent or recurring bacterial infections is the ability
of the pathogen to evade the host’s immune response. Many Enterobacteriaceae express
type 1 pili, a pre-adapted virulence trait, to invade host epithelial cells and
establish persistent infections. However, the molecular mechanisms and strategies
by which bacteria actively circumvent the immune response of the host remain poorly
understood. Here, we identified CD14, the major co-receptor for lipopolysaccharide
detection, on dendritic cells as a previously undescribed binding partner of FimH,
the protein located at the tip of the type 1 pilus of Escherichia coli. The FimH
amino acids involved in CD14 binding are highly conserved across pathogenic and
non-pathogenic strains. Binding of pathogenic bacteria to CD14 lead to reduced
dendritic cell migration and blunted expression of co-stimulatory molecules, both
rate-limiting factors of T cell activation. While defining an active molecular
mechanism of immune evasion by pathogens, the interaction between FimH and CD14
represents a potential target to interfere with persistent and recurrent infections,
such as urinary tract infections or Crohn’s disease.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
- _id: EM-Fac
acknowledgement: We thank Ulrich Dobrindt for providing UPEC strain CFT073, Vlad Gavra
and Maximilian Götz, Bor Kavčič, Jonna Alanko and Eva Kiermaier for help with experiments
and Robert Hauschild, Julian Stopp and Saren Tasciyan for help with data analysis.
We thank the IST Austria Scientific Service Units, especially the Bioimaging facility,
the Preclinical facility and the Electron microscopy facility for technical support,
Jakob Wallner and all members of the Guet and Sixt lab for fruitful discussions
and Daria Siekhaus for critically reading the manuscript. This work was supported
by grants from the Austrian Research Promotion Agency (FEMtech 868984) to I.G.,
the European Research Council (CoG 724373) and the Austrian Science Fund (FWF P29911)
to M.S.
article_processing_charge: No
author:
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Ivana
full_name: Glatzová, Ivana
id: 727b3c7d-4939-11ec-89b3-b9b0750ab74d
last_name: Glatzová
- first_name: Michael S.
full_name: Lukesch, Michael S.
last_name: Lukesch
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-4561-241X
citation:
ama: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated
uropathogenic Escherichia coli hijack the host immune response by binding to CD14.
bioRxiv. doi:10.1101/2021.10.18.464770
apa: Tomasek, K., Leithner, A. F., Glatzová, I., Lukesch, M. S., Guet, C. C., &
Sixt, M. K. (n.d.). Type 1 piliated uropathogenic Escherichia coli hijack the
host immune response by binding to CD14. bioRxiv. Cold Spring Harbor Laboratory.
https://doi.org/10.1101/2021.10.18.464770
chicago: Tomasek, Kathrin, Alexander F Leithner, Ivana Glatzová, Michael S. Lukesch,
Calin C Guet, and Michael K Sixt. “Type 1 Piliated Uropathogenic Escherichia Coli
Hijack the Host Immune Response by Binding to CD14.” BioRxiv. Cold Spring
Harbor Laboratory, n.d. https://doi.org/10.1101/2021.10.18.464770.
ieee: K. Tomasek, A. F. Leithner, I. Glatzová, M. S. Lukesch, C. C. Guet, and M.
K. Sixt, “Type 1 piliated uropathogenic Escherichia coli hijack the host immune
response by binding to CD14,” bioRxiv. Cold Spring Harbor Laboratory.
ista: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated
uropathogenic Escherichia coli hijack the host immune response by binding to CD14.
bioRxiv, 10.1101/2021.10.18.464770.
mla: Tomasek, Kathrin, et al. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack
the Host Immune Response by Binding to CD14.” BioRxiv, Cold Spring Harbor
Laboratory, doi:10.1101/2021.10.18.464770.
short: K. Tomasek, A.F. Leithner, I. Glatzová, M.S. Lukesch, C.C. Guet, M.K. Sixt,
BioRxiv (n.d.).
date_created: 2021-11-19T12:24:16Z
date_published: 2021-10-18T00:00:00Z
date_updated: 2024-03-28T23:30:35Z
day: '18'
department:
- _id: CaGu
- _id: MiSi
doi: 10.1101/2021.10.18.464770
ec_funded: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.biorxiv.org/content/10.1101/2021.10.18.464770v1
month: '10'
oa: 1
oa_version: Preprint
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
- _id: 26018E70-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29911
name: Mechanical adaptation of lamellipodial actin
publication: bioRxiv
publication_status: submitted
publisher: Cold Spring Harbor Laboratory
related_material:
record:
- id: '11843'
relation: later_version
status: public
- id: '10307'
relation: dissertation_contains
status: public
status: public
title: Type 1 piliated uropathogenic Escherichia coli hijack the host immune response
by binding to CD14
type: preprint
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2021'
...
---
_id: '7234'
abstract:
- lang: eng
text: T lymphocytes utilize amoeboid migration to navigate effectively within complex
microenvironments. The precise rearrangement of the actin cytoskeleton required
for cellular forward propulsion is mediated by actin regulators, including the
actin‐related protein 2/3 (Arp2/3) complex, a macromolecular machine that nucleates
branched actin filaments at the leading edge. The consequences of modulating Arp2/3
activity on the biophysical properties of the actomyosin cortex and downstream
T cell function are incompletely understood. We report that even a moderate decrease
of Arp3 levels in T cells profoundly affects actin cortex integrity. Reduction
in total F‐actin content leads to reduced cortical tension and disrupted lamellipodia
formation. Instead, in Arp3‐knockdown cells, the motility mode is dominated by
blebbing migration characterized by transient, balloon‐like protrusions at the
leading edge. Although this migration mode seems to be compatible with interstitial
migration in three‐dimensional environments, diminished locomotion kinetics and
impaired cytotoxicity interfere with optimal T cell function. These findings define
the importance of finely tuned, Arp2/3‐dependent mechanophysical membrane integrity
in cytotoxic effector T lymphocyte activities.
article_processing_charge: No
article_type: original
author:
- first_name: Peyman
full_name: Obeidy, Peyman
last_name: Obeidy
- first_name: Lining A.
full_name: Ju, Lining A.
last_name: Ju
- first_name: Stefan H.
full_name: Oehlers, Stefan H.
last_name: Oehlers
- first_name: Nursafwana S.
full_name: Zulkhernain, Nursafwana S.
last_name: Zulkhernain
- first_name: Quintin
full_name: Lee, Quintin
last_name: Lee
- first_name: Jorge L.
full_name: Galeano Niño, Jorge L.
last_name: Galeano Niño
- first_name: Rain Y.Q.
full_name: Kwan, Rain Y.Q.
last_name: Kwan
- first_name: Shweta
full_name: Tikoo, Shweta
last_name: Tikoo
- first_name: Lois L.
full_name: Cavanagh, Lois L.
last_name: Cavanagh
- first_name: Paulus
full_name: Mrass, Paulus
last_name: Mrass
- first_name: Adam J.L.
full_name: Cook, Adam J.L.
last_name: Cook
- first_name: Shaun P.
full_name: Jackson, Shaun P.
last_name: Jackson
- first_name: Maté
full_name: Biro, Maté
last_name: Biro
- first_name: Ben
full_name: Roediger, Ben
last_name: Roediger
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Wolfgang
full_name: Weninger, Wolfgang
last_name: Weninger
citation:
ama: Obeidy P, Ju LA, Oehlers SH, et al. Partial loss of actin nucleator actin-related
protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology
and Cell Biology. 2020;98(2):93-113. doi:10.1111/imcb.12304
apa: Obeidy, P., Ju, L. A., Oehlers, S. H., Zulkhernain, N. S., Lee, Q., Galeano
Niño, J. L., … Weninger, W. (2020). Partial loss of actin nucleator actin-related
protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology
and Cell Biology. Wiley. https://doi.org/10.1111/imcb.12304
chicago: Obeidy, Peyman, Lining A. Ju, Stefan H. Oehlers, Nursafwana S. Zulkhernain,
Quintin Lee, Jorge L. Galeano Niño, Rain Y.Q. Kwan, et al. “Partial Loss of Actin
Nucleator Actin-Related Protein 2/3 Activity Triggers Blebbing in Primary T Lymphocytes.”
Immunology and Cell Biology. Wiley, 2020. https://doi.org/10.1111/imcb.12304.
ieee: P. Obeidy et al., “Partial loss of actin nucleator actin-related protein
2/3 activity triggers blebbing in primary T lymphocytes,” Immunology and Cell
Biology, vol. 98, no. 2. Wiley, pp. 93–113, 2020.
ista: Obeidy P, Ju LA, Oehlers SH, Zulkhernain NS, Lee Q, Galeano Niño JL, Kwan
RYQ, Tikoo S, Cavanagh LL, Mrass P, Cook AJL, Jackson SP, Biro M, Roediger B,
Sixt MK, Weninger W. 2020. Partial loss of actin nucleator actin-related protein
2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology.
98(2), 93–113.
mla: Obeidy, Peyman, et al. “Partial Loss of Actin Nucleator Actin-Related Protein
2/3 Activity Triggers Blebbing in Primary T Lymphocytes.” Immunology and Cell
Biology, vol. 98, no. 2, Wiley, 2020, pp. 93–113, doi:10.1111/imcb.12304.
short: P. Obeidy, L.A. Ju, S.H. Oehlers, N.S. Zulkhernain, Q. Lee, J.L. Galeano
Niño, R.Y.Q. Kwan, S. Tikoo, L.L. Cavanagh, P. Mrass, A.J.L. Cook, S.P. Jackson,
M. Biro, B. Roediger, M.K. Sixt, W. Weninger, Immunology and Cell Biology 98 (2020)
93–113.
date_created: 2020-01-05T23:00:48Z
date_published: 2020-02-01T00:00:00Z
date_updated: 2023-08-17T14:21:12Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1111/imcb.12304
external_id:
isi:
- '000503885600001'
pmid:
- '31698518'
file:
- access_level: open_access
checksum: c389477b4b52172ef76afff8a06c6775
content_type: application/pdf
creator: dernst
date_created: 2020-11-19T11:22:33Z
date_updated: 2020-11-19T11:22:33Z
file_id: '8775'
file_name: 2020_ImmunologyCellBio_Obeidy.pdf
file_size: 8569945
relation: main_file
success: 1
file_date_updated: 2020-11-19T11:22:33Z
has_accepted_license: '1'
intvolume: ' 98'
isi: 1
issue: '2'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 93-113
pmid: 1
publication: Immunology and Cell Biology
publication_identifier:
eissn:
- '14401711'
issn:
- '08189641'
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Partial loss of actin nucleator actin-related protein 2/3 activity triggers
blebbing in primary T lymphocytes
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 98
year: '2020'
...
---
_id: '7623'
abstract:
- lang: eng
text: A two-dimensional mathematical model for cells migrating without adhesion
capabilities is presented and analyzed. Cells are represented by their cortex,
which is modeled as an elastic curve, subject to an internal pressure force. Net
polymerization or depolymerization in the cortex is modeled via local addition
or removal of material, driving a cortical flow. The model takes the form of a
fully nonlinear degenerate parabolic system. An existence analysis is carried
out by adapting ideas from the theory of gradient flows. Numerical simulations
show that these simple rules can account for the behavior observed in experiments,
suggesting a possible mechanical mechanism for adhesion-independent motility.
acknowledgement: This work has been supported by the Vienna Science and Technology
Fund, Grant no. LS13-029. G.J. and C.S. also acknowledge support by the Austrian
Science Fund, Grants no. W1245, F 65, and W1261, as well as by the Fondation Sciences
Mathématiques de Paris, and by Paris-Sciences-et-Lettres.
article_processing_charge: No
article_type: original
author:
- first_name: Gaspard
full_name: Jankowiak, Gaspard
last_name: Jankowiak
- first_name: Diane
full_name: Peurichard, Diane
last_name: Peurichard
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Christian
full_name: Schmeiser, Christian
last_name: Schmeiser
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Jankowiak G, Peurichard D, Reversat A, Schmeiser C, Sixt MK. Modeling adhesion-independent
cell migration. Mathematical Models and Methods in Applied Sciences. 2020;30(3):513-537.
doi:10.1142/S021820252050013X
apa: Jankowiak, G., Peurichard, D., Reversat, A., Schmeiser, C., & Sixt, M.
K. (2020). Modeling adhesion-independent cell migration. Mathematical Models
and Methods in Applied Sciences. World Scientific. https://doi.org/10.1142/S021820252050013X
chicago: Jankowiak, Gaspard, Diane Peurichard, Anne Reversat, Christian Schmeiser,
and Michael K Sixt. “Modeling Adhesion-Independent Cell Migration.” Mathematical
Models and Methods in Applied Sciences. World Scientific, 2020. https://doi.org/10.1142/S021820252050013X.
ieee: G. Jankowiak, D. Peurichard, A. Reversat, C. Schmeiser, and M. K. Sixt, “Modeling
adhesion-independent cell migration,” Mathematical Models and Methods in Applied
Sciences, vol. 30, no. 3. World Scientific, pp. 513–537, 2020.
ista: Jankowiak G, Peurichard D, Reversat A, Schmeiser C, Sixt MK. 2020. Modeling
adhesion-independent cell migration. Mathematical Models and Methods in Applied
Sciences. 30(3), 513–537.
mla: Jankowiak, Gaspard, et al. “Modeling Adhesion-Independent Cell Migration.”
Mathematical Models and Methods in Applied Sciences, vol. 30, no. 3, World
Scientific, 2020, pp. 513–37, doi:10.1142/S021820252050013X.
short: G. Jankowiak, D. Peurichard, A. Reversat, C. Schmeiser, M.K. Sixt, Mathematical
Models and Methods in Applied Sciences 30 (2020) 513–537.
date_created: 2020-03-31T11:25:05Z
date_published: 2020-03-18T00:00:00Z
date_updated: 2023-08-18T10:18:56Z
day: '18'
department:
- _id: MiSi
doi: 10.1142/S021820252050013X
external_id:
arxiv:
- '1903.09426'
isi:
- '000525349900003'
intvolume: ' 30'
isi: 1
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1903.09426
month: '03'
oa: 1
oa_version: Preprint
page: 513-537
project:
- _id: 25AD6156-B435-11E9-9278-68D0E5697425
grant_number: LS13-029
name: Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments
publication: Mathematical Models and Methods in Applied Sciences
publication_identifier:
issn:
- '02182025'
publication_status: published
publisher: World Scientific
quality_controlled: '1'
scopus_import: '1'
status: public
title: Modeling adhesion-independent cell migration
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 30
year: '2020'
...
---
_id: '7875'
abstract:
- lang: eng
text: 'Cells navigating through complex tissues face a fundamental challenge: while
multiple protrusions explore different paths, the cell needs to avoid entanglement.
How a cell surveys and then corrects its own shape is poorly understood. Here,
we demonstrate that spatially distinct microtubule dynamics regulate amoeboid
cell migration by locally promoting the retraction of protrusions. In migrating
dendritic cells, local microtubule depolymerization within protrusions remote
from the microtubule organizing center triggers actomyosin contractility controlled
by RhoA and its exchange factor Lfc. Depletion of Lfc leads to aberrant myosin
localization, thereby causing two effects that rate-limit locomotion: (1) impaired
cell edge coordination during path finding and (2) defective adhesion resolution.
Compromised shape control is particularly hindering in geometrically complex microenvironments,
where it leads to entanglement and ultimately fragmentation of the cell body.
We thus demonstrate that microtubules can act as a proprioceptive device: they
sense cell shape and control actomyosin retraction to sustain cellular coherence.'
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
- _id: PreCl
acknowledgement: "The authors thank the Scientific Service Units (Life Sciences, Bioimaging,
Preclinical) of the Institute of Science and Technology Austria for excellent support.
This work was funded by the European Research Council (ERC StG 281556 and CoG 724373),
two grants from the Austrian\r\nScience Fund (FWF; P29911 and DK Nanocell W1250-B20
to M. Sixt) and by the German Research Foundation (DFG SFB1032 project B09) to O.
Thorn-Seshold and D. Trauner. J. Renkawitz was supported by ISTFELLOW funding from
the People Program (Marie Curie Actions) of the European Union’s Seventh Framework
Programme (FP7/2007-2013) under the Research Executive Agency grant agreement (291734)
and a European Molecular Biology Organization long-term fellowship (ALTF 1396-2014)
co-funded by the European Commission (LTFCOFUND2013, GA-2013-609409), E. Kiermaier
by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany’s
Excellence Strategy—EXC 2151—390873048, and H. Hacker by the American Lebanese Syrian
Associated ¨Charities. K.-D. Fischer was supported by the Analysis, Imaging and
Modelling of Neuronal and Inflammatory Processes graduate school funded by the Ministry
of Economics, Science, and Digitisation of the State Saxony-Anhalt and by the European
Funds for Social and Regional Development."
article_number: e201907154
article_processing_charge: No
article_type: original
author:
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Irute
full_name: Girkontaite, Irute
last_name: Girkontaite
- first_name: Kerry
full_name: Tedford, Kerry
last_name: Tedford
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Oliver
full_name: Thorn-Seshold, Oliver
last_name: Thorn-Seshold
- first_name: Dirk
full_name: Trauner, Dirk
id: E8F27F48-3EBA-11E9-92A1-B709E6697425
last_name: Trauner
- first_name: Hans
full_name: Häcker, Hans
last_name: Häcker
- first_name: Klaus Dieter
full_name: Fischer, Klaus Dieter
last_name: Fischer
- first_name: Eva
full_name: Kiermaier, Eva
id: 3EB04B78-F248-11E8-B48F-1D18A9856A87
last_name: Kiermaier
orcid: 0000-0001-6165-5738
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Kopf A, Renkawitz J, Hauschild R, et al. Microtubules control cellular shape
and coherence in amoeboid migrating cells. The Journal of Cell Biology.
2020;219(6). doi:10.1083/jcb.201907154
apa: Kopf, A., Renkawitz, J., Hauschild, R., Girkontaite, I., Tedford, K., Merrin,
J., … Sixt, M. K. (2020). Microtubules control cellular shape and coherence in
amoeboid migrating cells. The Journal of Cell Biology. Rockefeller University
Press. https://doi.org/10.1083/jcb.201907154
chicago: Kopf, Aglaja, Jörg Renkawitz, Robert Hauschild, Irute Girkontaite, Kerry
Tedford, Jack Merrin, Oliver Thorn-Seshold, et al. “Microtubules Control Cellular
Shape and Coherence in Amoeboid Migrating Cells.” The Journal of Cell Biology.
Rockefeller University Press, 2020. https://doi.org/10.1083/jcb.201907154.
ieee: A. Kopf et al., “Microtubules control cellular shape and coherence
in amoeboid migrating cells,” The Journal of Cell Biology, vol. 219, no.
6. Rockefeller University Press, 2020.
ista: Kopf A, Renkawitz J, Hauschild R, Girkontaite I, Tedford K, Merrin J, Thorn-Seshold
O, Trauner D, Häcker H, Fischer KD, Kiermaier E, Sixt MK. 2020. Microtubules control
cellular shape and coherence in amoeboid migrating cells. The Journal of Cell
Biology. 219(6), e201907154.
mla: Kopf, Aglaja, et al. “Microtubules Control Cellular Shape and Coherence in
Amoeboid Migrating Cells.” The Journal of Cell Biology, vol. 219, no. 6,
e201907154, Rockefeller University Press, 2020, doi:10.1083/jcb.201907154.
short: A. Kopf, J. Renkawitz, R. Hauschild, I. Girkontaite, K. Tedford, J. Merrin,
O. Thorn-Seshold, D. Trauner, H. Häcker, K.D. Fischer, E. Kiermaier, M.K. Sixt,
The Journal of Cell Biology 219 (2020).
date_created: 2020-05-24T22:00:56Z
date_published: 2020-06-01T00:00:00Z
date_updated: 2023-08-21T06:28:17Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
- _id: NanoFab
doi: 10.1083/jcb.201907154
ec_funded: 1
external_id:
isi:
- '000538141100020'
pmid:
- '32379884'
file:
- access_level: open_access
checksum: cb0b9c77842ae1214caade7b77e4d82d
content_type: application/pdf
creator: dernst
date_created: 2020-11-24T13:25:13Z
date_updated: 2020-11-24T13:25:13Z
file_id: '8801'
file_name: 2020_JCellBiol_Kopf.pdf
file_size: 7536712
relation: main_file
success: 1
file_date_updated: 2020-11-24T13:25:13Z
has_accepted_license: '1'
intvolume: ' 219'
isi: 1
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
- _id: 26018E70-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29911
name: Mechanical adaptation of lamellipodial actin
- _id: 252C3B08-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W 1250-B20
name: Nano-Analytics of Cellular Systems
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25A48D24-B435-11E9-9278-68D0E5697425
grant_number: ALTF 1396-2014
name: Molecular and system level view of immune cell migration
publication: The Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Microtubules control cellular shape and coherence in amoeboid migrating cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 219
year: '2020'
...
---
_id: '7876'
abstract:
- lang: eng
text: 'In contrast to lymph nodes, the lymphoid regions of the spleen—the white
pulp—are located deep within the organ, yielding the trafficking paths of T cells
in the white pulp largely invisible. In an intravital microscopy tour de force
reported in this issue of Immunity, Chauveau et al. show that T cells perform
unidirectional, perivascular migration through the enigmatic marginal zone bridging
channels. '
article_processing_charge: No
article_type: original
author:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Tim
full_name: Lämmermann, Tim
last_name: Lämmermann
citation:
ama: 'Sixt MK, Lämmermann T. T cells: Bridge-and-channel commute to the white pulp.
Immunity. 2020;52(5):721-723. doi:10.1016/j.immuni.2020.04.020'
apa: 'Sixt, M. K., & Lämmermann, T. (2020). T cells: Bridge-and-channel commute
to the white pulp. Immunity. Elsevier. https://doi.org/10.1016/j.immuni.2020.04.020'
chicago: 'Sixt, Michael K, and Tim Lämmermann. “T Cells: Bridge-and-Channel Commute
to the White Pulp.” Immunity. Elsevier, 2020. https://doi.org/10.1016/j.immuni.2020.04.020.'
ieee: 'M. K. Sixt and T. Lämmermann, “T cells: Bridge-and-channel commute to the
white pulp,” Immunity, vol. 52, no. 5. Elsevier, pp. 721–723, 2020.'
ista: 'Sixt MK, Lämmermann T. 2020. T cells: Bridge-and-channel commute to the white
pulp. Immunity. 52(5), 721–723.'
mla: 'Sixt, Michael K., and Tim Lämmermann. “T Cells: Bridge-and-Channel Commute
to the White Pulp.” Immunity, vol. 52, no. 5, Elsevier, 2020, pp. 721–23,
doi:10.1016/j.immuni.2020.04.020.'
short: M.K. Sixt, T. Lämmermann, Immunity 52 (2020) 721–723.
date_created: 2020-05-24T22:00:57Z
date_published: 2020-05-19T00:00:00Z
date_updated: 2023-08-21T06:27:18Z
day: '19'
department:
- _id: MiSi
doi: 10.1016/j.immuni.2020.04.020
external_id:
isi:
- '000535371100002'
intvolume: ' 52'
isi: 1
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://pure.mpg.de/pubman/item/item_3265599_2/component/file_3265620/Sixt%20et%20al..pdf
month: '05'
oa: 1
oa_version: Published Version
page: 721-723
publication: Immunity
publication_identifier:
eissn:
- '10974180'
issn:
- '10747613'
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'T cells: Bridge-and-channel commute to the white pulp'
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 52
year: '2020'
...
---
_id: '7909'
abstract:
- lang: eng
text: Cell migration entails networks and bundles of actin filaments termed lamellipodia
and microspikes or filopodia, respectively, as well as focal adhesions, all of
which recruit Ena/VASP family members hitherto thought to antagonize efficient
cell motility. However, we find these proteins to act as positive regulators of
migration in different murine cell lines. CRISPR/Cas9-mediated loss of Ena/VASP
proteins reduced lamellipodial actin assembly and perturbed lamellipodial architecture,
as evidenced by changed network geometry as well as reduction of filament length
and number that was accompanied by abnormal Arp2/3 complex and heterodimeric capping
protein accumulation. Loss of Ena/VASP function also abolished the formation of
microspikes normally embedded in lamellipodia, but not of filopodia capable of
emanating without lamellipodia. Ena/VASP-deficiency also impaired integrin-mediated
adhesion accompanied by reduced traction forces exerted through these structures.
Our data thus uncover novel Ena/VASP functions of these actin polymerases that
are fully consistent with their promotion of cell migration.
article_number: e55351
article_processing_charge: No
article_type: original
author:
- first_name: Julia
full_name: Damiano-Guercio, Julia
last_name: Damiano-Guercio
- first_name: Laëtitia
full_name: Kurzawa, Laëtitia
last_name: Kurzawa
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Georgi A
full_name: Dimchev, Georgi A
id: 38C393BE-F248-11E8-B48F-1D18A9856A87
last_name: Dimchev
orcid: 0000-0001-8370-6161
- first_name: Matthias
full_name: Schaks, Matthias
last_name: Schaks
- first_name: Maria
full_name: Nemethova, Maria
id: 34E27F1C-F248-11E8-B48F-1D18A9856A87
last_name: Nemethova
- first_name: Thomas
full_name: Pokrant, Thomas
last_name: Pokrant
- first_name: Stefan
full_name: Brühmann, Stefan
last_name: Brühmann
- first_name: Joern
full_name: Linkner, Joern
last_name: Linkner
- first_name: Laurent
full_name: Blanchoin, Laurent
last_name: Blanchoin
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Jan
full_name: Faix, Jan
last_name: Faix
citation:
ama: Damiano-Guercio J, Kurzawa L, Müller J, et al. Loss of Ena/VASP interferes
with lamellipodium architecture, motility and integrin-dependent adhesion. eLife.
2020;9. doi:10.7554/eLife.55351
apa: Damiano-Guercio, J., Kurzawa, L., Müller, J., Dimchev, G. A., Schaks, M., Nemethova,
M., … Faix, J. (2020). Loss of Ena/VASP interferes with lamellipodium architecture,
motility and integrin-dependent adhesion. ELife. eLife Sciences Publications.
https://doi.org/10.7554/eLife.55351
chicago: Damiano-Guercio, Julia, Laëtitia Kurzawa, Jan Müller, Georgi A Dimchev,
Matthias Schaks, Maria Nemethova, Thomas Pokrant, et al. “Loss of Ena/VASP Interferes
with Lamellipodium Architecture, Motility and Integrin-Dependent Adhesion.” ELife.
eLife Sciences Publications, 2020. https://doi.org/10.7554/eLife.55351.
ieee: J. Damiano-Guercio et al., “Loss of Ena/VASP interferes with lamellipodium
architecture, motility and integrin-dependent adhesion,” eLife, vol. 9.
eLife Sciences Publications, 2020.
ista: Damiano-Guercio J, Kurzawa L, Müller J, Dimchev GA, Schaks M, Nemethova M,
Pokrant T, Brühmann S, Linkner J, Blanchoin L, Sixt MK, Rottner K, Faix J. 2020.
Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent
adhesion. eLife. 9, e55351.
mla: Damiano-Guercio, Julia, et al. “Loss of Ena/VASP Interferes with Lamellipodium
Architecture, Motility and Integrin-Dependent Adhesion.” ELife, vol. 9,
e55351, eLife Sciences Publications, 2020, doi:10.7554/eLife.55351.
short: J. Damiano-Guercio, L. Kurzawa, J. Müller, G.A. Dimchev, M. Schaks, M. Nemethova,
T. Pokrant, S. Brühmann, J. Linkner, L. Blanchoin, M.K. Sixt, K. Rottner, J. Faix,
ELife 9 (2020).
date_created: 2020-05-31T22:00:49Z
date_published: 2020-05-11T00:00:00Z
date_updated: 2023-08-21T06:32:25Z
day: '11'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.7554/eLife.55351
ec_funded: 1
external_id:
isi:
- '000537208000001'
file:
- access_level: open_access
checksum: d33bd4441b9a0195718ce1ba5d2c48a6
content_type: application/pdf
creator: dernst
date_created: 2020-06-02T10:35:37Z
date_updated: 2020-07-14T12:48:05Z
file_id: '7914'
file_name: 2020_eLife_Damiano_Guercio.pdf
file_size: 10535713
relation: main_file
file_date_updated: 2020-07-14T12:48:05Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
publication: eLife
publication_identifier:
eissn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent
adhesion
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 9
year: '2020'
...
---
_id: '8132'
abstract:
- lang: eng
text: The WAVE regulatory complex (WRC) is crucial for assembly of the peripheral
branched actin network constituting one of the main drivers of eukaryotic cell
migration. Here, we uncover an essential role of the hematopoietic-specific WRC
component HEM1 for immune cell development. Germline-encoded HEM1 deficiency underlies
an inborn error of immunity with systemic autoimmunity, at cellular level marked
by WRC destabilization, reduced filamentous actin, and failure to assemble lamellipodia.
Hem1−/− mice display systemic autoimmunity, phenocopying the human disease. In
the absence of Hem1, B cells become deprived of extracellular stimuli necessary
to maintain the strength of B cell receptor signaling at a level permissive for
survival of non-autoreactive B cells. This shifts the balance of B cell fate choices
toward autoreactive B cells and thus autoimmunity.
article_number: eabc3979
article_processing_charge: No
article_type: original
author:
- first_name: Elisabeth
full_name: Salzer, Elisabeth
last_name: Salzer
- first_name: Samaneh
full_name: Zoghi, Samaneh
last_name: Zoghi
- first_name: Máté G.
full_name: Kiss, Máté G.
last_name: Kiss
- first_name: Frieda
full_name: Kage, Frieda
last_name: Kage
- first_name: Christina
full_name: Rashkova, Christina
last_name: Rashkova
- first_name: Stephanie
full_name: Stahnke, Stephanie
last_name: Stahnke
- first_name: Matthias
full_name: Haimel, Matthias
last_name: Haimel
- first_name: René
full_name: Platzer, René
last_name: Platzer
- first_name: Michael
full_name: Caldera, Michael
last_name: Caldera
- first_name: Rico Chandra
full_name: Ardy, Rico Chandra
last_name: Ardy
- first_name: Birgit
full_name: Hoeger, Birgit
last_name: Hoeger
- first_name: Jana
full_name: Block, Jana
last_name: Block
- first_name: David
full_name: Medgyesi, David
last_name: Medgyesi
- first_name: Celine
full_name: Sin, Celine
last_name: Sin
- first_name: Sepideh
full_name: Shahkarami, Sepideh
last_name: Shahkarami
- first_name: Renate
full_name: Kain, Renate
last_name: Kain
- first_name: Vahid
full_name: Ziaee, Vahid
last_name: Ziaee
- first_name: Peter
full_name: Hammerl, Peter
last_name: Hammerl
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
- first_name: Jörg
full_name: Menche, Jörg
last_name: Menche
- first_name: Loïc
full_name: Dupré, Loïc
last_name: Dupré
- first_name: Johannes B.
full_name: Huppa, Johannes B.
last_name: Huppa
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Alexis
full_name: Lomakin, Alexis
last_name: Lomakin
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Christoph J.
full_name: Binder, Christoph J.
last_name: Binder
- first_name: Theresia E.B.
full_name: Stradal, Theresia E.B.
last_name: Stradal
- first_name: Nima
full_name: Rezaei, Nima
last_name: Rezaei
- first_name: Kaan
full_name: Boztug, Kaan
last_name: Boztug
citation:
ama: Salzer E, Zoghi S, Kiss MG, et al. The cytoskeletal regulator HEM1 governs
B cell development and prevents autoimmunity. Science Immunology. 2020;5(49).
doi:10.1126/sciimmunol.abc3979
apa: Salzer, E., Zoghi, S., Kiss, M. G., Kage, F., Rashkova, C., Stahnke, S., …
Boztug, K. (2020). The cytoskeletal regulator HEM1 governs B cell development
and prevents autoimmunity. Science Immunology. AAAS. https://doi.org/10.1126/sciimmunol.abc3979
chicago: Salzer, Elisabeth, Samaneh Zoghi, Máté G. Kiss, Frieda Kage, Christina
Rashkova, Stephanie Stahnke, Matthias Haimel, et al. “The Cytoskeletal Regulator
HEM1 Governs B Cell Development and Prevents Autoimmunity.” Science Immunology.
AAAS, 2020. https://doi.org/10.1126/sciimmunol.abc3979.
ieee: E. Salzer et al., “The cytoskeletal regulator HEM1 governs B cell development
and prevents autoimmunity,” Science Immunology, vol. 5, no. 49. AAAS, 2020.
ista: Salzer E, Zoghi S, Kiss MG, Kage F, Rashkova C, Stahnke S, Haimel M, Platzer
R, Caldera M, Ardy RC, Hoeger B, Block J, Medgyesi D, Sin C, Shahkarami S, Kain
R, Ziaee V, Hammerl P, Bock C, Menche J, Dupré L, Huppa JB, Sixt MK, Lomakin A,
Rottner K, Binder CJ, Stradal TEB, Rezaei N, Boztug K. 2020. The cytoskeletal
regulator HEM1 governs B cell development and prevents autoimmunity. Science Immunology.
5(49), eabc3979.
mla: Salzer, Elisabeth, et al. “The Cytoskeletal Regulator HEM1 Governs B Cell Development
and Prevents Autoimmunity.” Science Immunology, vol. 5, no. 49, eabc3979,
AAAS, 2020, doi:10.1126/sciimmunol.abc3979.
short: E. Salzer, S. Zoghi, M.G. Kiss, F. Kage, C. Rashkova, S. Stahnke, M. Haimel,
R. Platzer, M. Caldera, R.C. Ardy, B. Hoeger, J. Block, D. Medgyesi, C. Sin, S.
Shahkarami, R. Kain, V. Ziaee, P. Hammerl, C. Bock, J. Menche, L. Dupré, J.B.
Huppa, M.K. Sixt, A. Lomakin, K. Rottner, C.J. Binder, T.E.B. Stradal, N. Rezaei,
K. Boztug, Science Immunology 5 (2020).
date_created: 2020-07-19T22:00:58Z
date_published: 2020-07-10T00:00:00Z
date_updated: 2023-08-22T07:56:04Z
day: '10'
department:
- _id: MiSi
doi: 10.1126/sciimmunol.abc3979
external_id:
isi:
- '000546994600004'
pmid:
- '32646852'
intvolume: ' 5'
isi: 1
issue: '49'
language:
- iso: eng
month: '07'
oa_version: None
pmid: 1
publication: Science Immunology
publication_identifier:
eissn:
- '24709468'
publication_status: published
publisher: AAAS
quality_controlled: '1'
scopus_import: '1'
status: public
title: The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 5
year: '2020'
...
---
_id: '8787'
abstract:
- lang: eng
text: Breakdown of vascular barriers is a major complication of inflammatory diseases.
Anucleate platelets form blood-clots during thrombosis, but also play a crucial
role in inflammation. While spatio-temporal dynamics of clot formation are well
characterized, the cell-biological mechanisms of platelet recruitment to inflammatory
micro-environments remain incompletely understood. Here we identify Arp2/3-dependent
lamellipodia formation as a prominent morphological feature of immune-responsive
platelets. Platelets use lamellipodia to scan for fibrin(ogen) deposited on the
inflamed vasculature and to directionally spread, to polarize and to govern haptotactic
migration along gradients of the adhesive ligand. Platelet-specific abrogation
of Arp2/3 interferes with haptotactic repositioning of platelets to microlesions,
thus impairing vascular sealing and provoking inflammatory microbleeding. During
infection, haptotaxis promotes capture of bacteria and prevents hematogenic dissemination,
rendering platelets gate-keepers of the inflamed microvasculature. Consequently,
these findings identify haptotaxis as a key effector function of immune-responsive
platelets.
acknowledgement: "We thank Sebastian Helmer, Nicole Blount, Christine Mann, and Beate
Jantz for technical assistance; Hellen Ishikawa-Ankerhold for help and advice; Michael
Sixt for critical\r\ndiscussions. This study was supported by the DFG SFB 914 (S.M.
[B02 and Z01], K.Sch.\r\n[B02], B.W. [A02 and Z03], C.A.R. [B03], C.S. [A10], J.P.
[Gerok position]), the DFG\r\nSFB 1123 (S.M. [B06]), the DFG FOR 2033 (S.M. and
F.G.), the German Center for\r\nCardiovascular Research (DZHK) (Clinician Scientist
Program [L.N.], MHA 1.4VD\r\n[S.M.], Postdoc Start-up Grant, 81×3600213 [F.G.]),
FP7 program (project 260309,\r\nPRESTIGE [S.M.]), FöFoLe project 1015/1009 (L.N.),
FöFoLe project 947 (F.G.), the\r\nFriedrich-Baur-Stiftung project 41/16 (F.G.),
and LMUexcellence NFF (F.G.). This project has received funding from the European
Research Council (ERC) under the European Union’s Horizon 2020 research and innovation
program (grant agreement no.\r\n833440) (S.M.). F.G. received funding from the European
Union’s Horizon 2020 research\r\nand innovation program under the Marie Skłodowska-Curie
grant agreement no.\r\n747687."
article_number: '5778'
article_processing_charge: No
article_type: original
author:
- first_name: Leo
full_name: Nicolai, Leo
last_name: Nicolai
- first_name: Karin
full_name: Schiefelbein, Karin
last_name: Schiefelbein
- first_name: Silvia
full_name: Lipsky, Silvia
last_name: Lipsky
- first_name: Alexander
full_name: Leunig, Alexander
last_name: Leunig
- first_name: Marie
full_name: Hoffknecht, Marie
last_name: Hoffknecht
- first_name: Kami
full_name: Pekayvaz, Kami
last_name: Pekayvaz
- first_name: Ben
full_name: Raude, Ben
last_name: Raude
- first_name: Charlotte
full_name: Marx, Charlotte
last_name: Marx
- first_name: Andreas
full_name: Ehrlich, Andreas
last_name: Ehrlich
- first_name: Joachim
full_name: Pircher, Joachim
last_name: Pircher
- first_name: Zhe
full_name: Zhang, Zhe
last_name: Zhang
- first_name: Inas
full_name: Saleh, Inas
last_name: Saleh
- first_name: Anna-Kristina
full_name: Marel, Anna-Kristina
last_name: Marel
- first_name: Achim
full_name: Löf, Achim
last_name: Löf
- first_name: Tobias
full_name: Petzold, Tobias
last_name: Petzold
- first_name: Michael
full_name: Lorenz, Michael
last_name: Lorenz
- first_name: Konstantin
full_name: Stark, Konstantin
last_name: Stark
- first_name: Robert
full_name: Pick, Robert
last_name: Pick
- first_name: Gerhild
full_name: Rosenberger, Gerhild
last_name: Rosenberger
- first_name: Ludwig
full_name: Weckbach, Ludwig
last_name: Weckbach
- first_name: Bernd
full_name: Uhl, Bernd
last_name: Uhl
- first_name: Sheng
full_name: Xia, Sheng
last_name: Xia
- first_name: Christoph Andreas
full_name: Reichel, Christoph Andreas
last_name: Reichel
- first_name: Barbara
full_name: Walzog, Barbara
last_name: Walzog
- first_name: Christian
full_name: Schulz, Christian
last_name: Schulz
- first_name: Vanessa
full_name: Zheden, Vanessa
id: 39C5A68A-F248-11E8-B48F-1D18A9856A87
last_name: Zheden
orcid: 0000-0002-9438-4783
- first_name: Markus
full_name: Bender, Markus
last_name: Bender
- first_name: Rong
full_name: Li, Rong
last_name: Li
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
citation:
ama: Nicolai L, Schiefelbein K, Lipsky S, et al. Vascular surveillance by haptotactic
blood platelets in inflammation and infection. Nature Communications. 2020;11.
doi:10.1038/s41467-020-19515-0
apa: Nicolai, L., Schiefelbein, K., Lipsky, S., Leunig, A., Hoffknecht, M., Pekayvaz,
K., … Gärtner, F. R. (2020). Vascular surveillance by haptotactic blood platelets
in inflammation and infection. Nature Communications. Springer Nature.
https://doi.org/10.1038/s41467-020-19515-0
chicago: Nicolai, Leo, Karin Schiefelbein, Silvia Lipsky, Alexander Leunig, Marie
Hoffknecht, Kami Pekayvaz, Ben Raude, et al. “Vascular Surveillance by Haptotactic
Blood Platelets in Inflammation and Infection.” Nature Communications.
Springer Nature, 2020. https://doi.org/10.1038/s41467-020-19515-0.
ieee: L. Nicolai et al., “Vascular surveillance by haptotactic blood platelets
in inflammation and infection,” Nature Communications, vol. 11. Springer
Nature, 2020.
ista: Nicolai L, Schiefelbein K, Lipsky S, Leunig A, Hoffknecht M, Pekayvaz K, Raude
B, Marx C, Ehrlich A, Pircher J, Zhang Z, Saleh I, Marel A-K, Löf A, Petzold T,
Lorenz M, Stark K, Pick R, Rosenberger G, Weckbach L, Uhl B, Xia S, Reichel CA,
Walzog B, Schulz C, Zheden V, Bender M, Li R, Massberg S, Gärtner FR. 2020. Vascular
surveillance by haptotactic blood platelets in inflammation and infection. Nature
Communications. 11, 5778.
mla: Nicolai, Leo, et al. “Vascular Surveillance by Haptotactic Blood Platelets
in Inflammation and Infection.” Nature Communications, vol. 11, 5778, Springer
Nature, 2020, doi:10.1038/s41467-020-19515-0.
short: L. Nicolai, K. Schiefelbein, S. Lipsky, A. Leunig, M. Hoffknecht, K. Pekayvaz,
B. Raude, C. Marx, A. Ehrlich, J. Pircher, Z. Zhang, I. Saleh, A.-K. Marel, A.
Löf, T. Petzold, M. Lorenz, K. Stark, R. Pick, G. Rosenberger, L. Weckbach, B.
Uhl, S. Xia, C.A. Reichel, B. Walzog, C. Schulz, V. Zheden, M. Bender, R. Li,
S. Massberg, F.R. Gärtner, Nature Communications 11 (2020).
date_created: 2020-11-22T23:01:23Z
date_published: 2020-11-13T00:00:00Z
date_updated: 2023-08-22T13:26:26Z
day: '13'
ddc:
- '570'
department:
- _id: MiSi
- _id: EM-Fac
doi: 10.1038/s41467-020-19515-0
ec_funded: 1
external_id:
isi:
- '000594648000014'
pmid:
- '33188196'
file:
- access_level: open_access
checksum: 485b7b6cf30198ba0ce126491a28f125
content_type: application/pdf
creator: dernst
date_created: 2020-11-23T13:29:49Z
date_updated: 2020-11-23T13:29:49Z
file_id: '8798'
file_name: 2020_NatureComm_Nicolai.pdf
file_size: 7035340
relation: main_file
success: 1
file_date_updated: 2020-11-23T13:29:49Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Nature Communications
publication_identifier:
eissn:
- '20411723'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1038/s41467-022-31310-7
scopus_import: '1'
status: public
title: Vascular surveillance by haptotactic blood platelets in inflammation and infection
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2020'
...
---
_id: '8142'
abstract:
- lang: eng
text: Cell production and differentiation for the acquisition of specific functions
are key features of living systems. The dynamic network of cellular microtubules
provides the necessary platform to accommodate processes associated with the transition
of cells through the individual phases of cytogenesis. Here, we show that the
plant hormone cytokinin fine‐tunes the activity of the microtubular cytoskeleton
during cell differentiation and counteracts microtubular rearrangements driven
by the hormone auxin. The endogenous upward gradient of cytokinin activity along
the longitudinal growth axis in Arabidopsis thaliana roots correlates with robust
rearrangements of the microtubule cytoskeleton in epidermal cells progressing
from the proliferative to the differentiation stage. Controlled increases in cytokinin
activity result in premature re‐organization of the microtubule network from transversal
to an oblique disposition in cells prior to their differentiation, whereas attenuated
hormone perception delays cytoskeleton conversion into a configuration typical
for differentiated cells. Intriguingly, cytokinin can interfere with microtubules
also in animal cells, such as leukocytes, suggesting that a cytokinin‐sensitive
control pathway for the microtubular cytoskeleton may be at least partially conserved
between plant and animal cells.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
acknowledgement: We thank Takashi Aoyama, David Alabadi, and Bert De Rybel for sharing
material, Jiří Friml, Maciek Adamowski, and Katerina Schwarzerová for inspiring
discussions, and Martine De Cock for help in preparing the manuscript. This research
was supported by the Scientific Service Units (SSUs) of IST Austria through resources
provided by the Bioimaging Facility (BIF), especially to Robert Hauschild; and the
Life Science Facility (LSF). J.C.M. is the recipient of a EMBO Long‐Term Fellowship
(ALTF number 710‐2016). This work was supported with MEYS CR, project no.CZ.02.1.01/0.0/0.0/16_019/0000738
to J.P., and by the Austrian Science Fund (FWF01_I1774S) to E.B.
article_number: e104238
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Juan C
full_name: Montesinos López, Juan C
id: 310A8E3E-F248-11E8-B48F-1D18A9856A87
last_name: Montesinos López
orcid: 0000-0001-9179-6099
- first_name: A
full_name: Abuzeineh, A
last_name: Abuzeineh
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- first_name: Alba
full_name: Juanes Garcia, Alba
id: 40F05888-F248-11E8-B48F-1D18A9856A87
last_name: Juanes Garcia
orcid: 0000-0002-1009-9652
- first_name: Krisztina
full_name: Ötvös, Krisztina
id: 29B901B0-F248-11E8-B48F-1D18A9856A87
last_name: Ötvös
orcid: 0000-0002-5503-4983
- first_name: J
full_name: Petrášek, J
last_name: Petrášek
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
citation:
ama: Montesinos López JC, Abuzeineh A, Kopf A, et al. Phytohormone cytokinin guides
microtubule dynamics during cell progression from proliferative to differentiated
stage. The Embo Journal. 2020;39(17). doi:10.15252/embj.2019104238
apa: Montesinos López, J. C., Abuzeineh, A., Kopf, A., Juanes Garcia, A., Ötvös,
K., Petrášek, J., … Benková, E. (2020). Phytohormone cytokinin guides microtubule
dynamics during cell progression from proliferative to differentiated stage. The
Embo Journal. Embo Press. https://doi.org/10.15252/embj.2019104238
chicago: Montesinos López, Juan C, A Abuzeineh, Aglaja Kopf, Alba Juanes Garcia,
Krisztina Ötvös, J Petrášek, Michael K Sixt, and Eva Benková. “Phytohormone Cytokinin
Guides Microtubule Dynamics during Cell Progression from Proliferative to Differentiated
Stage.” The Embo Journal. Embo Press, 2020. https://doi.org/10.15252/embj.2019104238.
ieee: J. C. Montesinos López et al., “Phytohormone cytokinin guides microtubule
dynamics during cell progression from proliferative to differentiated stage,”
The Embo Journal, vol. 39, no. 17. Embo Press, 2020.
ista: Montesinos López JC, Abuzeineh A, Kopf A, Juanes Garcia A, Ötvös K, Petrášek
J, Sixt MK, Benková E. 2020. Phytohormone cytokinin guides microtubule dynamics
during cell progression from proliferative to differentiated stage. The Embo Journal.
39(17), e104238.
mla: Montesinos López, Juan C., et al. “Phytohormone Cytokinin Guides Microtubule
Dynamics during Cell Progression from Proliferative to Differentiated Stage.”
The Embo Journal, vol. 39, no. 17, e104238, Embo Press, 2020, doi:10.15252/embj.2019104238.
short: J.C. Montesinos López, A. Abuzeineh, A. Kopf, A. Juanes Garcia, K. Ötvös,
J. Petrášek, M.K. Sixt, E. Benková, The Embo Journal 39 (2020).
date_created: 2020-07-21T09:08:38Z
date_published: 2020-09-01T00:00:00Z
date_updated: 2023-09-05T13:05:47Z
day: '01'
ddc:
- '580'
department:
- _id: MiSi
- _id: EvBe
doi: 10.15252/embj.2019104238
external_id:
isi:
- '000548311800001'
pmid:
- '32667089'
file:
- access_level: open_access
checksum: 43d2b36598708e6ab05c69074e191d57
content_type: application/pdf
creator: dernst
date_created: 2020-12-02T09:13:23Z
date_updated: 2020-12-02T09:13:23Z
file_id: '8827'
file_name: 2020_EMBO_Montesinos.pdf
file_size: 3497156
relation: main_file
success: 1
file_date_updated: 2020-12-02T09:13:23Z
has_accepted_license: '1'
intvolume: ' 39'
isi: 1
issue: '17'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 253E54C8-B435-11E9-9278-68D0E5697425
grant_number: ALTF710-2016
name: Molecular mechanism of auxindriven formative divisions delineating lateral
root organogenesis in plants
- _id: 2542D156-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I 1774-B16
name: Hormone cross-talk drives nutrient dependent plant development
publication: The Embo Journal
publication_identifier:
eissn:
- 1460-2075
issn:
- 0261-4189
publication_status: published
publisher: Embo Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Phytohormone cytokinin guides microtubule dynamics during cell progression
from proliferative to differentiated stage
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 39
year: '2020'
...
---
_id: '7885'
abstract:
- lang: eng
text: Eukaryotic cells migrate by coupling the intracellular force of the actin
cytoskeleton to the environment. While force coupling is usually mediated by transmembrane
adhesion receptors, especially those of the integrin family, amoeboid cells such
as leukocytes can migrate extremely fast despite very low adhesive forces1. Here
we show that leukocytes cannot only migrate under low adhesion but can also transmit
forces in the complete absence of transmembrane force coupling. When confined
within three-dimensional environments, they use the topographical features of
the substrate to propel themselves. Here the retrograde flow of the actin cytoskeleton
follows the texture of the substrate, creating retrograde shear forces that are
sufficient to drive the cell body forwards. Notably, adhesion-dependent and adhesion-independent
migration are not mutually exclusive, but rather are variants of the same principle
of coupling retrograde actin flow to the environment and thus can potentially
operate interchangeably and simultaneously. As adhesion-free migration is independent
of the chemical composition of the environment, it renders cells completely autonomous
in their locomotive behaviour.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: M-Shop
acknowledgement: We thank A. Leithner and J. Renkawitz for discussion and critical
reading of the manuscript; J. Schwarz and M. Mehling for establishing the microfluidic
setups; the Bioimaging Facility of IST Austria for excellent support, as well as
the Life Science Facility and the Miba Machine Shop of IST Austria; and F. N. Arslan,
L. E. Burnett and L. Li for their work during their rotation in the IST PhD programme.
This work was supported by the European Research Council (ERC StG 281556 and CoG
724373) to M.S. and grants from the Austrian Science Fund (FWF P29911) and the WWTF
to M.S. M.H. was supported by the European Regional Development Fund Project (CZ.02.1.01/0.0/0.0/15_003/0000476).
F.G. received funding from the European Union’s Horizon 2020 research and innovation
programme under the Marie Skłodowska-Curie grant agreement no. 747687.
article_processing_charge: No
article_type: original
author:
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Julian A
full_name: Stopp, Julian A
id: 489E3F00-F248-11E8-B48F-1D18A9856A87
last_name: Stopp
- first_name: Saren
full_name: Tasciyan, Saren
id: 4323B49C-F248-11E8-B48F-1D18A9856A87
last_name: Tasciyan
orcid: 0000-0003-1671-393X
- first_name: Juan L
full_name: Aguilera Servin, Juan L
id: 2A67C376-F248-11E8-B48F-1D18A9856A87
last_name: Aguilera Servin
orcid: 0000-0002-2862-8372
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Matthieu
full_name: Piel, Matthieu
last_name: Piel
- first_name: Andrew
full_name: Callan-Jones, Andrew
last_name: Callan-Jones
- first_name: Raphael
full_name: Voituriez, Raphael
last_name: Voituriez
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Reversat A, Gärtner FR, Merrin J, et al. Cellular locomotion using environmental
topography. Nature. 2020;582:582–585. doi:10.1038/s41586-020-2283-z
apa: Reversat, A., Gärtner, F. R., Merrin, J., Stopp, J. A., Tasciyan, S., Aguilera
Servin, J. L., … Sixt, M. K. (2020). Cellular locomotion using environmental topography.
Nature. Springer Nature. https://doi.org/10.1038/s41586-020-2283-z
chicago: Reversat, Anne, Florian R Gärtner, Jack Merrin, Julian A Stopp, Saren Tasciyan,
Juan L Aguilera Servin, Ingrid de Vries, et al. “Cellular Locomotion Using Environmental
Topography.” Nature. Springer Nature, 2020. https://doi.org/10.1038/s41586-020-2283-z.
ieee: A. Reversat et al., “Cellular locomotion using environmental topography,”
Nature, vol. 582. Springer Nature, pp. 582–585, 2020.
ista: Reversat A, Gärtner FR, Merrin J, Stopp JA, Tasciyan S, Aguilera Servin JL,
de Vries I, Hauschild R, Hons M, Piel M, Callan-Jones A, Voituriez R, Sixt MK.
2020. Cellular locomotion using environmental topography. Nature. 582, 582–585.
mla: Reversat, Anne, et al. “Cellular Locomotion Using Environmental Topography.”
Nature, vol. 582, Springer Nature, 2020, pp. 582–585, doi:10.1038/s41586-020-2283-z.
short: A. Reversat, F.R. Gärtner, J. Merrin, J.A. Stopp, S. Tasciyan, J.L. Aguilera
Servin, I. de Vries, R. Hauschild, M. Hons, M. Piel, A. Callan-Jones, R. Voituriez,
M.K. Sixt, Nature 582 (2020) 582–585.
date_created: 2020-05-24T22:01:01Z
date_published: 2020-06-25T00:00:00Z
date_updated: 2024-03-28T23:30:24Z
day: '25'
department:
- _id: NanoFab
- _id: Bio
- _id: MiSi
doi: 10.1038/s41586-020-2283-z
ec_funded: 1
external_id:
isi:
- '000532688300008'
intvolume: ' 582'
isi: 1
language:
- iso: eng
month: '06'
oa_version: None
page: 582–585
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
- _id: 26018E70-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29911
name: Mechanical adaptation of lamellipodial actin
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Nature
publication_identifier:
eissn:
- '14764687'
issn:
- '00280836'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/off-road-mode-enables-mobile-cells-to-move-freely/
record:
- id: '14697'
relation: dissertation_contains
status: public
- id: '12401'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Cellular locomotion using environmental topography
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 582
year: '2020'
...
---
_id: '8190'
article_number: e202007029
article_processing_charge: No
article_type: letter_note
author:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Anna
full_name: Huttenlocher, Anna
last_name: Huttenlocher
citation:
ama: 'Sixt MK, Huttenlocher A. Zena Werb (1945-2020): Cell biology in context. The
Journal of Cell Biology. 2020;219(8). doi:10.1083/jcb.202007029'
apa: 'Sixt, M. K., & Huttenlocher, A. (2020). Zena Werb (1945-2020): Cell biology
in context. The Journal of Cell Biology. Rockefeller University Press.
https://doi.org/10.1083/jcb.202007029'
chicago: 'Sixt, Michael K, and Anna Huttenlocher. “Zena Werb (1945-2020): Cell Biology
in Context.” The Journal of Cell Biology. Rockefeller University Press,
2020. https://doi.org/10.1083/jcb.202007029.'
ieee: 'M. K. Sixt and A. Huttenlocher, “Zena Werb (1945-2020): Cell biology in context,”
The Journal of Cell Biology, vol. 219, no. 8. Rockefeller University Press,
2020.'
ista: 'Sixt MK, Huttenlocher A. 2020. Zena Werb (1945-2020): Cell biology in context.
The Journal of Cell Biology. 219(8), e202007029.'
mla: 'Sixt, Michael K., and Anna Huttenlocher. “Zena Werb (1945-2020): Cell Biology
in Context.” The Journal of Cell Biology, vol. 219, no. 8, e202007029,
Rockefeller University Press, 2020, doi:10.1083/jcb.202007029.'
short: M.K. Sixt, A. Huttenlocher, The Journal of Cell Biology 219 (2020).
date_created: 2020-08-02T22:00:57Z
date_published: 2020-07-22T00:00:00Z
date_updated: 2023-10-17T10:04:49Z
day: '22'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1083/jcb.202007029
external_id:
isi:
- '000573631000004'
file:
- access_level: open_access
checksum: 30016d778d266b8e17d01094917873b8
content_type: application/pdf
creator: dernst
date_created: 2020-08-04T13:11:52Z
date_updated: 2021-02-02T23:30:03Z
embargo: 2021-02-01
file_id: '8200'
file_name: 2020_JCB_Sixt.pdf
file_size: 830725
relation: main_file
file_date_updated: 2021-02-02T23:30:03Z
has_accepted_license: '1'
intvolume: ' 219'
isi: 1
issue: '8'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
publication: The Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
publication_status: published
publisher: Rockefeller University Press
scopus_import: '1'
status: public
title: 'Zena Werb (1945-2020): Cell biology in context'
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 219
year: '2020'
...
---
_id: '6824'
abstract:
- lang: eng
text: Platelets are small anucleate cellular fragments that are released by megakaryocytes
and safeguard vascular integrity through a process termed ‘haemostasis’. However,
platelets have important roles beyond haemostasis as they contribute to the initiation
and coordination of intravascular immune responses. They continuously monitor
blood vessel integrity and tightly coordinate vascular trafficking and functions
of multiple cell types. In this way platelets act as ‘patrolling officers of the
vascular highway’ that help to establish effective immune responses to infections
and cancer. Here we discuss the distinct biological features of platelets that
allow them to shape immune responses to pathogens and tumour cells, highlighting
the parallels between these responses.
article_processing_charge: No
article_type: original
author:
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
citation:
ama: 'Gärtner FR, Massberg S. Patrolling the vascular borders: Platelets in immunity
to infection and cancer. Nature Reviews Immunology. 2019;19(12):747–760.
doi:10.1038/s41577-019-0202-z'
apa: 'Gärtner, F. R., & Massberg, S. (2019). Patrolling the vascular borders:
Platelets in immunity to infection and cancer. Nature Reviews Immunology.
Springer Nature. https://doi.org/10.1038/s41577-019-0202-z'
chicago: 'Gärtner, Florian R, and Steffen Massberg. “Patrolling the Vascular Borders:
Platelets in Immunity to Infection and Cancer.” Nature Reviews Immunology.
Springer Nature, 2019. https://doi.org/10.1038/s41577-019-0202-z.'
ieee: 'F. R. Gärtner and S. Massberg, “Patrolling the vascular borders: Platelets
in immunity to infection and cancer,” Nature Reviews Immunology, vol. 19,
no. 12. Springer Nature, pp. 747–760, 2019.'
ista: 'Gärtner FR, Massberg S. 2019. Patrolling the vascular borders: Platelets
in immunity to infection and cancer. Nature Reviews Immunology. 19(12), 747–760.'
mla: 'Gärtner, Florian R., and Steffen Massberg. “Patrolling the Vascular Borders:
Platelets in Immunity to Infection and Cancer.” Nature Reviews Immunology,
vol. 19, no. 12, Springer Nature, 2019, pp. 747–760, doi:10.1038/s41577-019-0202-z.'
short: F.R. Gärtner, S. Massberg, Nature Reviews Immunology 19 (2019) 747–760.
date_created: 2019-08-20T17:24:32Z
date_published: 2019-12-01T00:00:00Z
date_updated: 2023-08-29T07:16:14Z
day: '01'
department:
- _id: MiSi
doi: 10.1038/s41577-019-0202-z
ec_funded: 1
external_id:
isi:
- '000499090600011'
pmid:
- '31409920'
intvolume: ' 19'
isi: 1
issue: '12'
language:
- iso: eng
month: '12'
oa_version: None
page: 747–760
pmid: 1
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Nature Reviews Immunology
publication_identifier:
eissn:
- 1474-1741
issn:
- 1474-1733
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Patrolling the vascular borders: Platelets in immunity to infection and cancer'
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 19
year: '2019'
...
---
_id: '7009'
abstract:
- lang: eng
text: Cell migration is essential for physiological processes as diverse as development,
immune defence and wound healing. It is also a hallmark of cancer malignancy.
Thousands of publications have elucidated detailed molecular and biophysical mechanisms
of cultured cells migrating on flat, 2D substrates of glass and plastic. However,
much less is known about how cells successfully navigate the complex 3D environments
of living tissues. In these more complex, native environments, cells use multiple
modes of migration, including mesenchymal, amoeboid, lobopodial and collective,
and these are governed by the local extracellular microenvironment, specific modalities
of Rho GTPase signalling and non- muscle myosin contractility. Migration through
3D environments is challenging because it requires the cell to squeeze through
complex or dense extracellular structures. Doing so requires specific cellular
adaptations to mechanical features of the extracellular matrix (ECM) or its remodelling.
In addition, besides navigating through diverse ECM environments and overcoming
extracellular barriers, cells often interact with neighbouring cells and tissues
through physical and signalling interactions. Accordingly, cells need to call
on an impressively wide diversity of mechanisms to meet these challenges. This
Review examines how cells use both classical and novel mechanisms of locomotion
as they traverse challenging 3D matrices and cellular environments. It focuses
on principles rather than details of migratory mechanisms and draws comparisons
between 1D, 2D and 3D migration.
article_processing_charge: No
article_type: review
author:
- first_name: KM
full_name: Yamada, KM
last_name: Yamada
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Yamada K, Sixt MK. Mechanisms of 3D cell migration. Nature Reviews Molecular
Cell Biology. 2019;20(12):738–752. doi:10.1038/s41580-019-0172-9
apa: Yamada, K., & Sixt, M. K. (2019). Mechanisms of 3D cell migration. Nature
Reviews Molecular Cell Biology. Springer Nature. https://doi.org/10.1038/s41580-019-0172-9
chicago: Yamada, KM, and Michael K Sixt. “Mechanisms of 3D Cell Migration.” Nature
Reviews Molecular Cell Biology. Springer Nature, 2019. https://doi.org/10.1038/s41580-019-0172-9.
ieee: K. Yamada and M. K. Sixt, “Mechanisms of 3D cell migration,” Nature Reviews
Molecular Cell Biology, vol. 20, no. 12. Springer Nature, pp. 738–752, 2019.
ista: Yamada K, Sixt MK. 2019. Mechanisms of 3D cell migration. Nature Reviews Molecular
Cell Biology. 20(12), 738–752.
mla: Yamada, KM, and Michael K. Sixt. “Mechanisms of 3D Cell Migration.” Nature
Reviews Molecular Cell Biology, vol. 20, no. 12, Springer Nature, 2019, pp.
738–752, doi:10.1038/s41580-019-0172-9.
short: K. Yamada, M.K. Sixt, Nature Reviews Molecular Cell Biology 20 (2019) 738–752.
date_created: 2019-11-12T14:54:42Z
date_published: 2019-12-01T00:00:00Z
date_updated: 2023-08-30T07:22:20Z
day: '01'
department:
- _id: MiSi
doi: 10.1038/s41580-019-0172-9
external_id:
isi:
- '000497966900007'
pmid:
- '31582855'
intvolume: ' 20'
isi: 1
issue: '12'
language:
- iso: eng
month: '12'
oa_version: None
page: 738–752
pmid: 1
publication: Nature Reviews Molecular Cell Biology
publication_identifier:
eissn:
- 1471-0080
issn:
- 1471-0072
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mechanisms of 3D cell migration
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 20
year: '2019'
...
---
_id: '6988'
abstract:
- lang: eng
text: 'Platelets are central players in thrombosis and hemostasis but are increasingly
recognized as key components of the immune system. They shape ensuing immune responses
by recruiting leukocytes, and support the development of adaptive immunity. Recent
data shed new light on the complex role of platelets in immunity. Here, we summarize
experimental and clinical data on the role of platelets in host defense against
bacteria. Platelets bind, contain, and kill bacteria directly; however, platelet
proinflammatory effector functions and cross-talk with the coagulation system,
can also result in damage to the host (e.g., acute lung injury and sepsis). Novel
clinical insights support this dichotomy: platelet inhibition/thrombocytopenia
can be either harmful or protective, depending on pathophysiological context.
Clinical studies are currently addressing this aspect in greater depth.'
article_processing_charge: No
article_type: review
author:
- first_name: Leo
full_name: Nicolai, Leo
last_name: Nicolai
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
citation:
ama: 'Nicolai L, Gärtner FR, Massberg S. Platelets in host defense: Experimental
and clinical insights. Trends in Immunology. 2019;40(10):922-938. doi:10.1016/j.it.2019.08.004'
apa: 'Nicolai, L., Gärtner, F. R., & Massberg, S. (2019). Platelets in host
defense: Experimental and clinical insights. Trends in Immunology. Cell
Press. https://doi.org/10.1016/j.it.2019.08.004'
chicago: 'Nicolai, Leo, Florian R Gärtner, and Steffen Massberg. “Platelets in Host
Defense: Experimental and Clinical Insights.” Trends in Immunology. Cell
Press, 2019. https://doi.org/10.1016/j.it.2019.08.004.'
ieee: 'L. Nicolai, F. R. Gärtner, and S. Massberg, “Platelets in host defense: Experimental
and clinical insights,” Trends in Immunology, vol. 40, no. 10. Cell Press,
pp. 922–938, 2019.'
ista: 'Nicolai L, Gärtner FR, Massberg S. 2019. Platelets in host defense: Experimental
and clinical insights. Trends in Immunology. 40(10), 922–938.'
mla: 'Nicolai, Leo, et al. “Platelets in Host Defense: Experimental and Clinical
Insights.” Trends in Immunology, vol. 40, no. 10, Cell Press, 2019, pp.
922–38, doi:10.1016/j.it.2019.08.004.'
short: L. Nicolai, F.R. Gärtner, S. Massberg, Trends in Immunology 40 (2019) 922–938.
date_created: 2019-11-04T16:27:36Z
date_published: 2019-10-01T00:00:00Z
date_updated: 2023-08-30T07:19:23Z
day: '01'
department:
- _id: MiSi
doi: 10.1016/j.it.2019.08.004
ec_funded: 1
external_id:
isi:
- '000493292100005'
pmid:
- '31601520'
intvolume: ' 40'
isi: 1
issue: '10'
language:
- iso: eng
month: '10'
oa_version: None
page: 922-938
pmid: 1
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Trends in Immunology
publication_identifier:
issn:
- 1471-4906
publication_status: published
publisher: Cell Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Platelets in host defense: Experimental and clinical insights'
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 40
year: '2019'
...
---
_id: '6979'
article_processing_charge: No
article_type: original
author:
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Kopf A, Sixt MK. Gut homeostasis: Active migration of intestinal epithelial
cells in tissue renewal. Current Biology. 2019;29(20):R1091-R1093. doi:10.1016/j.cub.2019.08.068'
apa: 'Kopf, A., & Sixt, M. K. (2019). Gut homeostasis: Active migration of intestinal
epithelial cells in tissue renewal. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2019.08.068'
chicago: 'Kopf, Aglaja, and Michael K Sixt. “Gut Homeostasis: Active Migration of
Intestinal Epithelial Cells in Tissue Renewal.” Current Biology. Cell Press,
2019. https://doi.org/10.1016/j.cub.2019.08.068.'
ieee: 'A. Kopf and M. K. Sixt, “Gut homeostasis: Active migration of intestinal
epithelial cells in tissue renewal,” Current Biology, vol. 29, no. 20.
Cell Press, pp. R1091–R1093, 2019.'
ista: 'Kopf A, Sixt MK. 2019. Gut homeostasis: Active migration of intestinal epithelial
cells in tissue renewal. Current Biology. 29(20), R1091–R1093.'
mla: 'Kopf, Aglaja, and Michael K. Sixt. “Gut Homeostasis: Active Migration of Intestinal
Epithelial Cells in Tissue Renewal.” Current Biology, vol. 29, no. 20,
Cell Press, 2019, pp. R1091–93, doi:10.1016/j.cub.2019.08.068.'
short: A. Kopf, M.K. Sixt, Current Biology 29 (2019) R1091–R1093.
date_created: 2019-11-04T15:18:29Z
date_published: 2019-10-21T00:00:00Z
date_updated: 2023-09-05T12:43:43Z
day: '21'
department:
- _id: MiSi
doi: 10.1016/j.cub.2019.08.068
external_id:
isi:
- '000491286200016'
pmid:
- '31639357'
intvolume: ' 29'
isi: 1
issue: '20'
language:
- iso: eng
month: '10'
oa_version: None
page: R1091-R1093
pmid: 1
publication: Current Biology
publication_identifier:
eissn:
- 1879-0445
issn:
- 0960-9822
publication_status: published
publisher: Cell Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Gut homeostasis: Active migration of intestinal epithelial cells in tissue
renewal'
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 29
year: '2019'
...
---
_id: '7105'
abstract:
- lang: eng
text: Cell migration is hypothesized to involve a cycle of behaviours beginning
with leading edge extension. However, recent evidence suggests that the leading
edge may be dispensable for migration, raising the question of what actually controls
cell directionality. Here, we exploit the embryonic migration of Drosophila macrophages
to bridge the different temporal scales of the behaviours controlling motility.
This approach reveals that edge fluctuations during random motility are not persistent
and are weakly correlated with motion. In contrast, flow of the actin network
behind the leading edge is highly persistent. Quantification of actin flow structure
during migration reveals a stable organization and asymmetry in the cell-wide
flowfield that strongly correlates with cell directionality. This organization
is regulated by a gradient of actin network compression and destruction, which
is controlled by myosin contraction and cofilin-mediated disassembly. It is this
stable actin-flow polarity, which integrates rapid fluctuations of the leading
edge, that controls inherent cellular persistence.
article_processing_charge: No
article_type: original
author:
- first_name: Lawrence
full_name: Yolland, Lawrence
last_name: Yolland
- first_name: Mubarik
full_name: Burki, Mubarik
last_name: Burki
- first_name: Stefania
full_name: Marcotti, Stefania
last_name: Marcotti
- first_name: Andrei
full_name: Luchici, Andrei
last_name: Luchici
- first_name: Fiona N.
full_name: Kenny, Fiona N.
last_name: Kenny
- first_name: John Robert
full_name: Davis, John Robert
last_name: Davis
- first_name: Eduardo
full_name: Serna-Morales, Eduardo
last_name: Serna-Morales
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Andrew
full_name: Davidson, Andrew
last_name: Davidson
- first_name: Will
full_name: Wood, Will
last_name: Wood
- first_name: Linus J.
full_name: Schumacher, Linus J.
last_name: Schumacher
- first_name: Robert G.
full_name: Endres, Robert G.
last_name: Endres
- first_name: Mark
full_name: Miodownik, Mark
last_name: Miodownik
- first_name: Brian M.
full_name: Stramer, Brian M.
last_name: Stramer
citation:
ama: Yolland L, Burki M, Marcotti S, et al. Persistent and polarized global actin
flow is essential for directionality during cell migration. Nature Cell Biology.
2019;21(11):1370-1381. doi:10.1038/s41556-019-0411-5
apa: Yolland, L., Burki, M., Marcotti, S., Luchici, A., Kenny, F. N., Davis, J.
R., … Stramer, B. M. (2019). Persistent and polarized global actin flow is essential
for directionality during cell migration. Nature Cell Biology. Springer
Nature. https://doi.org/10.1038/s41556-019-0411-5
chicago: Yolland, Lawrence, Mubarik Burki, Stefania Marcotti, Andrei Luchici, Fiona
N. Kenny, John Robert Davis, Eduardo Serna-Morales, et al. “Persistent and Polarized
Global Actin Flow Is Essential for Directionality during Cell Migration.” Nature
Cell Biology. Springer Nature, 2019. https://doi.org/10.1038/s41556-019-0411-5.
ieee: L. Yolland et al., “Persistent and polarized global actin flow is essential
for directionality during cell migration,” Nature Cell Biology, vol. 21,
no. 11. Springer Nature, pp. 1370–1381, 2019.
ista: Yolland L, Burki M, Marcotti S, Luchici A, Kenny FN, Davis JR, Serna-Morales
E, Müller J, Sixt MK, Davidson A, Wood W, Schumacher LJ, Endres RG, Miodownik
M, Stramer BM. 2019. Persistent and polarized global actin flow is essential for
directionality during cell migration. Nature Cell Biology. 21(11), 1370–1381.
mla: Yolland, Lawrence, et al. “Persistent and Polarized Global Actin Flow Is Essential
for Directionality during Cell Migration.” Nature Cell Biology, vol. 21,
no. 11, Springer Nature, 2019, pp. 1370–81, doi:10.1038/s41556-019-0411-5.
short: L. Yolland, M. Burki, S. Marcotti, A. Luchici, F.N. Kenny, J.R. Davis, E.
Serna-Morales, J. Müller, M.K. Sixt, A. Davidson, W. Wood, L.J. Schumacher, R.G.
Endres, M. Miodownik, B.M. Stramer, Nature Cell Biology 21 (2019) 1370–1381.
date_created: 2019-11-25T08:55:00Z
date_published: 2019-11-01T00:00:00Z
date_updated: 2023-09-06T11:08:52Z
day: '01'
department:
- _id: MiSi
doi: 10.1038/s41556-019-0411-5
external_id:
isi:
- '000495888300009'
pmid:
- '31685997'
intvolume: ' 21'
isi: 1
issue: '11'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7025891
month: '11'
oa: 1
oa_version: Submitted Version
page: 1370-1381
pmid: 1
publication: Nature Cell Biology
publication_identifier:
eissn:
- 1476-4679
issn:
- 1465-7392
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Persistent and polarized global actin flow is essential for directionality
during cell migration
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 21
year: '2019'
...
---
_id: '7420'
abstract:
- lang: eng
text: β1-integrins mediate cell–matrix interactions and their trafficking is important
in the dynamic regulation of cell adhesion, migration and malignant processes,
including cancer cell invasion. Here, we employ an RNAi screen to characterize
regulators of integrin traffic and identify the association of Golgi-localized
gamma ear-containing Arf-binding protein 2 (GGA2) with β1-integrin, and its role
in recycling of active but not inactive β1-integrin receptors. Silencing of GGA2
limits active β1-integrin levels in focal adhesions and decreases cancer cell
migration and invasion, which is in agreement with its ability to regulate the
dynamics of active integrins. By using the proximity-dependent biotin identification
(BioID) method, we identified two RAB family small GTPases, i.e. RAB13 and RAB10,
as novel interactors of GGA2. Functionally, RAB13 silencing triggers the intracellular
accumulation of active β1-integrin, and reduces integrin activity in focal adhesions
and cell migration similarly to GGA2 depletion, indicating that both facilitate
active β1-integrin recycling to the plasma membrane. Thus, GGA2 and RAB13 are
important specificity determinants for integrin activity-dependent traffic.
article_number: jcs233387
article_processing_charge: No
article_type: original
author:
- first_name: Pranshu
full_name: Sahgal, Pranshu
last_name: Sahgal
- first_name: Jonna H
full_name: Alanko, Jonna H
id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87
last_name: Alanko
orcid: 0000-0002-7698-3061
- first_name: Jaroslav
full_name: Icha, Jaroslav
last_name: Icha
- first_name: Ilkka
full_name: Paatero, Ilkka
last_name: Paatero
- first_name: Hellyeh
full_name: Hamidi, Hellyeh
last_name: Hamidi
- first_name: Antti
full_name: Arjonen, Antti
last_name: Arjonen
- first_name: Mika
full_name: Pietilä, Mika
last_name: Pietilä
- first_name: Anne
full_name: Rokka, Anne
last_name: Rokka
- first_name: Johanna
full_name: Ivaska, Johanna
last_name: Ivaska
citation:
ama: Sahgal P, Alanko JH, Icha J, et al. GGA2 and RAB13 promote activity-dependent
β1-integrin recycling. Journal of Cell Science. 2019;132(11). doi:10.1242/jcs.233387
apa: Sahgal, P., Alanko, J. H., Icha, J., Paatero, I., Hamidi, H., Arjonen, A.,
… Ivaska, J. (2019). GGA2 and RAB13 promote activity-dependent β1-integrin recycling.
Journal of Cell Science. The Company of Biologists. https://doi.org/10.1242/jcs.233387
chicago: Sahgal, Pranshu, Jonna H Alanko, Jaroslav Icha, Ilkka Paatero, Hellyeh
Hamidi, Antti Arjonen, Mika Pietilä, Anne Rokka, and Johanna Ivaska. “GGA2 and
RAB13 Promote Activity-Dependent Β1-Integrin Recycling.” Journal of Cell Science.
The Company of Biologists, 2019. https://doi.org/10.1242/jcs.233387.
ieee: P. Sahgal et al., “GGA2 and RAB13 promote activity-dependent β1-integrin
recycling,” Journal of Cell Science, vol. 132, no. 11. The Company of Biologists,
2019.
ista: Sahgal P, Alanko JH, Icha J, Paatero I, Hamidi H, Arjonen A, Pietilä M, Rokka
A, Ivaska J. 2019. GGA2 and RAB13 promote activity-dependent β1-integrin recycling.
Journal of Cell Science. 132(11), jcs233387.
mla: Sahgal, Pranshu, et al. “GGA2 and RAB13 Promote Activity-Dependent Β1-Integrin
Recycling.” Journal of Cell Science, vol. 132, no. 11, jcs233387, The Company
of Biologists, 2019, doi:10.1242/jcs.233387.
short: P. Sahgal, J.H. Alanko, J. Icha, I. Paatero, H. Hamidi, A. Arjonen, M. Pietilä,
A. Rokka, J. Ivaska, Journal of Cell Science 132 (2019).
date_created: 2020-01-30T10:31:42Z
date_published: 2019-06-07T00:00:00Z
date_updated: 2023-09-06T15:01:00Z
day: '07'
department:
- _id: MiSi
doi: 10.1242/jcs.233387
external_id:
isi:
- '000473327900017'
pmid:
- '31076515'
intvolume: ' 132'
isi: 1
issue: '11'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1242/jcs.233387
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Cell Science
publication_identifier:
eissn:
- 1477-9137
issn:
- 0021-9533
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
status: public
title: GGA2 and RAB13 promote activity-dependent β1-integrin recycling
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 132
year: '2019'
...
---
_id: '7404'
abstract:
- lang: eng
text: The formation of neuronal dendrite branches is fundamental for the wiring
and function of the nervous system. Indeed, dendrite branching enhances the coverage
of the neuron's receptive field and modulates the initial processing of incoming
stimuli. Complex dendrite patterns are achieved in vivo through a dynamic process
of de novo branch formation, branch extension and retraction. The first step towards
branch formation is the generation of a dynamic filopodium-like branchlet. The
mechanisms underlying the initiation of dendrite branchlets are therefore crucial
to the shaping of dendrites. Through in vivo time-lapse imaging of the subcellular
localization of actin during the process of branching of Drosophila larva sensory
neurons, combined with genetic analysis and electron tomography, we have identified
the Actin-related protein (Arp) 2/3 complex as the major actin nucleator involved
in the initiation of dendrite branchlet formation, under the control of the activator
WAVE and of the small GTPase Rac1. Transient recruitment of an Arp2/3 component
marks the site of branchlet initiation in vivo. These data position the activation
of Arp2/3 as an early hub for the initiation of branchlet formation.
article_number: dev171397
article_processing_charge: No
article_type: original
author:
- first_name: Tomke
full_name: Stürner, Tomke
last_name: Stürner
- first_name: Anastasia
full_name: Tatarnikova, Anastasia
last_name: Tatarnikova
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Barbara
full_name: Schaffran, Barbara
last_name: Schaffran
- first_name: Hermann
full_name: Cuntz, Hermann
last_name: Cuntz
- first_name: Yun
full_name: Zhang, Yun
last_name: Zhang
- first_name: Maria
full_name: Nemethova, Maria
id: 34E27F1C-F248-11E8-B48F-1D18A9856A87
last_name: Nemethova
- first_name: Sven
full_name: Bogdan, Sven
last_name: Bogdan
- first_name: Vic
full_name: Small, Vic
last_name: Small
- first_name: Gaia
full_name: Tavosanis, Gaia
last_name: Tavosanis
citation:
ama: Stürner T, Tatarnikova A, Müller J, et al. Transient localization of the Arp2/3
complex initiates neuronal dendrite branching in vivo. Development. 2019;146(7).
doi:10.1242/dev.171397
apa: Stürner, T., Tatarnikova, A., Müller, J., Schaffran, B., Cuntz, H., Zhang,
Y., … Tavosanis, G. (2019). Transient localization of the Arp2/3 complex initiates
neuronal dendrite branching in vivo. Development. The Company of Biologists.
https://doi.org/10.1242/dev.171397
chicago: Stürner, Tomke, Anastasia Tatarnikova, Jan Müller, Barbara Schaffran, Hermann
Cuntz, Yun Zhang, Maria Nemethova, Sven Bogdan, Vic Small, and Gaia Tavosanis.
“Transient Localization of the Arp2/3 Complex Initiates Neuronal Dendrite Branching
in Vivo.” Development. The Company of Biologists, 2019. https://doi.org/10.1242/dev.171397.
ieee: T. Stürner et al., “Transient localization of the Arp2/3 complex initiates
neuronal dendrite branching in vivo,” Development, vol. 146, no. 7. The
Company of Biologists, 2019.
ista: Stürner T, Tatarnikova A, Müller J, Schaffran B, Cuntz H, Zhang Y, Nemethova
M, Bogdan S, Small V, Tavosanis G. 2019. Transient localization of the Arp2/3
complex initiates neuronal dendrite branching in vivo. Development. 146(7), dev171397.
mla: Stürner, Tomke, et al. “Transient Localization of the Arp2/3 Complex Initiates
Neuronal Dendrite Branching in Vivo.” Development, vol. 146, no. 7, dev171397,
The Company of Biologists, 2019, doi:10.1242/dev.171397.
short: T. Stürner, A. Tatarnikova, J. Müller, B. Schaffran, H. Cuntz, Y. Zhang,
M. Nemethova, S. Bogdan, V. Small, G. Tavosanis, Development 146 (2019).
date_created: 2020-01-29T16:27:10Z
date_published: 2019-04-04T00:00:00Z
date_updated: 2023-09-07T14:47:00Z
day: '04'
department:
- _id: MiSi
doi: 10.1242/dev.171397
external_id:
isi:
- '000464583200006'
pmid:
- '30910826'
intvolume: ' 146'
isi: 1
issue: '7'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1242/dev.171397
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
publication: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Transient localization of the Arp2/3 complex initiates neuronal dendrite branching
in vivo
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 146
year: '2019'
...
---
_id: '6947'
abstract:
- lang: eng
text: Lymph nodes are es s ential organs of the immune s ys tem where adaptive
immune responses originate, and consist of various leukocyte populations and a
stromal backbone. Fibroblastic reticular cells (FRCs) are the main stromal cells
and form a sponge-like extracellular matrix network, called conduits , which they thems
elves enwrap and contract. Lymph, containing s oluble antigens , arrive
in lymph nodes via afferent lymphatic vessels that connect to the s ubcaps
ular s inus and conduit network. According to the current paradigm, the conduit network dis
tributes afferent lymph through lymph nodes and thus provides acces
s for immune cells to lymph-borne antigens. An elas tic caps ule s urrounds the organ and confines the
immune cells and FRC network. Lymph nodes are completely packed with lymphocytes and lymphocyte numbers directly dictates the
size of the organ. Although lymphocytes cons tantly enter and leave the lymph node, its s
ize remains remarkedly s table under homeostatic conditions. It is only
partly known how the cellularity and s ize of the lymph node is regulated and how the lymph node is
able to swell in inflammation. The role of the FRC network in lymph node s
welling and trans fer of fluids are inves tigated in this thes is. Furthermore, we s
tudied what trafficking routes are us ed by cancer cells in lymph nodes to form distal
metastases.We examined the role of a mechanical feedback in regulation of lymph node
swelling. Using parallel plate compression and UV-las er cutting experiments we dis
s ected the mechanical force dynamics of the whole lymph node, and individually
for FRCs and the caps ule. Physical forces generated by packed lymphocytes directly affect the tens
ion on the FRC network and capsule, which increases its resistance to swelling. This implies a feedback mechanism between tis
s ue pres s ure and ability of lymphocytes to enter the organ. Following inflammation, the lymph node swells
∼10 fold in two weeks . Yet, what is the role for tens ion on the FRC network and caps
ule, and how are lymphocytes able to enter in conditions that resist
swelling remain open ques tions . We s how that tens ion on the FRC network is important
to limit the swelling rate of the organ so that the FRC network can grow in a coordinated fashion.
This is illustrated by interfering with FRC contractility, which leads to faster
swelling rates and a dis organized FRC network in the inflamed lymph node.
Growth of the FRC network in turn is expected to releas e tens ion on thes
e s tructures and lowers the res is tance to swelling, thereby allowing
more lymphocytes to enter the organ and drive more swelling. Halt of swelling
coincides with a thickening of the caps ule, which forms a thick res
is tant band around the organ and lowers tens ion on the FRC network to form
a new force equilibrium.The FRC and conduit network are further believed to be a privileged s
ite of s oluble information within the lymph node, although many details remain uns
olved. We s how by 3D ultra-recons truction that FRCs and antigen pres
enting cells cover the s urface of conduit s ys tem for more than 99%
and we dis cus s the implications for s oluble information exchangeat the conduit
level.Finally, there is an ongoing debate in the cancer field whether and how
cancer cells in lymph nodes s eed dis tal metas tas es . We s how that cancer cells infus
ed into the lymph node can utilize trafficking routes of immune cells and rapidly migrate to blood vessels.
Once in the blood circulation, these cells are able to form metastases in
distal tissues.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
- _id: EM-Fac
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
citation:
ama: 'Assen FP. Lymph node mechanics: Deciphering the interplay between stroma contractility,
morphology and lymphocyte trafficking. 2019. doi:10.15479/AT:ISTA:6947'
apa: 'Assen, F. P. (2019). Lymph node mechanics: Deciphering the interplay between
stroma contractility, morphology and lymphocyte trafficking. Institute of
Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:6947'
chicago: 'Assen, Frank P. “Lymph Node Mechanics: Deciphering the Interplay between
Stroma Contractility, Morphology and Lymphocyte Trafficking.” Institute of Science
and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6947.'
ieee: 'F. P. Assen, “Lymph node mechanics: Deciphering the interplay between stroma
contractility, morphology and lymphocyte trafficking,” Institute of Science and
Technology Austria, 2019.'
ista: 'Assen FP. 2019. Lymph node mechanics: Deciphering the interplay between stroma
contractility, morphology and lymphocyte trafficking. Institute of Science and
Technology Austria.'
mla: 'Assen, Frank P. Lymph Node Mechanics: Deciphering the Interplay between
Stroma Contractility, Morphology and Lymphocyte Trafficking. Institute of
Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:6947.'
short: 'F.P. Assen, Lymph Node Mechanics: Deciphering the Interplay between Stroma
Contractility, Morphology and Lymphocyte Trafficking, Institute of Science and
Technology Austria, 2019.'
date_created: 2019-10-14T16:54:52Z
date_published: 2019-10-09T00:00:00Z
date_updated: 2023-09-13T08:50:57Z
day: '9'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:6947
file:
- access_level: closed
checksum: 53a739752a500f84d0f8ec953cbbd0b6
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: fassen
date_created: 2019-11-06T12:30:02Z
date_updated: 2020-11-07T23:30:03Z
embargo_to: open_access
file_id: '6990'
file_name: PhDthesis_FrankAssen_revised2.docx
file_size: 214172667
relation: source_file
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checksum: 8c156b65d9347bb599623a4b09f15d15
content_type: application/pdf
creator: fassen
date_created: 2019-11-06T12:30:57Z
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file_id: '6991'
file_name: PhDthesis_FrankAssen_revised2.pdf
file_size: 83637532
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file_date_updated: 2020-11-07T23:30:03Z
has_accepted_license: '1'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: '142'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '664'
relation: part_of_dissertation
status: public
- id: '402'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: 'Lymph node mechanics: Deciphering the interplay between stroma contractility,
morphology and lymphocyte trafficking'
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2019'
...
---
_id: '6891'
abstract:
- lang: eng
text: "While cells of mesenchymal or epithelial origin perform their effector functions
in a purely anchorage dependent manner, cells derived from the hematopoietic lineage
are not committed to operate only within a specific niche. Instead, these cells
are able to function autonomously of the molecular composition in a broad range
of tissue compartments. By this means, cells of the hematopoietic lineage retain
the capacity to disseminate into connective tissue and recirculate between organs,
building the foundation for essential processes such as tissue regeneration or
immune surveillance. \r\nCells of the immune system, specifically leukocytes,
are extraordinarily good at performing this task. These cells are able to flexibly
shift their mode of migration between an adhesion-mediated and an adhesion-independent
manner, instantaneously accommodating for any changes in molecular composition
of the external scaffold. The key component driving directed leukocyte migration
is the chemokine receptor 7, which guides the cell along gradients of chemokine
ligand. Therefore, the physical destination of migrating leukocytes is purely
deterministic, i.e. given by global directional cues such as chemokine gradients.
\r\nNevertheless, these cells typically reside in three-dimensional scaffolds
of inhomogeneous complexity, raising the question whether cells are able to locally
discriminate between multiple optional migration routes. Current literature provides
evidence that leukocytes, specifically dendritic cells, do indeed probe their
surrounding by virtue of multiple explorative protrusions. However, it remains
enigmatic how these cells decide which one is the more favorable route to follow
and what are the key players involved in performing this task. Due to the heterogeneous
environment of most tissues, and the vast adaptability of migrating leukocytes,
at this time it is not clear to what extent leukocytes are able to optimize their
migratory strategy by adapting their level of adhesiveness. And, given the fact
that leukocyte migration is characterized by branched cell shapes in combination
with high migration velocities, it is reasonable to assume that these cells require
fine tuned shape maintenance mechanisms that tightly coordinate protrusion and
adhesion dynamics in a spatiotemporal manner. \r\nTherefore, this study aimed
to elucidate how rapidly migrating leukocytes opt for an ideal migratory path
while maintaining a continuous cell shape and balancing adhesive forces to efficiently
navigate through complex microenvironments. \r\nThe results of this study unraveled
a role for the microtubule cytoskeleton in promoting the decision making process
during path finding and for the first time point towards a microtubule-mediated
function in cell shape maintenance of highly ramified cells such as dendritic
cells. Furthermore, we found that migrating low-adhesive leukocytes are able to
instantaneously adapt to increased tensile load by engaging adhesion receptors.
This response was only occurring tangential to the substrate while adhesive properties
in the vertical direction were not increased. As leukocytes are primed for rapid
migration velocities, these results demonstrate that leukocyte integrins are able
to confer a high level of traction forces parallel to the cell membrane along
the direction of migration without wasting energy in gluing the cell to the substrate.
\r\nThus, the data in the here presented thesis provide new insights into the
pivotal role of cytoskeletal dynamics and the mechanisms of force transduction
during leukocyte migration. \r\nThereby the here presented results help to further
define fundamental principles underlying leukocyte migration and open up potential
therapeutic avenues of clinical relevance.\r\n"
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
citation:
ama: Kopf A. The implication of cytoskeletal dynamics on leukocyte migration. 2019.
doi:10.15479/AT:ISTA:6891
apa: Kopf, A. (2019). The implication of cytoskeletal dynamics on leukocyte migration.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:6891
chicago: Kopf, Aglaja. “The Implication of Cytoskeletal Dynamics on Leukocyte Migration.”
Institute of Science and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6891.
ieee: A. Kopf, “The implication of cytoskeletal dynamics on leukocyte migration,”
Institute of Science and Technology Austria, 2019.
ista: Kopf A. 2019. The implication of cytoskeletal dynamics on leukocyte migration.
Institute of Science and Technology Austria.
mla: Kopf, Aglaja. The Implication of Cytoskeletal Dynamics on Leukocyte Migration.
Institute of Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:6891.
short: A. Kopf, The Implication of Cytoskeletal Dynamics on Leukocyte Migration,
Institute of Science and Technology Austria, 2019.
date_created: 2019-09-19T08:19:44Z
date_published: 2019-07-24T00:00:00Z
date_updated: 2023-10-18T08:49:17Z
day: '24'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:6891
file:
- access_level: closed
checksum: 00d100d6468e31e583051e0a006b640c
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: akopf
date_created: 2019-10-15T05:28:42Z
date_updated: 2020-10-17T22:30:03Z
embargo_to: open_access
file_id: '6950'
file_name: Kopf_PhD_Thesis.docx
file_size: 74735267
relation: source_file
- access_level: open_access
checksum: 5d1baa899993ae6ca81aebebe1797000
content_type: application/pdf
creator: akopf
date_created: 2019-10-15T05:28:47Z
date_updated: 2020-10-17T22:30:03Z
embargo: 2020-10-16
file_id: '6951'
file_name: Kopf_PhD_Thesis1.pdf
file_size: 52787224
relation: main_file
file_date_updated: 2020-10-17T22:30:03Z
has_accepted_license: '1'
keyword:
- cell biology
- immunology
- leukocyte
- migration
- microfluidics
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: '171'
project:
- _id: 265E2996-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W01250-B20
name: Nano-Analytics of Cellular Systems
publication_identifier:
eissn:
- 2663-337X
isbn:
- 978-3-99078-002-2
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
link:
- relation: press_release
url: https://ist.ac.at/en/news/feeling-like-a-cell/
record:
- id: '6328'
relation: part_of_dissertation
status: public
- id: '15'
relation: part_of_dissertation
status: public
- id: '6877'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: The implication of cytoskeletal dynamics on leukocyte migration
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2019'
...
---
_id: '6328'
abstract:
- lang: eng
text: During metazoan development, immune surveillance and cancer dissemination,
cells migrate in complex three-dimensional microenvironments1,2,3. These spaces
are crowded by cells and extracellular matrix, generating mazes with differently
sized gaps that are typically smaller than the diameter of the migrating cell4,5.
Most mesenchymal and epithelial cells and some—but not all—cancer cells actively
generate their migratory path using pericellular tissue proteolysis6. By contrast,
amoeboid cells such as leukocytes use non-destructive strategies of locomotion7,
raising the question how these extremely fast cells navigate through dense tissues.
Here we reveal that leukocytes sample their immediate vicinity for large pore
sizes, and are thereby able to choose the path of least resistance. This allows
them to circumnavigate local obstacles while effectively following global directional
cues such as chemotactic gradients. Pore-size discrimination is facilitated by
frontward positioning of the nucleus, which enables the cells to use their bulkiest
compartment as a mechanical gauge. Once the nucleus and the closely associated
microtubule organizing centre pass the largest pore, cytoplasmic protrusions still
lingering in smaller pores are retracted. These retractions are coordinated by
dynamic microtubules; when microtubules are disrupted, migrating cells lose coherence
and frequently fragment into migratory cytoplasmic pieces. As nuclear positioning
in front of the microtubule organizing centre is a typical feature of amoeboid
migration, our findings link the fundamental organization of cellular polarity
to the strategy of locomotion.
acknowledged_ssus:
- _id: SSU
article_processing_charge: No
article_type: letter_note
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- first_name: Julian A
full_name: Stopp, Julian A
id: 489E3F00-F248-11E8-B48F-1D18A9856A87
last_name: Stopp
- first_name: Ingrid
full_name: de Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: de Vries
- first_name: Meghan K.
full_name: Driscoll, Meghan K.
last_name: Driscoll
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Erik S.
full_name: Welf, Erik S.
last_name: Welf
- first_name: Gaudenz
full_name: Danuser, Gaudenz
last_name: Danuser
- first_name: Reto
full_name: Fiolka, Reto
last_name: Fiolka
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Renkawitz J, Kopf A, Stopp JA, et al. Nuclear positioning facilitates amoeboid
migration along the path of least resistance. Nature. 2019;568:546-550.
doi:10.1038/s41586-019-1087-5
apa: Renkawitz, J., Kopf, A., Stopp, J. A., de Vries, I., Driscoll, M. K., Merrin,
J., … Sixt, M. K. (2019). Nuclear positioning facilitates amoeboid migration along
the path of least resistance. Nature. Springer Nature. https://doi.org/10.1038/s41586-019-1087-5
chicago: Renkawitz, Jörg, Aglaja Kopf, Julian A Stopp, Ingrid de Vries, Meghan K.
Driscoll, Jack Merrin, Robert Hauschild, et al. “Nuclear Positioning Facilitates
Amoeboid Migration along the Path of Least Resistance.” Nature. Springer
Nature, 2019. https://doi.org/10.1038/s41586-019-1087-5.
ieee: J. Renkawitz et al., “Nuclear positioning facilitates amoeboid migration
along the path of least resistance,” Nature, vol. 568. Springer Nature,
pp. 546–550, 2019.
ista: Renkawitz J, Kopf A, Stopp JA, de Vries I, Driscoll MK, Merrin J, Hauschild
R, Welf ES, Danuser G, Fiolka R, Sixt MK. 2019. Nuclear positioning facilitates
amoeboid migration along the path of least resistance. Nature. 568, 546–550.
mla: Renkawitz, Jörg, et al. “Nuclear Positioning Facilitates Amoeboid Migration
along the Path of Least Resistance.” Nature, vol. 568, Springer Nature,
2019, pp. 546–50, doi:10.1038/s41586-019-1087-5.
short: J. Renkawitz, A. Kopf, J.A. Stopp, I. de Vries, M.K. Driscoll, J. Merrin,
R. Hauschild, E.S. Welf, G. Danuser, R. Fiolka, M.K. Sixt, Nature 568 (2019) 546–550.
date_created: 2019-04-17T06:52:28Z
date_published: 2019-04-25T00:00:00Z
date_updated: 2024-03-28T23:30:40Z
day: '25'
department:
- _id: MiSi
- _id: NanoFab
- _id: Bio
doi: 10.1038/s41586-019-1087-5
ec_funded: 1
external_id:
isi:
- '000465594200050'
pmid:
- '30944468'
intvolume: ' 568'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217284/
month: '04'
oa: 1
oa_version: Submitted Version
page: 546-550
pmid: 1
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
- _id: 265FAEBA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W01250-B20
name: Nano-Analytics of Cellular Systems
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25A48D24-B435-11E9-9278-68D0E5697425
grant_number: ALTF 1396-2014
name: Molecular and system level view of immune cell migration
publication: Nature
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/leukocytes-use-their-nucleus-as-a-ruler-to-choose-path-of-least-resistance/
record:
- id: '14697'
relation: dissertation_contains
status: public
- id: '6891'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Nuclear positioning facilitates amoeboid migration along the path of least
resistance
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 568
year: '2019'
...
---
_id: '6877'
article_processing_charge: No
article_type: original
author:
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Kopf A, Sixt MK. The neural crest pitches in to remove apoptotic debris. Cell.
2019;179(1):51-53. doi:10.1016/j.cell.2019.08.047
apa: Kopf, A., & Sixt, M. K. (2019). The neural crest pitches in to remove apoptotic
debris. Cell. Elsevier. https://doi.org/10.1016/j.cell.2019.08.047
chicago: Kopf, Aglaja, and Michael K Sixt. “The Neural Crest Pitches in to Remove
Apoptotic Debris.” Cell. Elsevier, 2019. https://doi.org/10.1016/j.cell.2019.08.047.
ieee: A. Kopf and M. K. Sixt, “The neural crest pitches in to remove apoptotic debris,”
Cell, vol. 179, no. 1. Elsevier, pp. 51–53, 2019.
ista: Kopf A, Sixt MK. 2019. The neural crest pitches in to remove apoptotic debris.
Cell. 179(1), 51–53.
mla: Kopf, Aglaja, and Michael K. Sixt. “The Neural Crest Pitches in to Remove Apoptotic
Debris.” Cell, vol. 179, no. 1, Elsevier, 2019, pp. 51–53, doi:10.1016/j.cell.2019.08.047.
short: A. Kopf, M.K. Sixt, Cell 179 (2019) 51–53.
date_created: 2019-09-15T22:00:46Z
date_published: 2019-09-19T00:00:00Z
date_updated: 2024-03-28T23:30:40Z
day: '19'
department:
- _id: MiSi
doi: 10.1016/j.cell.2019.08.047
external_id:
isi:
- '000486618500011'
pmid:
- '31539498'
intvolume: ' 179'
isi: 1
issue: '1'
language:
- iso: eng
month: '09'
oa_version: None
page: 51-53
pmid: 1
publication: Cell
publication_identifier:
eissn:
- 1097-4172
issn:
- 0092-8674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
record:
- id: '6891'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: The neural crest pitches in to remove apoptotic debris
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 179
year: '2019'
...
---
_id: '6354'
abstract:
- lang: eng
text: Blood platelets are critical for hemostasis and thrombosis, but also play
diverse roles during immune responses. We have recently reported that platelets
migrate at sites of infection in vitro and in vivo. Importantly, platelets use
their ability to migrate to collect and bundle fibrin (ogen)-bound bacteria accomplishing
efficient intravascular bacterial trapping. Here, we describe a method that allows
analyzing platelet migration in vitro, focusing on their ability to collect bacteria
and trap bacteria under flow.
acknowledgement: ' FöFoLe project 947 (F.G.), the Friedrich-Baur-Stiftung project
41/16 (F.G.)'
article_number: e3018
author:
- first_name: Shuxia
full_name: Fan, Shuxia
last_name: Fan
- first_name: Michael
full_name: Lorenz, Michael
last_name: Lorenz
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
citation:
ama: Fan S, Lorenz M, Massberg S, Gärtner FR. Platelet migration and bacterial trapping
assay under flow. Bio-Protocol. 2018;8(18). doi:10.21769/bioprotoc.3018
apa: Fan, S., Lorenz, M., Massberg, S., & Gärtner, F. R. (2018). Platelet migration
and bacterial trapping assay under flow. Bio-Protocol. Bio-Protocol. https://doi.org/10.21769/bioprotoc.3018
chicago: Fan, Shuxia, Michael Lorenz, Steffen Massberg, and Florian R Gärtner. “Platelet
Migration and Bacterial Trapping Assay under Flow.” Bio-Protocol. Bio-Protocol,
2018. https://doi.org/10.21769/bioprotoc.3018.
ieee: S. Fan, M. Lorenz, S. Massberg, and F. R. Gärtner, “Platelet migration and
bacterial trapping assay under flow,” Bio-Protocol, vol. 8, no. 18. Bio-Protocol,
2018.
ista: Fan S, Lorenz M, Massberg S, Gärtner FR. 2018. Platelet migration and bacterial
trapping assay under flow. Bio-Protocol. 8(18), e3018.
mla: Fan, Shuxia, et al. “Platelet Migration and Bacterial Trapping Assay under
Flow.” Bio-Protocol, vol. 8, no. 18, e3018, Bio-Protocol, 2018, doi:10.21769/bioprotoc.3018.
short: S. Fan, M. Lorenz, S. Massberg, F.R. Gärtner, Bio-Protocol 8 (2018).
date_created: 2019-04-29T09:40:33Z
date_published: 2018-09-20T00:00:00Z
date_updated: 2021-01-12T08:07:12Z
day: '20'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.21769/bioprotoc.3018
ec_funded: 1
file:
- access_level: open_access
checksum: d4588377e789da7f360b553ae02c5119
content_type: application/pdf
creator: dernst
date_created: 2019-04-30T08:04:33Z
date_updated: 2020-07-14T12:47:28Z
file_id: '6360'
file_name: 2018_BioProtocol_Fan.pdf
file_size: 2928337
relation: main_file
file_date_updated: 2020-07-14T12:47:28Z
has_accepted_license: '1'
intvolume: ' 8'
issue: '18'
keyword:
- Platelets
- Cell migration
- Bacteria
- Shear flow
- Fibrinogen
- E. coli
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Bio-Protocol
publication_identifier:
issn:
- 2331-8325
publication_status: published
publisher: Bio-Protocol
quality_controlled: '1'
status: public
title: Platelet migration and bacterial trapping assay under flow
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2018'
...
---
_id: '318'
abstract:
- lang: eng
text: The insect’s fat body combines metabolic and immunological functions. In this
issue of Developmental Cell, Franz et al. (2018) show that in Drosophila, cells
of the fat body are not static, but can actively “swim” toward sites of epithelial
injury, where they physically clog the wound and locally secrete antimicrobial
peptides.
acknowledgement: Short Survey
article_processing_charge: No
author:
- first_name: Alessandra M
full_name: Casano, Alessandra M
id: 3DBA3F4E-F248-11E8-B48F-1D18A9856A87
last_name: Casano
orcid: 0000-0002-6009-6804
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Casano AM, Sixt MK. A fat lot of good for wound healing. Developmental Cell.
2018;44(4):405-406. doi:10.1016/j.devcel.2018.02.009
apa: Casano, A. M., & Sixt, M. K. (2018). A fat lot of good for wound healing.
Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2018.02.009
chicago: Casano, Alessandra M, and Michael K Sixt. “A Fat Lot of Good for Wound
Healing.” Developmental Cell. Cell Press, 2018. https://doi.org/10.1016/j.devcel.2018.02.009.
ieee: A. M. Casano and M. K. Sixt, “A fat lot of good for wound healing,” Developmental
Cell, vol. 44, no. 4. Cell Press, pp. 405–406, 2018.
ista: Casano AM, Sixt MK. 2018. A fat lot of good for wound healing. Developmental
Cell. 44(4), 405–406.
mla: Casano, Alessandra M., and Michael K. Sixt. “A Fat Lot of Good for Wound Healing.”
Developmental Cell, vol. 44, no. 4, Cell Press, 2018, pp. 405–06, doi:10.1016/j.devcel.2018.02.009.
short: A.M. Casano, M.K. Sixt, Developmental Cell 44 (2018) 405–406.
date_created: 2018-12-11T11:45:47Z
date_published: 2018-02-26T00:00:00Z
date_updated: 2023-09-08T11:42:28Z
day: '26'
department:
- _id: MiSi
doi: 10.1016/j.devcel.2018.02.009
external_id:
isi:
- '000426150700002'
pmid:
- '29486189'
intvolume: ' 44'
isi: 1
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/29486189
month: '02'
oa: 1
oa_version: Published Version
page: 405 - 406
pmid: 1
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '7547'
quality_controlled: '1'
scopus_import: '1'
status: public
title: A fat lot of good for wound healing
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 44
year: '2018'
...
---
_id: '308'
abstract:
- lang: eng
text: Migrating cells penetrate tissue barriers during development, inflammatory
responses, and tumor metastasis. We study if migration in vivo in such three-dimensionally
confined environments requires changes in the mechanical properties of the surrounding
cells using embryonic Drosophila melanogaster hemocytes, also called macrophages,
as a model. We find that macrophage invasion into the germband through transient
separation of the apposing ectoderm and mesoderm requires cell deformations and
reductions in apical tension in the ectoderm. Interestingly, the genetic pathway
governing these mechanical shifts acts downstream of the only known tumor necrosis
factor superfamily member in Drosophila, Eiger, and its receptor, Grindelwald.
Eiger-Grindelwald signaling reduces levels of active Myosin in the germband ectodermal
cortex through the localization of a Crumbs complex component, Patj (Pals-1-associated
tight junction protein). We therefore elucidate a distinct molecular pathway that
controls tissue tension and demonstrate the importance of such regulation for
invasive migration in vivo.
acknowledged_ssus:
- _id: SSU
article_processing_charge: No
article_type: original
author:
- first_name: Aparna
full_name: Ratheesh, Aparna
id: 2F064CFE-F248-11E8-B48F-1D18A9856A87
last_name: Ratheesh
orcid: 0000-0001-7190-0776
- first_name: Julia
full_name: Biebl, Julia
id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87
last_name: Biebl
- first_name: Michael
full_name: Smutny, Michael
last_name: Smutny
- first_name: Jana
full_name: Veselá, Jana
id: 433253EE-F248-11E8-B48F-1D18A9856A87
last_name: Veselá
- first_name: Ekaterina
full_name: Papusheva, Ekaterina
id: 41DB591E-F248-11E8-B48F-1D18A9856A87
last_name: Papusheva
- first_name: Gabriel
full_name: Krens, Gabriel
id: 2B819732-F248-11E8-B48F-1D18A9856A87
last_name: Krens
orcid: 0000-0003-4761-5996
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Alessandra M
full_name: Casano, Alessandra M
id: 3DBA3F4E-F248-11E8-B48F-1D18A9856A87
last_name: Casano
orcid: 0000-0002-6009-6804
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
citation:
ama: Ratheesh A, Bicher J, Smutny M, et al. Drosophila TNF modulates tissue tension
in the embryo to facilitate macrophage invasive migration. Developmental Cell.
2018;45(3):331-346. doi:10.1016/j.devcel.2018.04.002
apa: Ratheesh, A., Bicher, J., Smutny, M., Veselá, J., Papusheva, E., Krens, G.,
… Siekhaus, D. E. (2018). Drosophila TNF modulates tissue tension in the embryo
to facilitate macrophage invasive migration. Developmental Cell. Elsevier.
https://doi.org/10.1016/j.devcel.2018.04.002
chicago: Ratheesh, Aparna, Julia Bicher, Michael Smutny, Jana Veselá, Ekaterina
Papusheva, Gabriel Krens, Walter Kaufmann, Attila György, Alessandra M Casano,
and Daria E Siekhaus. “Drosophila TNF Modulates Tissue Tension in the Embryo to
Facilitate Macrophage Invasive Migration.” Developmental Cell. Elsevier,
2018. https://doi.org/10.1016/j.devcel.2018.04.002.
ieee: A. Ratheesh et al., “Drosophila TNF modulates tissue tension in the
embryo to facilitate macrophage invasive migration,” Developmental Cell,
vol. 45, no. 3. Elsevier, pp. 331–346, 2018.
ista: Ratheesh A, Bicher J, Smutny M, Veselá J, Papusheva E, Krens G, Kaufmann W,
György A, Casano AM, Siekhaus DE. 2018. Drosophila TNF modulates tissue tension
in the embryo to facilitate macrophage invasive migration. Developmental Cell.
45(3), 331–346.
mla: Ratheesh, Aparna, et al. “Drosophila TNF Modulates Tissue Tension in the Embryo
to Facilitate Macrophage Invasive Migration.” Developmental Cell, vol.
45, no. 3, Elsevier, 2018, pp. 331–46, doi:10.1016/j.devcel.2018.04.002.
short: A. Ratheesh, J. Bicher, M. Smutny, J. Veselá, E. Papusheva, G. Krens, W.
Kaufmann, A. György, A.M. Casano, D.E. Siekhaus, Developmental Cell 45 (2018)
331–346.
date_created: 2018-12-11T11:45:44Z
date_published: 2018-05-07T00:00:00Z
date_updated: 2023-09-11T13:22:13Z
day: '07'
department:
- _id: DaSi
- _id: CaHe
- _id: Bio
- _id: EM-Fac
- _id: MiSi
doi: 10.1016/j.devcel.2018.04.002
ec_funded: 1
external_id:
isi:
- '000432461400009'
pmid:
- '29738712'
intvolume: ' 45'
isi: 1
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.devcel.2018.04.002
month: '05'
oa: 1
oa_version: Published Version
page: 331 - 346
pmid: 1
project:
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: Drosophila TNFa´s Funktion in Immunzellen
- _id: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
publication: Developmental Cell
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/cells-change-tension-to-make-tissue-barriers-easier-to-get-through/
scopus_import: '1'
status: public
title: Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage
invasive migration
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 45
year: '2018'
...
---
_id: '437'
abstract:
- lang: eng
text: Dendritic cells (DCs) are sentinels of the adaptive immune system that reside
in peripheral organs of mammals. Upon pathogen encounter, they undergo maturation
and up-regulate the chemokine receptor CCR7 that guides them along gradients of
its chemokine ligands CCL19 and 21 to the next draining lymph node. There, DCs
present peripherally acquired antigen to naïve T cells, thereby triggering adaptive
immunity.
acknowledged_ssus:
- _id: SSU
acknowledgement: "This work was supported by grants of the European Research Council
(ERC CoG 724373) and the Austrian Science Fund (FWF) to M.S. We thank the scientific
support units at IST Austria for excellent technical support.\r\nWe thank the scientific
\ support units at IST Austria for excellent technical support. "
article_processing_charge: Yes (via OA deal)
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Hans
full_name: Haecker, Hans
last_name: Haecker
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Leithner AF, Renkawitz J, de Vries I, Hauschild R, Haecker H, Sixt MK. Fast
and efficient genetic engineering of hematopoietic precursor cells for the study
of dendritic cell migration. European Journal of Immunology. 2018;48(6):1074-1077.
doi:10.1002/eji.201747358
apa: Leithner, A. F., Renkawitz, J., de Vries, I., Hauschild, R., Haecker, H., &
Sixt, M. K. (2018). Fast and efficient genetic engineering of hematopoietic precursor
cells for the study of dendritic cell migration. European Journal of Immunology.
Wiley-Blackwell. https://doi.org/10.1002/eji.201747358
chicago: Leithner, Alexander F, Jörg Renkawitz, Ingrid de Vries, Robert Hauschild,
Hans Haecker, and Michael K Sixt. “Fast and Efficient Genetic Engineering of Hematopoietic
Precursor Cells for the Study of Dendritic Cell Migration.” European Journal
of Immunology. Wiley-Blackwell, 2018. https://doi.org/10.1002/eji.201747358.
ieee: A. F. Leithner, J. Renkawitz, I. de Vries, R. Hauschild, H. Haecker, and M.
K. Sixt, “Fast and efficient genetic engineering of hematopoietic precursor cells
for the study of dendritic cell migration,” European Journal of Immunology,
vol. 48, no. 6. Wiley-Blackwell, pp. 1074–1077, 2018.
ista: Leithner AF, Renkawitz J, de Vries I, Hauschild R, Haecker H, Sixt MK. 2018.
Fast and efficient genetic engineering of hematopoietic precursor cells for the
study of dendritic cell migration. European Journal of Immunology. 48(6), 1074–1077.
mla: Leithner, Alexander F., et al. “Fast and Efficient Genetic Engineering of Hematopoietic
Precursor Cells for the Study of Dendritic Cell Migration.” European Journal
of Immunology, vol. 48, no. 6, Wiley-Blackwell, 2018, pp. 1074–77, doi:10.1002/eji.201747358.
short: A.F. Leithner, J. Renkawitz, I. de Vries, R. Hauschild, H. Haecker, M.K.
Sixt, European Journal of Immunology 48 (2018) 1074–1077.
date_created: 2018-12-11T11:46:28Z
date_published: 2018-02-13T00:00:00Z
date_updated: 2023-09-11T14:01:18Z
day: '13'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
doi: 10.1002/eji.201747358
ec_funded: 1
external_id:
isi:
- '000434963700016'
file:
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creator: system
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date_updated: 2020-07-14T12:46:27Z
file_id: '5044'
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file_size: 590106
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has_accepted_license: '1'
intvolume: ' 48'
isi: 1
issue: '6'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc/4.0/
month: '02'
oa: 1
oa_version: Published Version
page: 1074 - 1077
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
publication: European Journal of Immunology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '7386'
pubrep_id: '1067'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Fast and efficient genetic engineering of hematopoietic precursor cells for
the study of dendritic cell migration
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 48
year: '2018'
...
---
_id: '5672'
abstract:
- lang: eng
text: The release of IgM is the first line of an antibody response and precedes
the generation of high affinity IgG in germinal centers. Once secreted by freshly
activated plasmablasts, IgM is released into the efferent lymph of reactive lymph
nodes as early as 3 d after immunization. As pentameric IgM has an enormous size
of 1,000 kD, its diffusibility is low, and one might wonder how it can pass through
the densely lymphocyte-packed environment of a lymph node parenchyma in order
to reach its exit. In this issue of JEM, Thierry et al. show that, in order to
reach the blood stream, IgM molecules take a specific micro-anatomical route via
lymph node conduits.
article_processing_charge: No
author:
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Reversat A, Sixt MK. IgM’s exit route. Journal of Experimental Medicine.
2018;215(12):2959-2961. doi:10.1084/jem.20181934
apa: Reversat, A., & Sixt, M. K. (2018). IgM’s exit route. Journal of Experimental
Medicine. Rockefeller University Press. https://doi.org/10.1084/jem.20181934
chicago: Reversat, Anne, and Michael K Sixt. “IgM’s Exit Route.” Journal of Experimental
Medicine. Rockefeller University Press, 2018. https://doi.org/10.1084/jem.20181934.
ieee: A. Reversat and M. K. Sixt, “IgM’s exit route,” Journal of Experimental
Medicine, vol. 215, no. 12. Rockefeller University Press, pp. 2959–2961, 2018.
ista: Reversat A, Sixt MK. 2018. IgM’s exit route. Journal of Experimental Medicine.
215(12), 2959–2961.
mla: Reversat, Anne, and Michael K. Sixt. “IgM’s Exit Route.” Journal of Experimental
Medicine, vol. 215, no. 12, Rockefeller University Press, 2018, pp. 2959–61,
doi:10.1084/jem.20181934.
short: A. Reversat, M.K. Sixt, Journal of Experimental Medicine 215 (2018) 2959–2961.
date_created: 2018-12-16T22:59:18Z
date_published: 2018-11-20T00:00:00Z
date_updated: 2023-09-11T14:12:06Z
day: '20'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1084/jem.20181934
external_id:
isi:
- '000451920600002'
file:
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isi: 1
issue: '12'
language:
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month: '11'
oa: 1
oa_version: Published Version
page: 2959-2961
publication: Journal of Experimental Medicine
publication_identifier:
issn:
- '00221007'
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: IgM's exit route
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 215
year: '2018'
...
---
_id: '275'
abstract:
- lang: eng
text: Lymphatic endothelial cells (LECs) release extracellular chemokines to guide
the migration of dendritic cells. In this study, we report that LECs also release
basolateral exosome-rich endothelial vesicles (EEVs) that are secreted in greater
numbers in the presence of inflammatory cytokines and accumulate in the perivascular
stroma of small lymphatic vessels in human chronic inflammatory diseases. Proteomic
analyses of EEV fractions identified > 1,700 cargo proteins and revealed a
dominant motility-promoting protein signature. In vitro and ex vivo EEV fractions
augmented cellular protrusion formation in a CX3CL1/fractalkine-dependent fashion
and enhanced the directional migratory response of human dendritic cells along
guidance cues. We conclude that perilymphatic LEC exosomes enhance exploratory
behavior and thus promote directional migration of CX3CR1-expressing cells in
complex tissue environments.
acknowledgement: M. Brown was supported by the Cell Communication in Health and Disease
Graduate Study Program of the Austrian Science Fund and Medizinische Universität
Wien, M. Sixt by the European Research Council (ERC GA 281556) and an Austrian Science
Fund START award, K.L. Bennett by the Austrian Academy of Sciences, D.G. Jackson
and L.A. Johnson by Unit Funding (MC_UU_12010/2) and project grants from the Medical
Research Council (G1100134 and MR/L008610/1), and M. Detmar by the Schweizerischer
Nationalfonds zur Förderung der Wissenschaftlichen Forschung and Advanced European
Research Council grant LYVICAM. K. Vaahtomeri was supported by an Academy of Finland
postdoctoral research grant (287853). This project has received funding from the
European Union’s Horizon 2020 research and innovation program under grant agreement
No. 668036 (RELENT).
article_processing_charge: No
author:
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Louise
full_name: Johnson, Louise
last_name: Johnson
- first_name: Dario
full_name: Leone, Dario
last_name: Leone
- first_name: Peter
full_name: Májek, Peter
last_name: Májek
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Daniel
full_name: Senfter, Daniel
last_name: Senfter
- first_name: Nora
full_name: Bukosza, Nora
last_name: Bukosza
- first_name: Helga
full_name: Schachner, Helga
last_name: Schachner
- first_name: Gabriele
full_name: Asfour, Gabriele
last_name: Asfour
- first_name: Brigitte
full_name: Langer, Brigitte
last_name: Langer
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Katja
full_name: Parapatics, Katja
last_name: Parapatics
- first_name: Young
full_name: Hong, Young
last_name: Hong
- first_name: Keiryn
full_name: Bennett, Keiryn
last_name: Bennett
- first_name: Renate
full_name: Kain, Renate
last_name: Kain
- first_name: Michael
full_name: Detmar, Michael
last_name: Detmar
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: David
full_name: Jackson, David
last_name: Jackson
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
citation:
ama: Brown M, Johnson L, Leone D, et al. Lymphatic exosomes promote dendritic cell
migration along guidance cues. Journal of Cell Biology. 2018;217(6):2205-2221.
doi:10.1083/jcb.201612051
apa: Brown, M., Johnson, L., Leone, D., Májek, P., Vaahtomeri, K., Senfter, D.,
… Kerjaschki, D. (2018). Lymphatic exosomes promote dendritic cell migration along
guidance cues. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201612051
chicago: Brown, Markus, Louise Johnson, Dario Leone, Peter Májek, Kari Vaahtomeri,
Daniel Senfter, Nora Bukosza, et al. “Lymphatic Exosomes Promote Dendritic Cell
Migration along Guidance Cues.” Journal of Cell Biology. Rockefeller University
Press, 2018. https://doi.org/10.1083/jcb.201612051.
ieee: M. Brown et al., “Lymphatic exosomes promote dendritic cell migration
along guidance cues,” Journal of Cell Biology, vol. 217, no. 6. Rockefeller
University Press, pp. 2205–2221, 2018.
ista: Brown M, Johnson L, Leone D, Májek P, Vaahtomeri K, Senfter D, Bukosza N,
Schachner H, Asfour G, Langer B, Hauschild R, Parapatics K, Hong Y, Bennett K,
Kain R, Detmar M, Sixt MK, Jackson D, Kerjaschki D. 2018. Lymphatic exosomes promote
dendritic cell migration along guidance cues. Journal of Cell Biology. 217(6),
2205–2221.
mla: Brown, Markus, et al. “Lymphatic Exosomes Promote Dendritic Cell Migration
along Guidance Cues.” Journal of Cell Biology, vol. 217, no. 6, Rockefeller
University Press, 2018, pp. 2205–21, doi:10.1083/jcb.201612051.
short: M. Brown, L. Johnson, D. Leone, P. Májek, K. Vaahtomeri, D. Senfter, N. Bukosza,
H. Schachner, G. Asfour, B. Langer, R. Hauschild, K. Parapatics, Y. Hong, K. Bennett,
R. Kain, M. Detmar, M.K. Sixt, D. Jackson, D. Kerjaschki, Journal of Cell Biology
217 (2018) 2205–2221.
date_created: 2018-12-11T11:45:33Z
date_published: 2018-04-12T00:00:00Z
date_updated: 2023-09-13T08:51:29Z
day: '12'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
doi: 10.1083/jcb.201612051
ec_funded: 1
external_id:
isi:
- '000438077800026'
pmid:
- '29650776'
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oa: 1
oa_version: Published Version
page: 2205 - 2221
pmid: 1
project:
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Journal of Cell Biology
publication_status: published
publisher: Rockefeller University Press
publist_id: '7627'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Lymphatic exosomes promote dendritic cell migration along guidance cues
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 217
year: '2018'
...
---
_id: '5858'
abstract:
- lang: eng
text: Spatial patterns are ubiquitous on the subcellular, cellular and tissue level,
and can be studied using imaging techniques such as light and fluorescence microscopy.
Imaging data provide quantitative information about biological systems; however,
mechanisms causing spatial patterning often remain elusive. In recent years, spatio-temporal
mathematical modelling has helped to overcome this problem. Yet, outliers and
structured noise limit modelling of whole imaging data, and models often consider
spatial summary statistics. Here, we introduce an integrated data-driven modelling
approach that can cope with measurement artefacts and whole imaging data. Our
approach combines mechanistic models of the biological processes with robust statistical
models of the measurement process. The parameters of the integrated model are
calibrated using a maximum-likelihood approach. We used this integrated modelling
approach to study in vivo gradients of the chemokine (C-C motif) ligand 21 (CCL21).
CCL21 gradients guide dendritic cells and are important in the adaptive immune
response. Using artificial data, we verified that the integrated modelling approach
provides reliable parameter estimates in the presence of measurement noise and
that bias and variance of these estimates are reduced compared to conventional
approaches. The application to experimental data allowed the parametrization and
subsequent refinement of the model using additional mechanisms. Among other results,
model-based hypothesis testing predicted lymphatic vessel-dependent concentration
of heparan sulfate, the binding partner of CCL21. The selected model provided
an accurate description of the experimental data and was partially validated using
published data. Our findings demonstrate that integrated statistical modelling
of whole imaging data is computationally feasible and can provide novel biological
insights.
article_number: '20180600'
article_processing_charge: No
author:
- first_name: Sabrina
full_name: Hross, Sabrina
last_name: Hross
- first_name: Fabian J.
full_name: Theis, Fabian J.
last_name: Theis
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Jan
full_name: Hasenauer, Jan
last_name: Hasenauer
citation:
ama: Hross S, Theis FJ, Sixt MK, Hasenauer J. Mechanistic description of spatial
processes using integrative modelling of noise-corrupted imaging data. Journal
of the Royal Society Interface. 2018;15(149). doi:10.1098/rsif.2018.0600
apa: Hross, S., Theis, F. J., Sixt, M. K., & Hasenauer, J. (2018). Mechanistic
description of spatial processes using integrative modelling of noise-corrupted
imaging data. Journal of the Royal Society Interface. Royal Society Publishing.
https://doi.org/10.1098/rsif.2018.0600
chicago: Hross, Sabrina, Fabian J. Theis, Michael K Sixt, and Jan Hasenauer. “Mechanistic
Description of Spatial Processes Using Integrative Modelling of Noise-Corrupted
Imaging Data.” Journal of the Royal Society Interface. Royal Society Publishing,
2018. https://doi.org/10.1098/rsif.2018.0600.
ieee: S. Hross, F. J. Theis, M. K. Sixt, and J. Hasenauer, “Mechanistic description
of spatial processes using integrative modelling of noise-corrupted imaging data,”
Journal of the Royal Society Interface, vol. 15, no. 149. Royal Society
Publishing, 2018.
ista: Hross S, Theis FJ, Sixt MK, Hasenauer J. 2018. Mechanistic description of
spatial processes using integrative modelling of noise-corrupted imaging data.
Journal of the Royal Society Interface. 15(149), 20180600.
mla: Hross, Sabrina, et al. “Mechanistic Description of Spatial Processes Using
Integrative Modelling of Noise-Corrupted Imaging Data.” Journal of the Royal
Society Interface, vol. 15, no. 149, 20180600, Royal Society Publishing, 2018,
doi:10.1098/rsif.2018.0600.
short: S. Hross, F.J. Theis, M.K. Sixt, J. Hasenauer, Journal of the Royal Society
Interface 15 (2018).
date_created: 2019-01-20T22:59:18Z
date_published: 2018-12-05T00:00:00Z
date_updated: 2023-09-13T08:55:05Z
day: '05'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1098/rsif.2018.0600
external_id:
isi:
- '000456783800011'
file:
- access_level: open_access
checksum: 56eb4308a15b7190bff938fab1f780e8
content_type: application/pdf
creator: dernst
date_created: 2019-02-05T14:46:44Z
date_updated: 2020-07-14T12:47:13Z
file_id: '5925'
file_name: 2018_Interface_Hross.pdf
file_size: 1464288
relation: main_file
file_date_updated: 2020-07-14T12:47:13Z
has_accepted_license: '1'
intvolume: ' 15'
isi: 1
issue: '149'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
publication: Journal of the Royal Society Interface
publication_identifier:
issn:
- '17425689'
publication_status: published
publisher: Royal Society Publishing
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mechanistic description of spatial processes using integrative modelling of
noise-corrupted imaging data
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 15
year: '2018'
...
---
_id: '153'
abstract:
- lang: eng
text: Cells migrating in multicellular organisms steadily traverse complex three-dimensional
(3D) environments. To decipher the underlying cell biology, current experimental
setups either use simplified 2D, tissue-mimetic 3D (e.g., collagen matrices) or
in vivo environments. While only in vivo experiments are truly physiological,
they do not allow for precise manipulation of environmental parameters. 2D in
vitro experiments do allow mechanical and chemical manipulations, but increasing
evidence demonstrates substantial differences of migratory mechanisms in 2D and
3D. Here, we describe simple, robust, and versatile “pillar forests” to investigate
cell migration in complex but fully controllable 3D environments. Pillar forests
are polydimethylsiloxane-based setups, in which two closely adjacent surfaces
are interconnected by arrays of micrometer-sized pillars. Changing the pillar
shape, size, height and the inter-pillar distance precisely manipulates microenvironmental
parameters (e.g., pore sizes, micro-geometry, micro-topology), while being easily
combined with chemotactic cues, surface coatings, diverse cell types and advanced
imaging techniques. Thus, pillar forests combine the advantages of 2D cell migration
assays with the precise definition of 3D environmental parameters.
article_processing_charge: No
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Renkawitz J, Reversat A, Leithner AF, Merrin J, Sixt MK. Micro-engineered
“pillar forests” to study cell migration in complex but controlled 3D environments.
In: Methods in Cell Biology. Vol 147. Academic Press; 2018:79-91. doi:10.1016/bs.mcb.2018.07.004'
apa: Renkawitz, J., Reversat, A., Leithner, A. F., Merrin, J., & Sixt, M. K.
(2018). Micro-engineered “pillar forests” to study cell migration in complex but
controlled 3D environments. In Methods in Cell Biology (Vol. 147, pp. 79–91).
Academic Press. https://doi.org/10.1016/bs.mcb.2018.07.004
chicago: Renkawitz, Jörg, Anne Reversat, Alexander F Leithner, Jack Merrin, and
Michael K Sixt. “Micro-Engineered ‘Pillar Forests’ to Study Cell Migration in
Complex but Controlled 3D Environments.” In Methods in Cell Biology, 147:79–91.
Academic Press, 2018. https://doi.org/10.1016/bs.mcb.2018.07.004.
ieee: J. Renkawitz, A. Reversat, A. F. Leithner, J. Merrin, and M. K. Sixt, “Micro-engineered
‘pillar forests’ to study cell migration in complex but controlled 3D environments,”
in Methods in Cell Biology, vol. 147, Academic Press, 2018, pp. 79–91.
ista: 'Renkawitz J, Reversat A, Leithner AF, Merrin J, Sixt MK. 2018.Micro-engineered
“pillar forests” to study cell migration in complex but controlled 3D environments.
In: Methods in Cell Biology. vol. 147, 79–91.'
mla: Renkawitz, Jörg, et al. “Micro-Engineered ‘Pillar Forests’ to Study Cell Migration
in Complex but Controlled 3D Environments.” Methods in Cell Biology, vol.
147, Academic Press, 2018, pp. 79–91, doi:10.1016/bs.mcb.2018.07.004.
short: J. Renkawitz, A. Reversat, A.F. Leithner, J. Merrin, M.K. Sixt, in:, Methods
in Cell Biology, Academic Press, 2018, pp. 79–91.
date_created: 2018-12-11T11:44:54Z
date_published: 2018-07-27T00:00:00Z
date_updated: 2023-09-13T08:56:35Z
day: '27'
department:
- _id: MiSi
- _id: NanoFab
doi: 10.1016/bs.mcb.2018.07.004
external_id:
isi:
- '000452412300006'
pmid:
- '30165964'
intvolume: ' 147'
isi: 1
language:
- iso: eng
month: '07'
oa_version: None
page: 79 - 91
pmid: 1
publication: Methods in Cell Biology
publication_identifier:
issn:
- 0091679X
publication_status: published
publisher: Academic Press
publist_id: '7768'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Micro-engineered “pillar forests” to study cell migration in complex but controlled
3D environments
type: book_chapter
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 147
year: '2018'
...
---
_id: '276'
abstract:
- lang: eng
text: Directed migration of cells relies on their ability to sense directional guidance
cues and to interact with pericellular structures in order to transduce contractile
cytoskeletal- into mechanical forces. These biomechanical processes depend highly
on microenvironmental factors such as exposure to 2D surfaces or 3D matrices.
In vivo, the majority of cells are exposed to 3D environments. Data on 3D cell
migration are mostly derived from intravital microscopy or collagen-based in vitro
assays. Both approaches offer only limited controlla-bility of experimental conditions.
Here, we developed an automated microfluidic system that allows positioning of
cells in 3D microenvironments containing highly controlled diffusion-based chemokine
gradients. Tracking migration in such gradients was feasible in real time at the
single cell level. Moreover, the setup allowed on-chip immunocytochemistry and
thus linking of functional with phenotypical properties in individual cells. Spatially
defined retrieval of cells from the device allows down-stream off-chip analysis.
Using dendritic cells as a model, our setup specifically allowed us for the first
time to quantitate key migration characteristics of cells exposed to identical
gradients of the chemokine CCL19 yet placed on 2D vs in 3D environments. Migration
properties between 2D and 3D migration were distinct. Morphological features of
cells migrating in an in vitro 3D environment were similar to those of cells migrating
in animal tissues, but different from cells migrating on a surface. Our system
thus offers a highly controllable in vitro-mimic of a 3D environment that cells
traffic in vivo.
acknowledgement: This work was supported by the Swiss National Science Foundation
(MD-PhD fellowships, 323530_164221 to C.F.; and 323630_151483 to A.J.; grant PZ00P3_144863
to M.R, grant 31003A_156431 to T.S.; PZ00P3_148000 to C.T.B.; PZ00P3_154733 to M.M.),
a Novartis “FreeNovation” grant to M.M. and T.S. and an EMBO long-term fellowship
(ALTF 1396-2014) co-funded by the European Commission (LTFCOFUND2013, GA-2013-609409)
to J.R.. M.R. was supported by the Gebert Rüf Foundation (GRS 058/14). The funders
had no role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
article_number: e0198330
article_processing_charge: No
article_type: original
author:
- first_name: Corina
full_name: Frick, Corina
last_name: Frick
- first_name: Philip
full_name: Dettinger, Philip
last_name: Dettinger
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Annaïse
full_name: Jauch, Annaïse
last_name: Jauch
- first_name: Christoph
full_name: Berger, Christoph
last_name: Berger
- first_name: Mike
full_name: Recher, Mike
last_name: Recher
- first_name: Timm
full_name: Schroeder, Timm
last_name: Schroeder
- first_name: Matthias
full_name: Mehling, Matthias
last_name: Mehling
citation:
ama: Frick C, Dettinger P, Renkawitz J, et al. Nano-scale microfluidics to study
3D chemotaxis at the single cell level. PLoS One. 2018;13(6). doi:10.1371/journal.pone.0198330
apa: Frick, C., Dettinger, P., Renkawitz, J., Jauch, A., Berger, C., Recher, M.,
… Mehling, M. (2018). Nano-scale microfluidics to study 3D chemotaxis at the single
cell level. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0198330
chicago: Frick, Corina, Philip Dettinger, Jörg Renkawitz, Annaïse Jauch, Christoph
Berger, Mike Recher, Timm Schroeder, and Matthias Mehling. “Nano-Scale Microfluidics
to Study 3D Chemotaxis at the Single Cell Level.” PLoS One. Public Library
of Science, 2018. https://doi.org/10.1371/journal.pone.0198330.
ieee: C. Frick et al., “Nano-scale microfluidics to study 3D chemotaxis at
the single cell level,” PLoS One, vol. 13, no. 6. Public Library of Science,
2018.
ista: Frick C, Dettinger P, Renkawitz J, Jauch A, Berger C, Recher M, Schroeder
T, Mehling M. 2018. Nano-scale microfluidics to study 3D chemotaxis at the single
cell level. PLoS One. 13(6), e0198330.
mla: Frick, Corina, et al. “Nano-Scale Microfluidics to Study 3D Chemotaxis at the
Single Cell Level.” PLoS One, vol. 13, no. 6, e0198330, Public Library
of Science, 2018, doi:10.1371/journal.pone.0198330.
short: C. Frick, P. Dettinger, J. Renkawitz, A. Jauch, C. Berger, M. Recher, T.
Schroeder, M. Mehling, PLoS One 13 (2018).
date_created: 2018-12-11T11:45:34Z
date_published: 2018-06-07T00:00:00Z
date_updated: 2023-09-13T09:00:15Z
day: '07'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1371/journal.pone.0198330
external_id:
isi:
- '000434384900031'
file:
- access_level: open_access
checksum: 95fc5dc3938b3ad3b7697d10c83cc143
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T14:10:32Z
date_updated: 2020-07-14T12:45:45Z
file_id: '5709'
file_name: 2018_Plos_Frick.pdf
file_size: 7682167
relation: main_file
file_date_updated: 2020-07-14T12:45:45Z
has_accepted_license: '1'
intvolume: ' 13'
isi: 1
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '7626'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nano-scale microfluidics to study 3D chemotaxis at the single cell level
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 13
year: '2018'
...
---
_id: '5861'
abstract:
- lang: eng
text: In zebrafish larvae, it is the cell type that determines how the cell responds
to a chemokine signal.
article_number: e37888
article_processing_charge: No
article_type: original
author:
- first_name: Jonna H
full_name: Alanko, Jonna H
id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87
last_name: Alanko
orcid: 0000-0002-7698-3061
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Alanko JH, Sixt MK. The cell sets the tone. eLife. 2018;7. doi:10.7554/eLife.37888
apa: Alanko, J. H., & Sixt, M. K. (2018). The cell sets the tone. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.37888
chicago: Alanko, Jonna H, and Michael K Sixt. “The Cell Sets the Tone.” ELife.
eLife Sciences Publications, 2018. https://doi.org/10.7554/eLife.37888.
ieee: J. H. Alanko and M. K. Sixt, “The cell sets the tone,” eLife, vol.
7. eLife Sciences Publications, 2018.
ista: Alanko JH, Sixt MK. 2018. The cell sets the tone. eLife. 7, e37888.
mla: Alanko, Jonna H., and Michael K. Sixt. “The Cell Sets the Tone.” ELife,
vol. 7, e37888, eLife Sciences Publications, 2018, doi:10.7554/eLife.37888.
short: J.H. Alanko, M.K. Sixt, ELife 7 (2018).
date_created: 2019-01-20T22:59:19Z
date_published: 2018-06-06T00:00:00Z
date_updated: 2023-09-19T10:01:39Z
day: '06'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.7554/eLife.37888
external_id:
isi:
- '000434375000001'
file:
- access_level: open_access
checksum: f1c7ec2a809408d763c4b529a98f9a3b
content_type: application/pdf
creator: dernst
date_created: 2019-02-13T10:52:11Z
date_updated: 2020-07-14T12:47:13Z
file_id: '5973'
file_name: 2018_eLife_Alanko.pdf
file_size: 358141
relation: main_file
file_date_updated: 2020-07-14T12:47:13Z
has_accepted_license: '1'
intvolume: ' 7'
isi: 1
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: The cell sets the tone
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 7
year: '2018'
...
---
_id: '5984'
abstract:
- lang: eng
text: G-protein-coupled receptors (GPCRs) form the largest receptor family, relay
environmental stimuli to changes in cell behavior and represent prime drug targets.
Many GPCRs are classified as orphan receptors because of the limited knowledge
on their ligands and coupling to cellular signaling machineries. Here, we engineer
a library of 63 chimeric receptors that contain the signaling domains of human
orphan and understudied GPCRs functionally linked to the light-sensing domain
of rhodopsin. Upon stimulation with visible light, we identify activation of canonical
cell signaling pathways, including cAMP-, Ca2+-, MAPK/ERK-, and Rho-dependent
pathways, downstream of the engineered receptors. For the human pseudogene GPR33,
we resurrect a signaling function that supports its hypothesized role as a pathogen
entry site. These results demonstrate that substituting unknown chemical activators
with a light switch can reveal information about protein function and provide
an optically controlled protein library for exploring the physiology and therapeutic
potential of understudied GPCRs.
article_number: '1950'
article_processing_charge: No
author:
- first_name: Maurizio
full_name: Morri, Maurizio
id: 4863116E-F248-11E8-B48F-1D18A9856A87
last_name: Morri
- first_name: Inmaculada
full_name: Sanchez-Romero, Inmaculada
id: 3D9C5D30-F248-11E8-B48F-1D18A9856A87
last_name: Sanchez-Romero
- first_name: Alexandra-Madelaine
full_name: Tichy, Alexandra-Madelaine
id: 29D8BB2C-F248-11E8-B48F-1D18A9856A87
last_name: Tichy
- first_name: Stephanie
full_name: Kainrath, Stephanie
id: 32CFBA64-F248-11E8-B48F-1D18A9856A87
last_name: Kainrath
- first_name: Elliot J.
full_name: Gerrard, Elliot J.
last_name: Gerrard
- first_name: Priscila
full_name: Hirschfeld, Priscila
id: 435ACB3A-F248-11E8-B48F-1D18A9856A87
last_name: Hirschfeld
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Harald L
full_name: Janovjak, Harald L
id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
last_name: Janovjak
orcid: 0000-0002-8023-9315
citation:
ama: Morri M, Sanchez-Romero I, Tichy A-M, et al. Optical functionalization of human
class A orphan G-protein-coupled receptors. Nature Communications. 2018;9(1).
doi:10.1038/s41467-018-04342-1
apa: Morri, M., Sanchez-Romero, I., Tichy, A.-M., Kainrath, S., Gerrard, E. J.,
Hirschfeld, P., … Janovjak, H. L. (2018). Optical functionalization of human class
A orphan G-protein-coupled receptors. Nature Communications. Springer Nature.
https://doi.org/10.1038/s41467-018-04342-1
chicago: Morri, Maurizio, Inmaculada Sanchez-Romero, Alexandra-Madelaine Tichy,
Stephanie Kainrath, Elliot J. Gerrard, Priscila Hirschfeld, Jan Schwarz, and Harald
L Janovjak. “Optical Functionalization of Human Class A Orphan G-Protein-Coupled
Receptors.” Nature Communications. Springer Nature, 2018. https://doi.org/10.1038/s41467-018-04342-1.
ieee: M. Morri et al., “Optical functionalization of human class A orphan
G-protein-coupled receptors,” Nature Communications, vol. 9, no. 1. Springer
Nature, 2018.
ista: Morri M, Sanchez-Romero I, Tichy A-M, Kainrath S, Gerrard EJ, Hirschfeld P,
Schwarz J, Janovjak HL. 2018. Optical functionalization of human class A orphan
G-protein-coupled receptors. Nature Communications. 9(1), 1950.
mla: Morri, Maurizio, et al. “Optical Functionalization of Human Class A Orphan
G-Protein-Coupled Receptors.” Nature Communications, vol. 9, no. 1, 1950,
Springer Nature, 2018, doi:10.1038/s41467-018-04342-1.
short: M. Morri, I. Sanchez-Romero, A.-M. Tichy, S. Kainrath, E.J. Gerrard, P. Hirschfeld,
J. Schwarz, H.L. Janovjak, Nature Communications 9 (2018).
date_created: 2019-02-14T10:50:24Z
date_published: 2018-12-01T00:00:00Z
date_updated: 2023-09-19T14:29:32Z
day: '01'
ddc:
- '570'
department:
- _id: HaJa
- _id: CaGu
- _id: MiSi
doi: 10.1038/s41467-018-04342-1
ec_funded: 1
external_id:
isi:
- '000432280000006'
file:
- access_level: open_access
checksum: 8325fcc194264af4749e662a73bf66b5
content_type: application/pdf
creator: kschuh
date_created: 2019-02-14T10:58:29Z
date_updated: 2020-07-14T12:47:14Z
file_id: '5985'
file_name: 2018_Springer_Morri.pdf
file_size: 1349914
relation: main_file
file_date_updated: 2020-07-14T12:47:14Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
issue: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 25548C20-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '303564'
name: Microbial Ion Channels for Synthetic Neurobiology
- _id: 255A6082-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W1232-B24
name: Molecular Drug Targets
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Optical functionalization of human class A orphan G-protein-coupled receptors
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 9
year: '2018'
...
---
_id: '5992'
abstract:
- lang: eng
text: Lamellipodia are flat membrane protrusions formed during mesenchymal motion.
Polymerization at the leading edge assembles the actin filament network and generates
protrusion force. How this force is supported by the network and how the assembly
rate is shared between protrusion and network retrograde flow determines the protrusion
rate. We use mathematical modeling to understand experiments changing the F-actin
density in lamellipodia of B16-F1 melanoma cells by modulation of Arp2/3 complex
activity or knockout of the formins FMNL2 and FMNL3. Cells respond to a reduction
of density with a decrease of protrusion velocity, an increase in the ratio of
force to filament number, but constant network assembly rate. The relation between
protrusion force and tension gradient in the F-actin network and the density dependency
of friction, elasticity, and viscosity of the network explain the experimental
observations. The formins act as filament nucleators and elongators with differential
rates. Modulation of their activity suggests an effect on network assembly rate.
Contrary to these expectations, the effect of changes in elongator composition
is much weaker than the consequences of the density change. We conclude that the
force acting on the leading edge membrane is the force required to drive F-actin
network retrograde flow.
article_processing_charge: No
author:
- first_name: Setareh
full_name: Dolati, Setareh
last_name: Dolati
- first_name: Frieda
full_name: Kage, Frieda
last_name: Kage
- first_name: Jan
full_name: Mueller, Jan
last_name: Mueller
- first_name: Mathias
full_name: Müsken, Mathias
last_name: Müsken
- first_name: Marieluise
full_name: Kirchner, Marieluise
last_name: Kirchner
- first_name: Gunnar
full_name: Dittmar, Gunnar
last_name: Dittmar
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Martin
full_name: Falcke, Martin
last_name: Falcke
citation:
ama: Dolati S, Kage F, Mueller J, et al. On the relation between filament density,
force generation, and protrusion rate in mesenchymal cell motility. Molecular
Biology of the Cell. 2018;29(22):2674-2686. doi:10.1091/mbc.e18-02-0082
apa: Dolati, S., Kage, F., Mueller, J., Müsken, M., Kirchner, M., Dittmar, G., …
Falcke, M. (2018). On the relation between filament density, force generation,
and protrusion rate in mesenchymal cell motility. Molecular Biology of the
Cell. American Society for Cell Biology . https://doi.org/10.1091/mbc.e18-02-0082
chicago: Dolati, Setareh, Frieda Kage, Jan Mueller, Mathias Müsken, Marieluise Kirchner,
Gunnar Dittmar, Michael K Sixt, Klemens Rottner, and Martin Falcke. “On the Relation
between Filament Density, Force Generation, and Protrusion Rate in Mesenchymal
Cell Motility.” Molecular Biology of the Cell. American Society for Cell
Biology , 2018. https://doi.org/10.1091/mbc.e18-02-0082.
ieee: S. Dolati et al., “On the relation between filament density, force
generation, and protrusion rate in mesenchymal cell motility,” Molecular Biology
of the Cell, vol. 29, no. 22. American Society for Cell Biology , pp. 2674–2686,
2018.
ista: Dolati S, Kage F, Mueller J, Müsken M, Kirchner M, Dittmar G, Sixt MK, Rottner
K, Falcke M. 2018. On the relation between filament density, force generation,
and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell.
29(22), 2674–2686.
mla: Dolati, Setareh, et al. “On the Relation between Filament Density, Force Generation,
and Protrusion Rate in Mesenchymal Cell Motility.” Molecular Biology of the
Cell, vol. 29, no. 22, American Society for Cell Biology , 2018, pp. 2674–86,
doi:10.1091/mbc.e18-02-0082.
short: S. Dolati, F. Kage, J. Mueller, M. Müsken, M. Kirchner, G. Dittmar, M.K.
Sixt, K. Rottner, M. Falcke, Molecular Biology of the Cell 29 (2018) 2674–2686.
date_created: 2019-02-14T12:25:47Z
date_published: 2018-11-01T00:00:00Z
date_updated: 2023-09-19T14:30:23Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1091/mbc.e18-02-0082
external_id:
isi:
- '000455641000011'
pmid:
- '30156465'
file:
- access_level: open_access
checksum: e98465b4416b3e804c47f40086932af2
content_type: application/pdf
creator: kschuh
date_created: 2019-02-14T12:34:29Z
date_updated: 2020-07-14T12:47:15Z
file_id: '5994'
file_name: 2018_ASCB_Dolati.pdf
file_size: 6668971
relation: main_file
file_date_updated: 2020-07-14T12:47:15Z
has_accepted_license: '1'
intvolume: ' 29'
isi: 1
issue: '22'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 2674-2686
pmid: 1
publication: Molecular Biology of the Cell
publication_identifier:
eissn:
- 1939-4586
publication_status: published
publisher: 'American Society for Cell Biology '
quality_controlled: '1'
scopus_import: '1'
status: public
title: On the relation between filament density, force generation, and protrusion
rate in mesenchymal cell motility
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 29
year: '2018'
...
---
_id: '6497'
abstract:
- lang: eng
text: T cells are actively scanning pMHC-presenting cells in lymphoid organs and
nonlymphoid tissues (NLTs) with divergent topologies and confinement. How the
T cell actomyosin cytoskeleton facilitates this task in distinct environments
is incompletely understood. Here, we show that lack of Myosin IXb (Myo9b), a negative
regulator of the small GTPase Rho, led to increased Rho-GTP levels and cell surface
stiffness in primary T cells. Nonetheless, intravital imaging revealed robust
motility of Myo9b−/− CD8+ T cells in lymphoid tissue and similar expansion and
differentiation during immune responses. In contrast, accumulation of Myo9b−/−
CD8+ T cells in NLTs was strongly impaired. Specifically, Myo9b was required for
T cell crossing of basement membranes, such as those which are present between
dermis and epidermis. As consequence, Myo9b−/− CD8+ T cells showed impaired control
of skin infections. In sum, we show that Myo9b is critical for the CD8+ T cell
adaptation from lymphoid to NLT surveillance and the establishment of protective
tissue–resident T cell populations.
article_processing_charge: No
author:
- first_name: Federica
full_name: Moalli, Federica
last_name: Moalli
- first_name: Xenia
full_name: Ficht, Xenia
last_name: Ficht
- first_name: Philipp
full_name: Germann, Philipp
last_name: Germann
- first_name: Mykhailo
full_name: Vladymyrov, Mykhailo
last_name: Vladymyrov
- first_name: Bettina
full_name: Stolp, Bettina
last_name: Stolp
- first_name: Ingrid
full_name: de Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: de Vries
- first_name: Ruth
full_name: Lyck, Ruth
last_name: Lyck
- first_name: Jasmin
full_name: Balmer, Jasmin
last_name: Balmer
- first_name: Amleto
full_name: Fiocchi, Amleto
last_name: Fiocchi
- first_name: Mario
full_name: Kreutzfeldt, Mario
last_name: Kreutzfeldt
- first_name: Doron
full_name: Merkler, Doron
last_name: Merkler
- first_name: Matteo
full_name: Iannacone, Matteo
last_name: Iannacone
- first_name: Akitaka
full_name: Ariga, Akitaka
last_name: Ariga
- first_name: Michael H.
full_name: Stoffel, Michael H.
last_name: Stoffel
- first_name: James
full_name: Sharpe, James
last_name: Sharpe
- first_name: Martin
full_name: Bähler, Martin
last_name: Bähler
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Alba
full_name: Diz-Muñoz, Alba
last_name: Diz-Muñoz
- first_name: Jens V.
full_name: Stein, Jens V.
last_name: Stein
citation:
ama: Moalli F, Ficht X, Germann P, et al. The Rho regulator Myosin IXb enables nonlymphoid
tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine.
2018;2015(7):1869–1890. doi:10.1084/jem.20170896
apa: Moalli, F., Ficht, X., Germann, P., Vladymyrov, M., Stolp, B., de Vries, I.,
… Stein, J. V. (2018). The Rho regulator Myosin IXb enables nonlymphoid tissue
seeding of protective CD8+T cells. The Journal of Experimental Medicine.
Rockefeller University Press. https://doi.org/10.1084/jem.20170896
chicago: Moalli, Federica, Xenia Ficht, Philipp Germann, Mykhailo Vladymyrov, Bettina
Stolp, Ingrid de Vries, Ruth Lyck, et al. “The Rho Regulator Myosin IXb Enables
Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” The Journal of Experimental
Medicine. Rockefeller University Press, 2018. https://doi.org/10.1084/jem.20170896.
ieee: F. Moalli et al., “The Rho regulator Myosin IXb enables nonlymphoid
tissue seeding of protective CD8+T cells,” The Journal of Experimental Medicine,
vol. 2015, no. 7. Rockefeller University Press, pp. 1869–1890, 2018.
ista: Moalli F, Ficht X, Germann P, Vladymyrov M, Stolp B, de Vries I, Lyck R, Balmer
J, Fiocchi A, Kreutzfeldt M, Merkler D, Iannacone M, Ariga A, Stoffel MH, Sharpe
J, Bähler M, Sixt MK, Diz-Muñoz A, Stein JV. 2018. The Rho regulator Myosin IXb
enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental
Medicine. 2015(7), 1869–1890.
mla: Moalli, Federica, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid
Tissue Seeding of Protective CD8+T Cells.” The Journal of Experimental Medicine,
vol. 2015, no. 7, Rockefeller University Press, 2018, pp. 1869–1890, doi:10.1084/jem.20170896.
short: F. Moalli, X. Ficht, P. Germann, M. Vladymyrov, B. Stolp, I. de Vries, R.
Lyck, J. Balmer, A. Fiocchi, M. Kreutzfeldt, D. Merkler, M. Iannacone, A. Ariga,
M.H. Stoffel, J. Sharpe, M. Bähler, M.K. Sixt, A. Diz-Muñoz, J.V. Stein, The Journal
of Experimental Medicine 2015 (2018) 1869–1890.
date_created: 2019-05-28T12:36:47Z
date_published: 2018-06-06T00:00:00Z
date_updated: 2023-09-19T14:52:08Z
day: '06'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1084/jem.20170896
external_id:
isi:
- '000440822900011'
file:
- access_level: open_access
checksum: 86ae5331f9bfced9a6358a790a04bef4
content_type: application/pdf
creator: kschuh
date_created: 2019-05-28T12:40:05Z
date_updated: 2020-07-14T12:47:32Z
file_id: '6498'
file_name: 2018_rupress_Moalli.pdf
file_size: 3841660
relation: main_file
file_date_updated: 2020-07-14T12:47:32Z
has_accepted_license: '1'
intvolume: ' 2015'
isi: 1
issue: '7'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 1869–1890
publication: The Journal of Experimental Medicine
publication_identifier:
eissn:
- 1540-9538
issn:
- 0022-1007
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective
CD8+T cells
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 2015
year: '2018'
...
---
_id: '402'
abstract:
- lang: eng
text: During metastasis, malignant cells escape the primary tumor, intravasate lymphatic
vessels, and reach draining sentinel lymph nodes before they colonize distant
organs via the blood circulation. Although lymph node metastasis in cancer patients
correlates with poor prognosis, evidence is lacking as to whether and how tumor
cells enter the bloodstream via lymph nodes. To investigate this question, we
delivered carcinoma cells into the lymph nodes of mice by microinfusing the cells
into afferent lymphatic vessels. We found that tumor cells rapidly infiltrated
the lymph node parenchyma, invaded blood vessels, and seeded lung metastases without
involvement of the thoracic duct. These results suggest that the lymph node blood
vessels can serve as an exit route for systemic dissemination of cancer cells
in experimental mouse models. Whether this form of tumor cell spreading occurs
in cancer patients remains to be determined.
acknowledged_ssus:
- _id: Bio
acknowledgement: "M.B. was supported by the Cell Communication in Health and Disease
graduate study program of the Austrian Science Fund (FWF) and the Medical University
of Vienna. M.S. was supported by the European Research Council (grant ERC GA 281556)
and an FWF START award.\r\nWe thank C. Moussion for establishing the intralymphatic
injection at IST Austria and for providing anti-PNAd hybridoma supernatant, R. Förster
and A. Braun for sharing the intralymphatic injection technology, K. Vaahtomeri
for the lentiviral constructs, M. Hons for establishing in vivo multiphoton imaging,
the Sixt lab for intellectual input, M. Schunn for help with the design of the in
vivo experiments, F. Langer for technical assistance with the in vivo experiments,
the bioimaging facility of IST Austria for support, and R. Efferl for providing
the CT26 cell line."
article_processing_charge: No
article_type: original
author:
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Helga
full_name: Schachner, Helga
last_name: Schachner
- first_name: Gabriele
full_name: Asfour, Gabriele
last_name: Asfour
- first_name: Zsuzsanna
full_name: Bagó Horváth, Zsuzsanna
last_name: Bagó Horváth
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- first_name: Pavel
full_name: Uhrin, Pavel
last_name: Uhrin
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
citation:
ama: Brown M, Assen FP, Leithner AF, et al. Lymph node blood vessels provide exit
routes for metastatic tumor cell dissemination in mice. Science. 2018;359(6382):1408-1411.
doi:10.1126/science.aal3662
apa: Brown, M., Assen, F. P., Leithner, A. F., Abe, J., Schachner, H., Asfour, G.,
… Kerjaschki, D. (2018). Lymph node blood vessels provide exit routes for metastatic
tumor cell dissemination in mice. Science. American Association for the
Advancement of Science. https://doi.org/10.1126/science.aal3662
chicago: Brown, Markus, Frank P Assen, Alexander F Leithner, Jun Abe, Helga Schachner,
Gabriele Asfour, Zsuzsanna Bagó Horváth, et al. “Lymph Node Blood Vessels Provide
Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” Science.
American Association for the Advancement of Science, 2018. https://doi.org/10.1126/science.aal3662.
ieee: M. Brown et al., “Lymph node blood vessels provide exit routes for
metastatic tumor cell dissemination in mice,” Science, vol. 359, no. 6382.
American Association for the Advancement of Science, pp. 1408–1411, 2018.
ista: Brown M, Assen FP, Leithner AF, Abe J, Schachner H, Asfour G, Bagó Horváth
Z, Stein J, Uhrin P, Sixt MK, Kerjaschki D. 2018. Lymph node blood vessels provide
exit routes for metastatic tumor cell dissemination in mice. Science. 359(6382),
1408–1411.
mla: Brown, Markus, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic
Tumor Cell Dissemination in Mice.” Science, vol. 359, no. 6382, American
Association for the Advancement of Science, 2018, pp. 1408–11, doi:10.1126/science.aal3662.
short: M. Brown, F.P. Assen, A.F. Leithner, J. Abe, H. Schachner, G. Asfour, Z.
Bagó Horváth, J. Stein, P. Uhrin, M.K. Sixt, D. Kerjaschki, Science 359 (2018)
1408–1411.
date_created: 2018-12-11T11:46:16Z
date_published: 2018-03-23T00:00:00Z
date_updated: 2024-03-28T23:30:09Z
day: '23'
department:
- _id: MiSi
doi: 10.1126/science.aal3662
ec_funded: 1
external_id:
isi:
- '000428043600047'
pmid:
- '29567714'
intvolume: ' 359'
isi: 1
issue: '6382'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1126/science.aal3662
month: '03'
oa: 1
oa_version: Published Version
page: 1408 - 1411
pmid: 1
project:
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7428'
quality_controlled: '1'
related_material:
record:
- id: '6947'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination
in mice
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 359
year: '2018'
...
---
_id: '323'
abstract:
- lang: eng
text: 'In the here presented thesis, we explore the role of branched actin networks
in cell migration and antigen presentation, the two most relevant processes in
dendritic cell biology. Branched actin networks construct lamellipodial protrusions
at the leading edge of migrating cells. These are typically seen as adhesive structures,
which mediate force transduction to the extracellular matrix that leads to forward
locomotion. We ablated Arp2/3 nucleation promoting factor WAVE in DCs and found
that the resulting cells lack lamellipodial protrusions. Instead, depending on
the maturation state, one or multiple filopodia were formed. By challenging these
cells in a variety of migration assays we found that lamellipodial protrusions
are dispensable for the locomotion of leukocytes and actually dampen the speed
of migration. However, lamellipodia are critically required to negotiate complex
environments that DCs experience while they travel to the next draining lymph
node. Taken together our results suggest that leukocyte lamellipodia have rather
a sensory- than a force transducing function. Furthermore, we show for the first
time structure and dynamics of dendritic cell F-actin at the immunological synapse
with naïve T cells. Dendritic cell F-actin appears as dynamic foci that are nucleated
by the Arp2/3 complex. WAVE ablated dendritic cells show increased membrane tension,
leading to an altered ultrastructure of the immunological synapse and severe T
cell priming defects. These results point towards a previously unappreciated role
of the cellular mechanics of dendritic cells in T cell activation. Additionally,
we present a novel cell culture based system for the differentiation of dendritic
cells from conditionally immortalized hematopoietic precursors. These precursor
cells are genetically tractable via the CRISPR/Cas9 system while they retain their
ability to differentiate into highly migratory dendritic cells and other immune
cells. This will foster the study of all aspects of dendritic cell biology and
beyond. '
acknowledged_ssus:
- _id: NanoFab
- _id: Bio
- _id: PreCl
- _id: EM-Fac
acknowledgement: "First of all I would like to thank Michael Sixt for giving me the
opportunity to work in \r\nhis group and for his support throughout the years. He
is a truly inspiring person and \r\nthe best boss one can imagine. I would
\ also like to thank all current and past \r\nmembers of the Sixt group for
their help and the great working atmosphere in the lab. \r\nIt is a true privilege
to work with such a bright, funny and friendly group of people and \r\nI’m proud
\ that I could be part of it. Furthermore, I would like to say ‘thank
\ you’ to Daria Siekhaus for all the meetings and discussion we had throughout
the years \r\nand to Federica Benvenuti for being part of my committee.
\ I am also grateful to Jack \r\nMerrin in the nanofabrication facility
\ and all the people working in the bioimaging-\r\n, the electron microscopy-
and the preclinical facilities."
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
citation:
ama: Leithner AF. Branched actin networks in dendritic cell biology. 2018. doi:10.15479/AT:ISTA:th_998
apa: Leithner, A. F. (2018). Branched actin networks in dendritic cell biology.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_998
chicago: Leithner, Alexander F. “Branched Actin Networks in Dendritic Cell Biology.”
Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_998.
ieee: A. F. Leithner, “Branched actin networks in dendritic cell biology,” Institute
of Science and Technology Austria, 2018.
ista: Leithner AF. 2018. Branched actin networks in dendritic cell biology. Institute
of Science and Technology Austria.
mla: Leithner, Alexander F. Branched Actin Networks in Dendritic Cell Biology.
Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_998.
short: A.F. Leithner, Branched Actin Networks in Dendritic Cell Biology, Institute
of Science and Technology Austria, 2018.
date_created: 2018-12-11T11:45:49Z
date_published: 2018-04-12T00:00:00Z
date_updated: 2023-09-07T12:39:44Z
day: '12'
ddc:
- '571'
- '599'
- '610'
degree_awarded: PhD
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:th_998
file:
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checksum: d5e3edbac548c26c1fa43a4b37a54a4c
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date_created: 2019-04-05T09:23:11Z
date_updated: 2021-02-11T23:30:17Z
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file_size: 29027671
relation: source_file
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checksum: 071f7476db29e41146824ebd0697cb10
content_type: application/pdf
creator: dernst
date_created: 2019-04-05T09:23:11Z
date_updated: 2021-02-11T11:17:16Z
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file_size: 66045341
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file_date_updated: 2021-02-11T23:30:17Z
has_accepted_license: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: '99'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '7542'
pubrep_id: '998'
related_material:
record:
- id: '1321'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: Branched actin networks in dendritic cell biology
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2018'
...
---
_id: '15'
abstract:
- lang: eng
text: Although much is known about the physiological framework of T cell motility,
and numerous rate-limiting molecules have been identified through loss-of-function
approaches, an integrated functional concept of T cell motility is lacking. Here,
we used in vivo precision morphometry together with analysis of cytoskeletal dynamics
in vitro to deconstruct the basic mechanisms of T cell migration within lymphatic
organs. We show that the contributions of the integrin LFA-1 and the chemokine
receptor CCR7 are complementary rather than positioned in a linear pathway, as
they are during leukocyte extravasation from the blood vasculature. Our data demonstrate
that CCR7 controls cortical actin flows, whereas integrins mediate substrate friction
that is sufficient to drive locomotion in the absence of considerable surface
adhesions and plasma membrane flux.
acknowledged_ssus:
- _id: SSU
acknowledgement: This work was funded by grants from the European Research Council
(ERC StG 281556 and CoG 724373) and the Austrian Science Foundation (FWF) to M.S.
and by Swiss National Foundation (SNF) project grants 31003A_135649, 31003A_153457
and CR23I3_156234 to J.V.S. F.G. received funding from the European Union’s Horizon
2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement
no. 747687, and J.R. was funded by an EMBO long-term fellowship (ALTF 1396-2014).
article_processing_charge: No
author:
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Hons M, Kopf A, Hauschild R, et al. Chemokines and integrins independently
tune actin flow and substrate friction during intranodal migration of T cells.
Nature Immunology. 2018;19(6):606-616. doi:10.1038/s41590-018-0109-z
apa: Hons, M., Kopf, A., Hauschild, R., Leithner, A. F., Gärtner, F. R., Abe, J.,
… Sixt, M. K. (2018). Chemokines and integrins independently tune actin flow and
substrate friction during intranodal migration of T cells. Nature Immunology.
Nature Publishing Group. https://doi.org/10.1038/s41590-018-0109-z
chicago: Hons, Miroslav, Aglaja Kopf, Robert Hauschild, Alexander F Leithner, Florian
R Gärtner, Jun Abe, Jörg Renkawitz, Jens Stein, and Michael K Sixt. “Chemokines
and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal
Migration of T Cells.” Nature Immunology. Nature Publishing Group, 2018.
https://doi.org/10.1038/s41590-018-0109-z.
ieee: M. Hons et al., “Chemokines and integrins independently tune actin
flow and substrate friction during intranodal migration of T cells,” Nature
Immunology, vol. 19, no. 6. Nature Publishing Group, pp. 606–616, 2018.
ista: Hons M, Kopf A, Hauschild R, Leithner AF, Gärtner FR, Abe J, Renkawitz J,
Stein J, Sixt MK. 2018. Chemokines and integrins independently tune actin flow
and substrate friction during intranodal migration of T cells. Nature Immunology.
19(6), 606–616.
mla: Hons, Miroslav, et al. “Chemokines and Integrins Independently Tune Actin Flow
and Substrate Friction during Intranodal Migration of T Cells.” Nature Immunology,
vol. 19, no. 6, Nature Publishing Group, 2018, pp. 606–16, doi:10.1038/s41590-018-0109-z.
short: M. Hons, A. Kopf, R. Hauschild, A.F. Leithner, F.R. Gärtner, J. Abe, J. Renkawitz,
J. Stein, M.K. Sixt, Nature Immunology 19 (2018) 606–616.
date_created: 2018-12-11T11:44:10Z
date_published: 2018-05-18T00:00:00Z
date_updated: 2024-03-28T23:30:40Z
day: '18'
department:
- _id: MiSi
- _id: Bio
doi: 10.1038/s41590-018-0109-z
ec_funded: 1
external_id:
isi:
- '000433041500026'
pmid:
- '29777221'
intvolume: ' 19'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/29777221
month: '05'
oa: 1
oa_version: Published Version
page: 606 - 616
pmid: 1
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
- _id: 25A48D24-B435-11E9-9278-68D0E5697425
grant_number: ALTF 1396-2014
name: Molecular and system level view of immune cell migration
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '8040'
quality_controlled: '1'
related_material:
record:
- id: '6891'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Chemokines and integrins independently tune actin flow and substrate friction
during intranodal migration of T cells
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 19
year: '2018'
...
---
_id: '569'
abstract:
- lang: eng
text: The actomyosin ring generates force to ingress the cytokinetic cleavage furrow
in animal cells, yet its filament organization and the mechanism of contractility
is not well understood. We quantified actin filament order in human cells using
fluorescence polarization microscopy and found that cleavage furrow ingression
initiates by contraction of an equatorial actin network with randomly oriented
filaments. The network subsequently gradually reoriented actin filaments along
the cell equator. This strictly depended on myosin II activity, suggesting local
network reorganization by mechanical forces. Cortical laser microsurgery revealed
that during cytokinesis progression, mechanical tension increased substantially
along the direction of the cell equator, while the network contracted laterally
along the pole-to-pole axis without a detectable increase in tension. Our data
suggest that an asymmetric increase in cortical tension promotes filament reorientation
along the cytokinetic cleavage furrow, which might have implications for diverse
other biological processes involving actomyosin rings.
article_number: e30867
author:
- first_name: Felix
full_name: Spira, Felix
last_name: Spira
- first_name: Sara
full_name: Cuylen Haering, Sara
last_name: Cuylen Haering
- first_name: Shalin
full_name: Mehta, Shalin
last_name: Mehta
- first_name: Matthias
full_name: Samwer, Matthias
last_name: Samwer
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Amitabh
full_name: Verma, Amitabh
last_name: Verma
- first_name: Rudolf
full_name: Oldenbourg, Rudolf
last_name: Oldenbourg
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Daniel
full_name: Gerlich, Daniel
last_name: Gerlich
citation:
ama: Spira F, Cuylen Haering S, Mehta S, et al. Cytokinesis in vertebrate cells
initiates by contraction of an equatorial actomyosin network composed of randomly
oriented filaments. eLife. 2017;6. doi:10.7554/eLife.30867
apa: Spira, F., Cuylen Haering, S., Mehta, S., Samwer, M., Reversat, A., Verma,
A., … Gerlich, D. (2017). Cytokinesis in vertebrate cells initiates by contraction
of an equatorial actomyosin network composed of randomly oriented filaments. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.30867
chicago: Spira, Felix, Sara Cuylen Haering, Shalin Mehta, Matthias Samwer, Anne
Reversat, Amitabh Verma, Rudolf Oldenbourg, Michael K Sixt, and Daniel Gerlich.
“Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin
Network Composed of Randomly Oriented Filaments.” ELife. eLife Sciences
Publications, 2017. https://doi.org/10.7554/eLife.30867.
ieee: F. Spira et al., “Cytokinesis in vertebrate cells initiates by contraction
of an equatorial actomyosin network composed of randomly oriented filaments,”
eLife, vol. 6. eLife Sciences Publications, 2017.
ista: Spira F, Cuylen Haering S, Mehta S, Samwer M, Reversat A, Verma A, Oldenbourg
R, Sixt MK, Gerlich D. 2017. Cytokinesis in vertebrate cells initiates by contraction
of an equatorial actomyosin network composed of randomly oriented filaments. eLife.
6, e30867.
mla: Spira, Felix, et al. “Cytokinesis in Vertebrate Cells Initiates by Contraction
of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.”
ELife, vol. 6, e30867, eLife Sciences Publications, 2017, doi:10.7554/eLife.30867.
short: F. Spira, S. Cuylen Haering, S. Mehta, M. Samwer, A. Reversat, A. Verma,
R. Oldenbourg, M.K. Sixt, D. Gerlich, ELife 6 (2017).
date_created: 2018-12-11T11:47:14Z
date_published: 2017-11-06T00:00:00Z
date_updated: 2023-02-23T12:30:29Z
day: '06'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.7554/eLife.30867
file:
- access_level: open_access
checksum: ba09c1451153d39e4f4b7cee013e314c
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:40Z
date_updated: 2020-07-14T12:47:10Z
file_id: '4829'
file_name: IST-2017-919-v1+1_elife-30867-figures-v1.pdf
file_size: 9666973
relation: main_file
- access_level: open_access
checksum: 01eb51f1d6ad679947415a51c988e137
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:41Z
date_updated: 2020-07-14T12:47:10Z
file_id: '4830'
file_name: IST-2017-919-v1+2_elife-30867-v1.pdf
file_size: 5951246
relation: main_file
file_date_updated: 2020-07-14T12:47:10Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '7245'
pubrep_id: '919'
quality_controlled: '1'
scopus_import: 1
status: public
title: Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin
network composed of randomly oriented filaments
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2017'
...
---
_id: '571'
abstract:
- lang: eng
text: Blood platelets are critical for hemostasis and thrombosis and play diverse
roles during immune responses. Despite these versatile tasks in mammalian biology,
their skills on a cellular level are deemed limited, mainly consisting in rolling,
adhesion, and aggregate formation. Here, we identify an unappreciated asset of
platelets and show that adherent platelets use adhesion receptors to mechanically
probe the adhesive substrate in their local microenvironment. When actomyosin-dependent
traction forces overcome substrate resistance, platelets migrate and pile up the
adhesive substrate together with any bound particulate material. They use this
ability to act as cellular scavengers, scanning the vascular surface for potential
invaders and collecting deposited bacteria. Microbe collection by migrating platelets
boosts the activity of professional phagocytes, exacerbating inflammatory tissue
injury in sepsis. This assigns platelets a central role in innate immune responses
and identifies them as potential targets to dampen inflammatory tissue damage
in clinical scenarios of severe systemic infection. In addition to their role
in thrombosis and hemostasis, platelets can also migrate to sites of infection
to help trap bacteria and clear the vascular surface.
author:
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Zerkah
full_name: Ahmad, Zerkah
last_name: Ahmad
- first_name: Gerhild
full_name: Rosenberger, Gerhild
last_name: Rosenberger
- first_name: Shuxia
full_name: Fan, Shuxia
last_name: Fan
- first_name: Leo
full_name: Nicolai, Leo
last_name: Nicolai
- first_name: Benjamin
full_name: Busch, Benjamin
last_name: Busch
- first_name: Gökce
full_name: Yavuz, Gökce
last_name: Yavuz
- first_name: Manja
full_name: Luckner, Manja
last_name: Luckner
- first_name: Hellen
full_name: Ishikawa Ankerhold, Hellen
last_name: Ishikawa Ankerhold
- first_name: Roman
full_name: Hennel, Roman
last_name: Hennel
- first_name: Alexandre
full_name: Benechet, Alexandre
last_name: Benechet
- first_name: Michael
full_name: Lorenz, Michael
last_name: Lorenz
- first_name: Sue
full_name: Chandraratne, Sue
last_name: Chandraratne
- first_name: Irene
full_name: Schubert, Irene
last_name: Schubert
- first_name: Sebastian
full_name: Helmer, Sebastian
last_name: Helmer
- first_name: Bianca
full_name: Striednig, Bianca
last_name: Striednig
- first_name: Konstantin
full_name: Stark, Konstantin
last_name: Stark
- first_name: Marek
full_name: Janko, Marek
last_name: Janko
- first_name: Ralph
full_name: Böttcher, Ralph
last_name: Böttcher
- first_name: Admar
full_name: Verschoor, Admar
last_name: Verschoor
- first_name: Catherine
full_name: Leon, Catherine
last_name: Leon
- first_name: Christian
full_name: Gachet, Christian
last_name: Gachet
- first_name: Thomas
full_name: Gudermann, Thomas
last_name: Gudermann
- first_name: Michael
full_name: Mederos Y Schnitzler, Michael
last_name: Mederos Y Schnitzler
- first_name: Zachary
full_name: Pincus, Zachary
last_name: Pincus
- first_name: Matteo
full_name: Iannacone, Matteo
last_name: Iannacone
- first_name: Rainer
full_name: Haas, Rainer
last_name: Haas
- first_name: Gerhard
full_name: Wanner, Gerhard
last_name: Wanner
- first_name: Kirsten
full_name: Lauber, Kirsten
last_name: Lauber
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
citation:
ama: Gärtner FR, Ahmad Z, Rosenberger G, et al. Migrating platelets are mechano
scavengers that collect and bundle bacteria. Cell Press. 2017;171(6):1368-1382.
doi:10.1016/j.cell.2017.11.001
apa: Gärtner, F. R., Ahmad, Z., Rosenberger, G., Fan, S., Nicolai, L., Busch, B.,
… Massberg, S. (2017). Migrating platelets are mechano scavengers that collect
and bundle bacteria. Cell Press. Cell Press. https://doi.org/10.1016/j.cell.2017.11.001
chicago: Gärtner, Florian R, Zerkah Ahmad, Gerhild Rosenberger, Shuxia Fan, Leo
Nicolai, Benjamin Busch, Gökce Yavuz, et al. “Migrating Platelets Are Mechano
Scavengers That Collect and Bundle Bacteria.” Cell Press. Cell Press, 2017.
https://doi.org/10.1016/j.cell.2017.11.001.
ieee: F. R. Gärtner et al., “Migrating platelets are mechano scavengers that
collect and bundle bacteria,” Cell Press, vol. 171, no. 6. Cell Press,
pp. 1368–1382, 2017.
ista: Gärtner FR, Ahmad Z, Rosenberger G, Fan S, Nicolai L, Busch B, Yavuz G, Luckner
M, Ishikawa Ankerhold H, Hennel R, Benechet A, Lorenz M, Chandraratne S, Schubert
I, Helmer S, Striednig B, Stark K, Janko M, Böttcher R, Verschoor A, Leon C, Gachet
C, Gudermann T, Mederos Y Schnitzler M, Pincus Z, Iannacone M, Haas R, Wanner
G, Lauber K, Sixt MK, Massberg S. 2017. Migrating platelets are mechano scavengers
that collect and bundle bacteria. Cell Press. 171(6), 1368–1382.
mla: Gärtner, Florian R., et al. “Migrating Platelets Are Mechano Scavengers That
Collect and Bundle Bacteria.” Cell Press, vol. 171, no. 6, Cell Press,
2017, pp. 1368–82, doi:10.1016/j.cell.2017.11.001.
short: F.R. Gärtner, Z. Ahmad, G. Rosenberger, S. Fan, L. Nicolai, B. Busch, G.
Yavuz, M. Luckner, H. Ishikawa Ankerhold, R. Hennel, A. Benechet, M. Lorenz, S.
Chandraratne, I. Schubert, S. Helmer, B. Striednig, K. Stark, M. Janko, R. Böttcher,
A. Verschoor, C. Leon, C. Gachet, T. Gudermann, M. Mederos Y Schnitzler, Z. Pincus,
M. Iannacone, R. Haas, G. Wanner, K. Lauber, M.K. Sixt, S. Massberg, Cell Press
171 (2017) 1368–1382.
date_created: 2018-12-11T11:47:15Z
date_published: 2017-11-30T00:00:00Z
date_updated: 2021-01-12T08:03:15Z
day: '30'
department:
- _id: MiSi
doi: 10.1016/j.cell.2017.11.001
ec_funded: 1
intvolume: ' 171'
issue: '6'
language:
- iso: eng
month: '11'
oa_version: None
page: 1368 - 1382
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Cell Press
publication_identifier:
issn:
- '00928674'
publication_status: published
publisher: Cell Press
publist_id: '7243'
quality_controlled: '1'
scopus_import: 1
status: public
title: Migrating platelets are mechano scavengers that collect and bundle bacteria
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 171
year: '2017'
...
---
_id: '659'
abstract:
- lang: eng
text: Migration frequently involves Rac-mediated protrusion of lamellipodia, formed
by Arp2/3 complex-dependent branching thought to be crucial for force generation
and stability of these networks. The formins FMNL2 and FMNL3 are Cdc42 effectors
targeting to the lamellipodium tip and shown here to nucleate and elongate actin
filaments with complementary activities in vitro. In migrating B16-F1 melanoma
cells, both formins contribute to the velocity of lamellipodium protrusion. Loss
of FMNL2/3 function in melanoma cells and fibroblasts reduces lamellipodial width,
actin filament density and -bundling, without changing patterns of Arp2/3 complex
incorporation. Strikingly, in melanoma cells, FMNL2/3 gene inactivation almost
completely abolishes protrusion forces exerted by lamellipodia and modifies their
ultrastructural organization. Consistently, CRISPR/Cas-mediated depletion of FMNL2/3
in fibroblasts reduces both migration and capability of cells to move against
viscous media. Together, we conclude that force generation in lamellipodia strongly
depends on FMNL formin activity, operating in addition to Arp2/3 complex-dependent
filament branching.
article_number: '14832'
article_processing_charge: No
author:
- first_name: Frieda
full_name: Kage, Frieda
last_name: Kage
- first_name: Moritz
full_name: Winterhoff, Moritz
last_name: Winterhoff
- first_name: Vanessa
full_name: Dimchev, Vanessa
last_name: Dimchev
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Tobias
full_name: Thalheim, Tobias
last_name: Thalheim
- first_name: Anika
full_name: Freise, Anika
last_name: Freise
- first_name: Stefan
full_name: Brühmann, Stefan
last_name: Brühmann
- first_name: Jana
full_name: Kollasser, Jana
last_name: Kollasser
- first_name: Jennifer
full_name: Block, Jennifer
last_name: Block
- first_name: Georgi A
full_name: Dimchev, Georgi A
last_name: Dimchev
- first_name: Matthias
full_name: Geyer, Matthias
last_name: Geyer
- first_name: Hams
full_name: Schnittler, Hams
last_name: Schnittler
- first_name: Cord
full_name: Brakebusch, Cord
last_name: Brakebusch
- first_name: Theresia
full_name: Stradal, Theresia
last_name: Stradal
- first_name: Marie
full_name: Carlier, Marie
last_name: Carlier
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Josef
full_name: Käs, Josef
last_name: Käs
- first_name: Jan
full_name: Faix, Jan
last_name: Faix
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
citation:
ama: Kage F, Winterhoff M, Dimchev V, et al. FMNL formins boost lamellipodial force
generation. Nature Communications. 2017;8. doi:10.1038/ncomms14832
apa: Kage, F., Winterhoff, M., Dimchev, V., Müller, J., Thalheim, T., Freise, A.,
… Rottner, K. (2017). FMNL formins boost lamellipodial force generation. Nature
Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms14832
chicago: Kage, Frieda, Moritz Winterhoff, Vanessa Dimchev, Jan Müller, Tobias Thalheim,
Anika Freise, Stefan Brühmann, et al. “FMNL Formins Boost Lamellipodial Force
Generation.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/ncomms14832.
ieee: F. Kage et al., “FMNL formins boost lamellipodial force generation,”
Nature Communications, vol. 8. Nature Publishing Group, 2017.
ista: Kage F, Winterhoff M, Dimchev V, Müller J, Thalheim T, Freise A, Brühmann
S, Kollasser J, Block J, Dimchev GA, Geyer M, Schnittler H, Brakebusch C, Stradal
T, Carlier M, Sixt MK, Käs J, Faix J, Rottner K. 2017. FMNL formins boost lamellipodial
force generation. Nature Communications. 8, 14832.
mla: Kage, Frieda, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature
Communications, vol. 8, 14832, Nature Publishing Group, 2017, doi:10.1038/ncomms14832.
short: F. Kage, M. Winterhoff, V. Dimchev, J. Müller, T. Thalheim, A. Freise, S.
Brühmann, J. Kollasser, J. Block, G.A. Dimchev, M. Geyer, H. Schnittler, C. Brakebusch,
T. Stradal, M. Carlier, M.K. Sixt, J. Käs, J. Faix, K. Rottner, Nature Communications
8 (2017).
date_created: 2018-12-11T11:47:46Z
date_published: 2017-03-22T00:00:00Z
date_updated: 2021-01-12T08:08:06Z
day: '22'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1038/ncomms14832
file:
- access_level: open_access
checksum: dae30190291c3630e8102d8714a8d23e
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:21Z
date_updated: 2020-07-14T12:47:34Z
file_id: '5072'
file_name: IST-2017-902-v1+1_Kage_et_al-2017-Nature_Communications.pdf
file_size: 9523746
relation: main_file
file_date_updated: 2020-07-14T12:47:34Z
has_accepted_license: '1'
intvolume: ' 8'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
issn:
- '20411723'
publication_status: published
publisher: Nature Publishing Group
publist_id: '7075'
pubrep_id: '902'
quality_controlled: '1'
scopus_import: 1
status: public
title: FMNL formins boost lamellipodial force generation
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2017'
...
---
_id: '668'
abstract:
- lang: eng
text: Macrophage filopodia, finger-like membrane protrusions, were first implicated
in phagocytosis more than 100 years ago, but little is still known about the involvement
of these actin-dependent structures in particle clearance. Using spinning disk
confocal microscopy to image filopodial dynamics in mouse resident Lifeact-EGFP
macrophages, we show that filopodia, or filopodia-like structures, support pathogen
clearance by multiple means. Filopodia supported the phagocytic uptake of bacterial
(Escherichia coli) particles by (i) capturing along the filopodial shaft and surfing
toward the cell body, the most common mode of capture; (ii) capturing via the
tip followed by retraction; (iii) combinations of surfing and retraction; or (iv)
sweeping actions. In addition, filopodia supported the uptake of zymosan (Saccharomyces
cerevisiae) particles by (i) providing fixation, (ii) capturing at the tip and
filopodia-guided actin anterograde flow with phagocytic cup formation, and (iii)
the rapid growth of new protrusions. To explore the role of filopodia-inducing
Cdc42, we generated myeloid-restricted Cdc42 knock-out mice. Cdc42-deficient macrophages
exhibited rapid phagocytic cup kinetics, but reduced particle clearance, which
could be explained by the marked rounded-up morphology of these cells. Macrophages
lacking Myo10, thought to act downstream of Cdc42, had normal morphology, motility,
and phagocytic cup formation, but displayed markedly reduced filopodia formation.
In conclusion, live-cell imaging revealed multiple mechanisms involving macrophage
filopodia in particle capture and engulfment. Cdc42 is not critical for filopodia
or phagocytic cup formation, but plays a key role in driving macrophage lamellipodial
spreading.
article_type: original
author:
- first_name: Markus
full_name: Horsthemke, Markus
last_name: Horsthemke
- first_name: Anne
full_name: Bachg, Anne
last_name: Bachg
- first_name: Katharina
full_name: Groll, Katharina
last_name: Groll
- first_name: Sven
full_name: Moyzio, Sven
last_name: Moyzio
- first_name: Barbara
full_name: Müther, Barbara
last_name: Müther
- first_name: Sandra
full_name: Hemkemeyer, Sandra
last_name: Hemkemeyer
- first_name: Roland
full_name: Wedlich Söldner, Roland
last_name: Wedlich Söldner
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Sebastian
full_name: Tacke, Sebastian
last_name: Tacke
- first_name: Martin
full_name: Bähler, Martin
last_name: Bähler
- first_name: Peter
full_name: Hanley, Peter
last_name: Hanley
citation:
ama: Horsthemke M, Bachg A, Groll K, et al. Multiple roles of filopodial dynamics
in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion.
Journal of Biological Chemistry. 2017;292(17):7258-7273. doi:10.1074/jbc.M116.766923
apa: Horsthemke, M., Bachg, A., Groll, K., Moyzio, S., Müther, B., Hemkemeyer, S.,
… Hanley, P. (2017). Multiple roles of filopodial dynamics in particle capture
and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological
Chemistry. American Society for Biochemistry and Molecular Biology. https://doi.org/10.1074/jbc.M116.766923
chicago: Horsthemke, Markus, Anne Bachg, Katharina Groll, Sven Moyzio, Barbara Müther,
Sandra Hemkemeyer, Roland Wedlich Söldner, et al. “Multiple Roles of Filopodial
Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10
Deletion.” Journal of Biological Chemistry. American Society for Biochemistry
and Molecular Biology, 2017. https://doi.org/10.1074/jbc.M116.766923.
ieee: M. Horsthemke et al., “Multiple roles of filopodial dynamics in particle
capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion,” Journal
of Biological Chemistry, vol. 292, no. 17. American Society for Biochemistry
and Molecular Biology, pp. 7258–7273, 2017.
ista: Horsthemke M, Bachg A, Groll K, Moyzio S, Müther B, Hemkemeyer S, Wedlich
Söldner R, Sixt MK, Tacke S, Bähler M, Hanley P. 2017. Multiple roles of filopodial
dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10
deletion. Journal of Biological Chemistry. 292(17), 7258–7273.
mla: Horsthemke, Markus, et al. “Multiple Roles of Filopodial Dynamics in Particle
Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal
of Biological Chemistry, vol. 292, no. 17, American Society for Biochemistry
and Molecular Biology, 2017, pp. 7258–73, doi:10.1074/jbc.M116.766923.
short: M. Horsthemke, A. Bachg, K. Groll, S. Moyzio, B. Müther, S. Hemkemeyer, R.
Wedlich Söldner, M.K. Sixt, S. Tacke, M. Bähler, P. Hanley, Journal of Biological
Chemistry 292 (2017) 7258–7273.
date_created: 2018-12-11T11:47:49Z
date_published: 2017-04-28T00:00:00Z
date_updated: 2021-01-12T08:08:34Z
day: '28'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1074/jbc.M116.766923
file:
- access_level: open_access
checksum: d488162874326a4bb056065fa549dc4a
content_type: application/pdf
creator: dernst
date_created: 2019-10-24T15:25:42Z
date_updated: 2020-07-14T12:47:37Z
file_id: '6971'
file_name: 2017_JBC_Horsthemke.pdf
file_size: 5647880
relation: main_file
file_date_updated: 2020-07-14T12:47:37Z
has_accepted_license: '1'
intvolume: ' 292'
issue: '17'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 7258 - 7273
publication: Journal of Biological Chemistry
publication_identifier:
issn:
- '00219258'
publication_status: published
publisher: American Society for Biochemistry and Molecular Biology
publist_id: '7059'
quality_controlled: '1'
scopus_import: 1
status: public
title: Multiple roles of filopodial dynamics in particle capture and phagocytosis
and phenotypes of Cdc42 and Myo10 deletion
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 292
year: '2017'
...
---
_id: '672'
abstract:
- lang: eng
text: Trafficking cells frequently transmigrate through epithelial and endothelial
monolayers. How monolayers cooperate with the penetrating cells to support their
transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic
capillaries as a model system for transendothelial migration. We find that the
chemokine CCL21, which is the decisive guidance cue for intravasation, mainly
localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial
cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes
extracellularly enriched at the sites of endothelial cell-cell junctions. When
we reconstitute the transmigration process in vitro, we find that secretion of
CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and
selective calcium chelation in lymphatic endothelium attenuates transmigration.
Altogether, our data demonstrate a chemokine-mediated feedback between DCs and
lymphatic endothelium, which facilitates transendothelial migration.
article_processing_charge: Yes
author:
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
- first_name: Matthias
full_name: Mehling, Matthias
id: 3C23B994-F248-11E8-B48F-1D18A9856A87
last_name: Mehling
orcid: 0000-0001-8599-1226
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the
chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia.
Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027
apa: Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling,
M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes
dendritic cell transmigration across lymphatic endothelia. Cell Reports.
Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027
chicago: Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander
F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered
Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic
Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027.
ieee: K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21
promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports,
vol. 19, no. 5. Cell Press, pp. 902–909, 2017.
ista: Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann
W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic
cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909.
mla: Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21
Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports,
vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027.
short: K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling,
W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.
date_created: 2018-12-11T11:47:50Z
date_published: 2017-05-02T00:00:00Z
date_updated: 2023-02-23T12:50:09Z
day: '02'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
- _id: EM-Fac
doi: 10.1016/j.celrep.2017.04.027
ec_funded: 1
file:
- access_level: open_access
checksum: 8fdddaab1f1d76a6ec9ca94dcb6b07a2
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:54Z
date_updated: 2020-07-14T12:47:38Z
file_id: '5109'
file_name: IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf
file_size: 2248814
relation: main_file
file_date_updated: 2020-07-14T12:47:38Z
has_accepted_license: '1'
intvolume: ' 19'
issue: '5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 902 - 909
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Cell Reports
publication_identifier:
issn:
- '22111247'
publication_status: published
publisher: Cell Press
publist_id: '7052'
pubrep_id: '900'
quality_controlled: '1'
scopus_import: 1
status: public
title: Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration
across lymphatic endothelia
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2017'
...
---
_id: '674'
abstract:
- lang: eng
text: Navigation of cells along gradients of guidance cues is a determining step
in many developmental and immunological processes. Gradients can either be soluble
or immobilized to tissues as demonstrated for the haptotactic migration of dendritic
cells (DCs) toward higher concentrations of immobilized chemokine CCL21. To elucidate
how gradient characteristics govern cellular response patterns, we here introduce
an in vitro system allowing to track migratory responses of DCs to precisely controlled
immobilized gradients of CCL21. We find that haptotactic sensing depends on the
absolute CCL21 concentration and local steepness of the gradient, consistent with
a scenario where DC directionality is governed by the signal-to-noise ratio of
CCL21 binding to the receptor CCR7. We find that the conditions for optimal DC
guidance are perfectly provided by the CCL21 gradients we measure in vivo. Furthermore,
we find that CCR7 signal termination by the G-protein-coupled receptor kinase
6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient
sensing in vitro and confirm those observations in vivo. These findings suggest
that stable, tissue-bound CCL21 gradients as sustainable “roads” ensure optimal
guidance in vivo.
author:
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Veronika
full_name: Bierbaum, Veronika
id: 3FD04378-F248-11E8-B48F-1D18A9856A87
last_name: Bierbaum
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Teresa
full_name: Tarrant, Teresa
last_name: Tarrant
- first_name: Tobias
full_name: Bollenbach, Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic
chemokine gradients in a manner governed by signal to noise ratio and dependent
on GRK6. Current Biology. 2017;27(9):1314-1325. doi:10.1016/j.cub.2017.04.004
apa: Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries,
I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients
in a manner governed by signal to noise ratio and dependent on GRK6. Current
Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.04.004
chicago: Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus
Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret
Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio
and Dependent on GRK6.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.04.004.
ieee: J. Schwarz et al., “Dendritic cells interpret haptotactic chemokine
gradients in a manner governed by signal to noise ratio and dependent on GRK6,”
Current Biology, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017.
ista: Schwarz J, Bierbaum V, Vaahtomeri K, Hauschild R, Brown M, de Vries I, Leithner
AF, Reversat A, Merrin J, Tarrant T, Bollenbach MT, Sixt MK. 2017. Dendritic cells
interpret haptotactic chemokine gradients in a manner governed by signal to noise
ratio and dependent on GRK6. Current Biology. 27(9), 1314–1325.
mla: Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients
in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current
Biology, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:10.1016/j.cub.2017.04.004.
short: J. Schwarz, V. Bierbaum, K. Vaahtomeri, R. Hauschild, M. Brown, I. de Vries,
A.F. Leithner, A. Reversat, J. Merrin, T. Tarrant, M.T. Bollenbach, M.K. Sixt,
Current Biology 27 (2017) 1314–1325.
date_created: 2018-12-11T11:47:51Z
date_published: 2017-05-09T00:00:00Z
date_updated: 2023-02-23T12:50:44Z
day: '09'
department:
- _id: MiSi
- _id: Bio
- _id: NanoFab
doi: 10.1016/j.cub.2017.04.004
ec_funded: 1
intvolume: ' 27'
issue: '9'
language:
- iso: eng
month: '05'
oa_version: None
page: 1314 - 1325
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Current Biology
publication_identifier:
issn:
- '09609822'
publication_status: published
publisher: Cell Press
publist_id: '7050'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dendritic cells interpret haptotactic chemokine gradients in a manner governed
by signal to noise ratio and dependent on GRK6
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 27
year: '2017'
...
---
_id: '677'
abstract:
- lang: eng
text: The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler
that acts in transcription, replication, and genome stability. It is required
for resistance against genotoxic agents and is involved in the repair of DNA double-strand
breaks (DSBs) by homologous recombination (HR). However, the causes of the HR
defect in INO80-C mutant cells are controversial. Here, we unite previous findings
using a system to study HR with high spatial resolution in budding yeast. We find
that INO80-C has at least two distinct functions during HR—DNA end resection and
presynaptic filament formation. Importantly, the second function is linked to
the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation
and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic
filament formation is the crucial INO80-C function during HR.
author:
- first_name: Claudio
full_name: Lademann, Claudio
last_name: Lademann
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Boris
full_name: Pfander, Boris
last_name: Pfander
- first_name: Stefan
full_name: Jentsch, Stefan
last_name: Jentsch
citation:
ama: Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z
to promote presynaptic filament formation during homologous recombination. Cell
Reports. 2017;19(7):1294-1303. doi:10.1016/j.celrep.2017.04.051
apa: Lademann, C., Renkawitz, J., Pfander, B., & Jentsch, S. (2017). The INO80
complex removes H2A.Z to promote presynaptic filament formation during homologous
recombination. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.051
chicago: Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The
INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous
Recombination.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.051.
ieee: C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex
removes H2A.Z to promote presynaptic filament formation during homologous recombination,”
Cell Reports, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017.
ista: Lademann C, Renkawitz J, Pfander B, Jentsch S. 2017. The INO80 complex removes
H2A.Z to promote presynaptic filament formation during homologous recombination.
Cell Reports. 19(7), 1294–1303.
mla: Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic
Filament Formation during Homologous Recombination.” Cell Reports, vol.
19, no. 7, Cell Press, 2017, pp. 1294–303, doi:10.1016/j.celrep.2017.04.051.
short: C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017)
1294–1303.
date_created: 2018-12-11T11:47:52Z
date_published: 2017-05-16T00:00:00Z
date_updated: 2021-01-12T08:08:57Z
day: '16'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.celrep.2017.04.051
file:
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intvolume: ' 19'
issue: '7'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 1294 - 1303
publication: Cell Reports
publication_identifier:
issn:
- '22111247'
publication_status: published
publisher: Cell Press
publist_id: '7046'
pubrep_id: '899'
quality_controlled: '1'
scopus_import: 1
status: public
title: The INO80 complex removes H2A.Z to promote presynaptic filament formation during
homologous recombination
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2017'
...
---
_id: '694'
abstract:
- lang: eng
text: A change regarding the extent of adhesion - hereafter referred to as adhesion
plasticity - between adhesive and less-adhesive states of mammalian cells is important
for their behavior. To investigate adhesion plasticity, we have selected a stable
isogenic subpopulation of human MDA-MB-468 breast carcinoma cells growing in suspension.
These suspension cells are unable to re-adhere to various matrices or to contract
three-dimensional collagen lattices. By using transcriptome analysis, we identified
the focal adhesion protein tensin3 (Tns3) as a determinant of adhesion plasticity.
Tns3 is strongly reduced at mRNA and protein levels in suspension cells. Furthermore,
by transiently challenging breast cancer cells to grow under non-adherent conditions
markedly reduces Tns3 protein expression, which is regained upon re-adhesion.
Stable knockdown of Tns3 in parental MDA-MB-468 cells results in defective adhesion,
spreading and migration. Tns3-knockdown cells display impaired structure and dynamics
of focal adhesion complexes as determined by immunostaining. Restoration of Tns3
protein expression in suspension cells partially rescues adhesion and focal contact
composition. Our work identifies Tns3 as a crucial focal adhesion component regulated
by, and functionally contributing to, the switch between adhesive and non-adhesive
states in MDA-MB-468 cancer cells.
article_type: original
author:
- first_name: Astrid
full_name: Veß, Astrid
last_name: Veß
- first_name: Ulrich
full_name: Blache, Ulrich
last_name: Blache
- first_name: Laura
full_name: Leitner, Laura
last_name: Leitner
- first_name: Angela
full_name: Kurz, Angela
last_name: Kurz
- first_name: Anja
full_name: Ehrenpfordt, Anja
last_name: Ehrenpfordt
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Guido
full_name: Posern, Guido
last_name: Posern
citation:
ama: Veß A, Blache U, Leitner L, et al. A dual phenotype of MDA MB 468 cancer cells
reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell
Science. 2017;130(13):2172-2184. doi:10.1242/jcs.200899
apa: Veß, A., Blache, U., Leitner, L., Kurz, A., Ehrenpfordt, A., Sixt, M. K., &
Posern, G. (2017). A dual phenotype of MDA MB 468 cancer cells reveals mutual
regulation of tensin3 and adhesion plasticity. Journal of Cell Science.
Company of Biologists. https://doi.org/10.1242/jcs.200899
chicago: Veß, Astrid, Ulrich Blache, Laura Leitner, Angela Kurz, Anja Ehrenpfordt,
Michael K Sixt, and Guido Posern. “A Dual Phenotype of MDA MB 468 Cancer Cells
Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell
Science. Company of Biologists, 2017. https://doi.org/10.1242/jcs.200899.
ieee: A. Veß et al., “A dual phenotype of MDA MB 468 cancer cells reveals
mutual regulation of tensin3 and adhesion plasticity,” Journal of Cell Science,
vol. 130, no. 13. Company of Biologists, pp. 2172–2184, 2017.
ista: Veß A, Blache U, Leitner L, Kurz A, Ehrenpfordt A, Sixt MK, Posern G. 2017.
A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3
and adhesion plasticity. Journal of Cell Science. 130(13), 2172–2184.
mla: Veß, Astrid, et al. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual
Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science,
vol. 130, no. 13, Company of Biologists, 2017, pp. 2172–84, doi:10.1242/jcs.200899.
short: A. Veß, U. Blache, L. Leitner, A. Kurz, A. Ehrenpfordt, M.K. Sixt, G. Posern,
Journal of Cell Science 130 (2017) 2172–2184.
date_created: 2018-12-11T11:47:58Z
date_published: 2017-07-01T00:00:00Z
date_updated: 2021-01-12T08:09:41Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1242/jcs.200899
external_id:
pmid:
- '28515231'
file:
- access_level: open_access
checksum: 42c81a0a4fc3128883b391c3af3f74bc
content_type: application/pdf
creator: dernst
date_created: 2019-10-24T09:43:56Z
date_updated: 2020-07-14T12:47:45Z
file_id: '6966'
file_name: 2017_CellScience_Vess.pdf
file_size: 10847596
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file_date_updated: 2020-07-14T12:47:45Z
has_accepted_license: '1'
intvolume: ' 130'
issue: '13'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: 2172 - 2184
pmid: 1
publication: Journal of Cell Science
publication_identifier:
issn:
- '00219533'
publication_status: published
publisher: Company of Biologists
publist_id: '7008'
quality_controlled: '1'
scopus_import: 1
status: public
title: A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3
and adhesion plasticity
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 130
year: '2017'
...
---
_id: '1161'
abstract:
- lang: eng
text: Coordinated changes of cell shape are often the result of the excitable, wave-like
dynamics of the actin cytoskeleton. New work shows that, in migrating cells, protrusion
waves arise from mechanochemical crosstalk between adhesion sites, membrane tension
and the actin protrusive machinery.
article_processing_charge: No
author:
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Müller J, Sixt MK. Cell migration: Making the waves. Current Biology.
2017;27(1):R24-R25. doi:10.1016/j.cub.2016.11.035'
apa: 'Müller, J., & Sixt, M. K. (2017). Cell migration: Making the waves. Current
Biology. Cell Press. https://doi.org/10.1016/j.cub.2016.11.035'
chicago: 'Müller, Jan, and Michael K Sixt. “Cell Migration: Making the Waves.” Current
Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2016.11.035.'
ieee: 'J. Müller and M. K. Sixt, “Cell migration: Making the waves,” Current
Biology, vol. 27, no. 1. Cell Press, pp. R24–R25, 2017.'
ista: 'Müller J, Sixt MK. 2017. Cell migration: Making the waves. Current Biology.
27(1), R24–R25.'
mla: 'Müller, Jan, and Michael K. Sixt. “Cell Migration: Making the Waves.” Current
Biology, vol. 27, no. 1, Cell Press, 2017, pp. R24–25, doi:10.1016/j.cub.2016.11.035.'
short: J. Müller, M.K. Sixt, Current Biology 27 (2017) R24–R25.
date_created: 2018-12-11T11:50:29Z
date_published: 2017-01-09T00:00:00Z
date_updated: 2023-09-20T11:28:19Z
day: '09'
department:
- _id: MiSi
doi: 10.1016/j.cub.2016.11.035
external_id:
isi:
- '000391902500010'
intvolume: ' 27'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: R24 - R25
publication: Current Biology
publication_identifier:
issn:
- '09609822'
publication_status: published
publisher: Cell Press
publist_id: '6197'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Cell migration: Making the waves'
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 27
year: '2017'
...