---
_id: '6091'
abstract:
- lang: eng
text: Cortical networks are characterized by sparse connectivity, with synapses
found at only a subset of axo-dendritic contacts. Yet within these networks, neurons
can exhibit high connection probabilities, suggesting that cell-intrinsic factors,
not proximity, determine connectivity. Here, we identify ephrin-B3 (eB3) as a
factor that determines synapse density by mediating a cell-cell competition that
requires ephrin-B-EphB signaling. In a microisland culture system designed to
isolate cell-cell competition, we find that eB3 determines winning and losing
neurons in a contest for synapses. In a Mosaic Analysis with Double Markers (MADM)
genetic mouse model system in vivo the relative levels of eB3 control spine density
in layer 5 and 6 neurons. MADM cortical neurons in vitro reveal that eB3 controls
synapse density independently of action potential-driven activity. Our findings
illustrate a new class of competitive mechanism mediated by trans-synaptic organizing
proteins which control the number of synapses neurons receive relative to neighboring
neurons.
article_number: e41563
article_processing_charge: No
author:
- first_name: Nathan T.
full_name: Henderson, Nathan T.
last_name: Henderson
- first_name: Sylvain J.
full_name: Le Marchand, Sylvain J.
last_name: Le Marchand
- first_name: Martin
full_name: Hruska, Martin
last_name: Hruska
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Matthew B.
full_name: Dalva, Matthew B.
last_name: Dalva
citation:
ama: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. Ephrin-B3
controls excitatory synapse density through cell-cell competition for EphBs. eLife.
2019;8. doi:10.7554/eLife.41563
apa: Henderson, N. T., Le Marchand, S. J., Hruska, M., Hippenmeyer, S., Luo, L.,
& Dalva, M. B. (2019). Ephrin-B3 controls excitatory synapse density through
cell-cell competition for EphBs. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.41563
chicago: Henderson, Nathan T., Sylvain J. Le Marchand, Martin Hruska, Simon Hippenmeyer,
Liqun Luo, and Matthew B. Dalva. “Ephrin-B3 Controls Excitatory Synapse Density
through Cell-Cell Competition for EphBs.” ELife. eLife Sciences Publications,
2019. https://doi.org/10.7554/eLife.41563.
ieee: N. T. Henderson, S. J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, and
M. B. Dalva, “Ephrin-B3 controls excitatory synapse density through cell-cell
competition for EphBs,” eLife, vol. 8. eLife Sciences Publications, 2019.
ista: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. 2019.
Ephrin-B3 controls excitatory synapse density through cell-cell competition for
EphBs. eLife. 8, e41563.
mla: Henderson, Nathan T., et al. “Ephrin-B3 Controls Excitatory Synapse Density
through Cell-Cell Competition for EphBs.” ELife, vol. 8, e41563, eLife
Sciences Publications, 2019, doi:10.7554/eLife.41563.
short: N.T. Henderson, S.J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, M.B.
Dalva, ELife 8 (2019).
date_created: 2019-03-10T22:59:20Z
date_published: 2019-02-21T00:00:00Z
date_updated: 2023-08-24T14:50:50Z
day: '21'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/eLife.41563
external_id:
isi:
- '000459380600001'
pmid:
- '30789343'
file:
- access_level: open_access
checksum: 7b0800d003f14cd06b1802dea0c52941
content_type: application/pdf
creator: dernst
date_created: 2019-03-11T16:15:37Z
date_updated: 2020-07-14T12:47:19Z
file_id: '6098'
file_name: 2019_eLife_Henderson.pdf
file_size: 7260753
relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Ephrin-B3 controls excitatory synapse density through cell-cell competition
for EphBs
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: 8
year: '2019'
...
---
_id: '6046'
abstract:
- lang: eng
text: Sudden stress often triggers diverse, temporally structured gene expression
responses in microbes, but it is largely unknown how variable in time such responses
are and if genes respond in the same temporal order in every single cell. Here,
we quantified timing variability of individual promoters responding to sublethal
antibiotic stress using fluorescent reporters, microfluidics, and time‐lapse microscopy.
We identified lower and upper bounds that put definite constraints on timing variability,
which varies strongly among promoters and conditions. Timing variability can be
interpreted using results from statistical kinetics, which enable us to estimate
the number of rate‐limiting molecular steps underlying different responses. We
found that just a few critical steps control some responses while others rely
on dozens of steps. To probe connections between different stress responses, we
then tracked the temporal order and response time correlations of promoter pairs
in individual cells. Our results support that, when bacteria are exposed to the
antibiotic nitrofurantoin, the ensuing oxidative stress and SOS responses are
part of the same causal chain of molecular events. In contrast, under trimethoprim,
the acid stress response and the SOS response are part of different chains of
events running in parallel. Our approach reveals fundamental constraints on gene
expression timing and provides new insights into the molecular events that underlie
the timing of stress responses.
acknowledged_ssus:
- _id: Bio
article_number: e8470
article_processing_charge: No
author:
- first_name: Karin
full_name: Mitosch, Karin
id: 39B66846-F248-11E8-B48F-1D18A9856A87
last_name: Mitosch
- first_name: Georg
full_name: Rieckh, Georg
id: 34DA8BD6-F248-11E8-B48F-1D18A9856A87
last_name: Rieckh
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Mitosch K, Rieckh G, Bollenbach MT. Temporal order and precision of complex
stress responses in individual bacteria. Molecular systems biology. 2019;15(2).
doi:10.15252/msb.20188470
apa: Mitosch, K., Rieckh, G., & Bollenbach, M. T. (2019). Temporal order and
precision of complex stress responses in individual bacteria. Molecular Systems
Biology. Embo Press. https://doi.org/10.15252/msb.20188470
chicago: Mitosch, Karin, Georg Rieckh, and Mark Tobias Bollenbach. “Temporal Order
and Precision of Complex Stress Responses in Individual Bacteria.” Molecular
Systems Biology. Embo Press, 2019. https://doi.org/10.15252/msb.20188470.
ieee: K. Mitosch, G. Rieckh, and M. T. Bollenbach, “Temporal order and precision
of complex stress responses in individual bacteria,” Molecular systems biology,
vol. 15, no. 2. Embo Press, 2019.
ista: Mitosch K, Rieckh G, Bollenbach MT. 2019. Temporal order and precision of
complex stress responses in individual bacteria. Molecular systems biology. 15(2),
e8470.
mla: Mitosch, Karin, et al. “Temporal Order and Precision of Complex Stress Responses
in Individual Bacteria.” Molecular Systems Biology, vol. 15, no. 2, e8470,
Embo Press, 2019, doi:10.15252/msb.20188470.
short: K. Mitosch, G. Rieckh, M.T. Bollenbach, Molecular Systems Biology 15 (2019).
date_created: 2019-02-24T22:59:18Z
date_published: 2019-02-14T00:00:00Z
date_updated: 2023-08-24T14:49:53Z
day: '14'
department:
- _id: GaTk
doi: 10.15252/msb.20188470
external_id:
isi:
- '000459628300003'
pmid:
- '30765425'
intvolume: ' 15'
isi: 1
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/30765425
month: '02'
oa: 1
oa_version: Submitted Version
pmid: 1
project:
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
- _id: 25EB3A80-B435-11E9-9278-68D0E5697425
grant_number: RGP0042/2013
name: Revealing the fundamental limits of cell growth
publication: Molecular systems biology
publication_status: published
publisher: Embo Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Temporal order and precision of complex stress responses in individual bacteria
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 15
year: '2019'
...
---
_id: '6105'
abstract:
- lang: eng
text: " Hosts can alter their strategy towards pathogens during their lifetime;
that is, they can show phenotypic plasticity in immunity or life history. Immune
priming is one such example, where a previous encounter with a pathogen confers
enhanced protection upon secondary challenge, resulting in reduced pathogen load
(i.e., resistance) and improved host survival. However, an initial encounter might
also enhance tolerance, particularly to less virulent opportunistic pathogens
that establish persistent infections. In this scenario, individuals are better
able to reduce the negative fecundity consequences that result from a high pathogen
burden. Finally, previous exposure may also lead to life‐history adjustments,
such as terminal investment into reproduction.\r\n Using different Drosophila
melanogaster host genotypes and two bacterial pathogens, Lactococcus lactis and
Pseudomonas entomophila, we tested whether previous exposure results in resistance
or tolerance and whether it modifies immune gene expression during an acute‐phase
infection (one day post‐challenge). We then asked whether previous pathogen exposure
affects chronic‐phase pathogen persistence and longer‐term survival (28 days post‐challenge).\r\n
\ We predicted that previous exposure would increase host resistance to an early
stage bacterial infection while it might come at a cost to host fecundity tolerance.
We reasoned that resistance would be due in part to stronger immune gene expression
after challenge. We expected that previous exposure would improve long‐term survival,
that it would reduce infection persistence, and we expected to find genetic variation
in these responses.\r\n We found that previous exposure to P. entomophila weakened
host resistance to a second infection independent of genotype and had no effect
on immune gene expression. Fecundity tolerance showed genotypic variation but
was not influenced by previous exposure. However, L. lactis persisted as a chronic
infection, whereas survivors cleared the more pathogenic P. entomophila infection.\r\n
\ To our knowledge, this is the first study that addresses host tolerance to
bacteria in relation to previous exposure, taking a multi‐faceted approach to
address the topic. Our results suggest that previous exposure comes with transient
costs to resistance during the early stage of infection in this host–pathogen
system and that infection persistence may be bacterium‐specific.\r\n"
article_processing_charge: No
article_type: original
author:
- first_name: Megan
full_name: Kutzer, Megan
id: 29D0B332-F248-11E8-B48F-1D18A9856A87
last_name: Kutzer
orcid: 0000-0002-8696-6978
- first_name: Joachim
full_name: Kurtz, Joachim
last_name: Kurtz
- first_name: Sophie A.O.
full_name: Armitage, Sophie A.O.
last_name: Armitage
citation:
ama: Kutzer M, Kurtz J, Armitage SAO. A multi-faceted approach testing the effects
of previous bacterial exposure on resistance and tolerance. Journal of Animal
Ecology. 2019;88(4):566-578. doi:10.1111/1365-2656.12953
apa: Kutzer, M., Kurtz, J., & Armitage, S. A. O. (2019). A multi-faceted approach
testing the effects of previous bacterial exposure on resistance and tolerance.
Journal of Animal Ecology. Wiley. https://doi.org/10.1111/1365-2656.12953
chicago: Kutzer, Megan, Joachim Kurtz, and Sophie A.O. Armitage. “A Multi-Faceted
Approach Testing the Effects of Previous Bacterial Exposure on Resistance and
Tolerance.” Journal of Animal Ecology. Wiley, 2019. https://doi.org/10.1111/1365-2656.12953.
ieee: M. Kutzer, J. Kurtz, and S. A. O. Armitage, “A multi-faceted approach testing
the effects of previous bacterial exposure on resistance and tolerance,” Journal
of Animal Ecology, vol. 88, no. 4. Wiley, pp. 566–578, 2019.
ista: Kutzer M, Kurtz J, Armitage SAO. 2019. A multi-faceted approach testing the
effects of previous bacterial exposure on resistance and tolerance. Journal of
Animal Ecology. 88(4), 566–578.
mla: Kutzer, Megan, et al. “A Multi-Faceted Approach Testing the Effects of Previous
Bacterial Exposure on Resistance and Tolerance.” Journal of Animal Ecology,
vol. 88, no. 4, Wiley, 2019, pp. 566–78, doi:10.1111/1365-2656.12953.
short: M. Kutzer, J. Kurtz, S.A.O. Armitage, Journal of Animal Ecology 88 (2019)
566–578.
date_created: 2019-03-17T22:59:15Z
date_published: 2019-04-01T00:00:00Z
date_updated: 2023-08-25T08:04:53Z
day: '01'
ddc:
- '570'
department:
- _id: SyCr
doi: 10.1111/1365-2656.12953
ec_funded: 1
external_id:
isi:
- '000467994800007'
file:
- access_level: open_access
checksum: 405cde15120de26018b3bd0dfa29986c
content_type: application/pdf
creator: dernst
date_created: 2019-03-18T07:43:06Z
date_updated: 2020-07-14T12:47:19Z
file_id: '6107'
file_name: 2019_JournalAnimalEcology_Kutzer.pdf
file_size: 1460662
relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
has_accepted_license: '1'
intvolume: ' 88'
isi: 1
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 566-578
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: Journal of Animal Ecology
publication_identifier:
eissn:
- '13652656'
issn:
- '00218790'
publication_status: published
publisher: Wiley
quality_controlled: '1'
related_material:
record:
- id: '9806'
relation: research_data
status: public
scopus_import: '1'
status: public
title: A multi-faceted approach testing the effects of previous bacterial exposure
on resistance and tolerance
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: 88
year: '2019'
...
---
_id: '6088'
abstract:
- lang: eng
text: P-Glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) are two
efflux transporters at the blood–brain barrier (BBB), which effectively restrict
brain distribution of diverse drugs, such as tyrosine kinase inhibitors. There
is a crucial need for pharmacological ABCB1 and ABCG2 inhibition protocols for
a more effective treatment of brain diseases. In the present study, seven marketed
drugs (osimertinib, erlotinib, nilotinib, imatinib, lapatinib, pazopanib, and
cyclosporine A) and one nonmarketed drug (tariquidar), with known in vitro ABCB1/ABCG2
inhibitory properties, were screened for their inhibitory potency at the BBB in
vivo. Positron emission tomography (PET) using the model ABCB1/ABCG2 substrate
[11C]erlotinib was performed in mice. Tested inhibitors were administered as i.v.
bolus injections at 30 min before the start of the PET scan, followed by a continuous
i.v. infusion for the duration of the PET scan. Five of the tested drugs increased
total distribution volume of [11C]erlotinib in the brain (VT,brain) compared to
vehicle-treated animals (tariquidar, + 69%; erlotinib, + 19% and +23% for the
21.5 mg/kg and the 43 mg/kg dose, respectively; imatinib, + 22%; lapatinib, +
25%; and cyclosporine A, + 49%). For all drugs, increases in [11C]erlotinib brain
distribution were lower than in Abcb1a/b(−/−)Abcg2(−/−) mice (+149%), which suggested
that only partial ABCB1/ABCG2 inhibition was reached at the mouse BBB. The plasma
concentrations of the tested drugs at the time of the PET scan were higher than
clinically achievable plasma concentrations. Some of the tested drugs led to significant
increases in blood radioactivity concentrations measured at the end of the PET
scan (erlotinib, + 103% and +113% for the 21.5 mg/kg and the 43 mg/kg dose, respectively;
imatinib, + 125%; and cyclosporine A, + 101%), which was most likely caused by
decreased hepatobiliary excretion of radioactivity. Taken together, our data suggest
that some marketed tyrosine kinase inhibitors may be repurposed to inhibit ABCB1
and ABCG2 at the BBB. From a clinical perspective, moderate increases in brain
delivery despite the administration of high i.v. doses as well as peripheral drug–drug
interactions due to transporter inhibition in clearance organs question the translatability
of this concept.
article_processing_charge: No
author:
- first_name: Alexander
full_name: Traxl, Alexander
last_name: Traxl
- first_name: Severin
full_name: Mairinger, Severin
last_name: Mairinger
- first_name: Thomas
full_name: Filip, Thomas
last_name: Filip
- first_name: Michael
full_name: Sauberer, Michael
last_name: Sauberer
- first_name: Johann
full_name: Stanek, Johann
last_name: Stanek
- first_name: Stefan
full_name: Poschner, Stefan
last_name: Poschner
- first_name: Walter
full_name: Jäger, Walter
last_name: Jäger
- first_name: Viktoria
full_name: Zoufal, Viktoria
last_name: Zoufal
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
- first_name: Nicolas
full_name: Tournier, Nicolas
last_name: Tournier
- first_name: Martin
full_name: Bauer, Martin
last_name: Bauer
- first_name: Thomas
full_name: Wanek, Thomas
last_name: Wanek
- first_name: Oliver
full_name: Langer, Oliver
last_name: Langer
citation:
ama: Traxl A, Mairinger S, Filip T, et al. Inhibition of ABCB1 and ABCG2 at the
mouse blood-brain barrier with marketed drugs to improve brain delivery of the
model ABCB1/ABCG2 substrate [11C]erlotinib. Molecular Pharmaceutics. 2019;16(3):1282-1293.
doi:10.1021/acs.molpharmaceut.8b01217
apa: Traxl, A., Mairinger, S., Filip, T., Sauberer, M., Stanek, J., Poschner, S.,
… Langer, O. (2019). Inhibition of ABCB1 and ABCG2 at the mouse blood-brain barrier
with marketed drugs to improve brain delivery of the model ABCB1/ABCG2 substrate
[11C]erlotinib. Molecular Pharmaceutics. American Chemical Society. https://doi.org/10.1021/acs.molpharmaceut.8b01217
chicago: Traxl, Alexander, Severin Mairinger, Thomas Filip, Michael Sauberer, Johann
Stanek, Stefan Poschner, Walter Jäger, et al. “Inhibition of ABCB1 and ABCG2 at
the Mouse Blood-Brain Barrier with Marketed Drugs to Improve Brain Delivery of
the Model ABCB1/ABCG2 Substrate [11C]Erlotinib.” Molecular Pharmaceutics.
American Chemical Society, 2019. https://doi.org/10.1021/acs.molpharmaceut.8b01217.
ieee: A. Traxl et al., “Inhibition of ABCB1 and ABCG2 at the mouse blood-brain
barrier with marketed drugs to improve brain delivery of the model ABCB1/ABCG2
substrate [11C]erlotinib,” Molecular Pharmaceutics, vol. 16, no. 3. American
Chemical Society, pp. 1282–1293, 2019.
ista: Traxl A, Mairinger S, Filip T, Sauberer M, Stanek J, Poschner S, Jäger W,
Zoufal V, Novarino G, Tournier N, Bauer M, Wanek T, Langer O. 2019. Inhibition
of ABCB1 and ABCG2 at the mouse blood-brain barrier with marketed drugs to improve
brain delivery of the model ABCB1/ABCG2 substrate [11C]erlotinib. Molecular Pharmaceutics.
16(3), 1282–1293.
mla: Traxl, Alexander, et al. “Inhibition of ABCB1 and ABCG2 at the Mouse Blood-Brain
Barrier with Marketed Drugs to Improve Brain Delivery of the Model ABCB1/ABCG2
Substrate [11C]Erlotinib.” Molecular Pharmaceutics, vol. 16, no. 3, American
Chemical Society, 2019, pp. 1282–93, doi:10.1021/acs.molpharmaceut.8b01217.
short: A. Traxl, S. Mairinger, T. Filip, M. Sauberer, J. Stanek, S. Poschner, W.
Jäger, V. Zoufal, G. Novarino, N. Tournier, M. Bauer, T. Wanek, O. Langer, Molecular
Pharmaceutics 16 (2019) 1282–1293.
date_created: 2019-03-10T22:59:19Z
date_published: 2019-03-04T00:00:00Z
date_updated: 2023-08-25T08:02:51Z
day: '04'
department:
- _id: GaNo
doi: 10.1021/acs.molpharmaceut.8b01217
external_id:
isi:
- '000460600400031'
pmid:
- '30694684'
intvolume: ' 16'
isi: 1
issue: '3'
language:
- iso: eng
month: '03'
oa_version: None
page: 1282-1293
pmid: 1
publication: Molecular Pharmaceutics
publication_status: published
publisher: American Chemical Society
quality_controlled: '1'
scopus_import: '1'
status: public
title: Inhibition of ABCB1 and ABCG2 at the mouse blood-brain barrier with marketed
drugs to improve brain delivery of the model ABCB1/ABCG2 substrate [11C]erlotinib
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 16
year: '2019'
...
---
_id: '6087'
abstract:
- lang: eng
text: Cell fate specification by lateral inhibition typically involves contact signaling
through the Delta-Notch signaling pathway. However, whether this is the only signaling
mode mediating lateral inhibition remains unclear. Here we show that in zebrafish
oogenesis, a group of cells within the granulosa cell layer at the oocyte animal
pole acquire elevated levels of the transcriptional coactivator TAZ in their nuclei.
One of these cells, the future micropyle precursor cell (MPC), accumulates increasingly
high levels of nuclear TAZ and grows faster than its surrounding cells, mechanically
compressing those cells, which ultimately lose TAZ from their nuclei. Strikingly,
relieving neighbor-cell compression by MPC ablation or aspiration restores nuclear
TAZ accumulation in neighboring cells, eventually leading to MPC re-specification
from these cells. Conversely, MPC specification is defective in taz−/− follicles.
These findings uncover a novel mode of lateral inhibition in cell fate specification
based on mechanical signals controlling TAZ activity.
acknowledged_ssus:
- _id: Bio
- _id: EM-Fac
- _id: LifeSc
acknowledgement: We thank Roland Dosch, Makoto Furutani-Seiki, Brian Link, Mary Mullins,
and Masazumi Tada for providing transgenic and/or mutant zebrafish lines; Alexandra
Schauer, Shayan Shami-Pour, and the rest of the Heisenberg lab for technical assistance
and feedback on the manuscript; and the Bioimaging, Electron Microscopy, and Zebrafish
facilities of IST Austria for continuous support. This work was supported by an
ERC advanced grant ( MECSPEC to C.-P.H.).
article_processing_charge: No
article_type: original
author:
- first_name: Peng
full_name: Xia, Peng
id: 4AB6C7D0-F248-11E8-B48F-1D18A9856A87
last_name: Xia
orcid: 0000-0002-5419-7756
- first_name: Daniel J
full_name: Gütl, Daniel J
id: 381929CE-F248-11E8-B48F-1D18A9856A87
last_name: Gütl
- first_name: Vanessa
full_name: Zheden, Vanessa
id: 39C5A68A-F248-11E8-B48F-1D18A9856A87
last_name: Zheden
orcid: 0000-0002-9438-4783
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Xia P, Gütl DJ, Zheden V, Heisenberg C-PJ. Lateral inhibition in cell specification
mediated by mechanical signals modulating TAZ activity. Cell. 2019;176(6):1379-1392.e14.
doi:10.1016/j.cell.2019.01.019
apa: Xia, P., Gütl, D. J., Zheden, V., & Heisenberg, C.-P. J. (2019). Lateral
inhibition in cell specification mediated by mechanical signals modulating TAZ
activity. Cell. Elsevier. https://doi.org/10.1016/j.cell.2019.01.019
chicago: Xia, Peng, Daniel J Gütl, Vanessa Zheden, and Carl-Philipp J Heisenberg.
“Lateral Inhibition in Cell Specification Mediated by Mechanical Signals Modulating
TAZ Activity.” Cell. Elsevier, 2019. https://doi.org/10.1016/j.cell.2019.01.019.
ieee: P. Xia, D. J. Gütl, V. Zheden, and C.-P. J. Heisenberg, “Lateral inhibition
in cell specification mediated by mechanical signals modulating TAZ activity,”
Cell, vol. 176, no. 6. Elsevier, p. 1379–1392.e14, 2019.
ista: Xia P, Gütl DJ, Zheden V, Heisenberg C-PJ. 2019. Lateral inhibition in cell
specification mediated by mechanical signals modulating TAZ activity. Cell. 176(6),
1379–1392.e14.
mla: Xia, Peng, et al. “Lateral Inhibition in Cell Specification Mediated by Mechanical
Signals Modulating TAZ Activity.” Cell, vol. 176, no. 6, Elsevier, 2019,
p. 1379–1392.e14, doi:10.1016/j.cell.2019.01.019.
short: P. Xia, D.J. Gütl, V. Zheden, C.-P.J. Heisenberg, Cell 176 (2019) 1379–1392.e14.
date_created: 2019-03-10T22:59:19Z
date_published: 2019-03-07T00:00:00Z
date_updated: 2023-08-25T08:02:23Z
day: '07'
department:
- _id: CaHe
- _id: EM-Fac
doi: 10.1016/j.cell.2019.01.019
ec_funded: 1
external_id:
isi:
- '000460509600013'
pmid:
- '30773315'
intvolume: ' 176'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cell.2019.01.019
month: '03'
oa: 1
oa_version: Published Version
page: 1379-1392.e14
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
publication: 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/in-zebrafish-eggs-most-rapidly-growing-cell-inhibits-its-neighbours-through-mechanical-signals/
scopus_import: '1'
status: public
title: Lateral inhibition in cell specification mediated by mechanical signals modulating
TAZ activity
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 176
year: '2019'
...
---
_id: '9806'
abstract:
- lang: eng
text: 1. Hosts can alter their strategy towards pathogens during their lifetime,
i.e., they can show phenotypic plasticity in immunity or life history. Immune
priming is one such example, where a previous encounter with a pathogen confers
enhanced protection upon secondary challenge, resulting in reduced pathogen load
(i.e. resistance) and improved host survival. However, an initial encounter might
also enhance tolerance, particularly to less virulent opportunistic pathogens
that establish persistent infections. In this scenario, individuals are better
able to reduce the negative fitness consequences that result from a high pathogen
load. Finally, previous exposure may also lead to life history adjustments, such
as terminal investment into reproduction. 2. Using different Drosophila melanogaster
host genotypes and two bacterial pathogens, Lactococcus lactis and Pseudomonas
entomophila, we tested if previous exposure results in resistance or tolerance
and whether it modifies immune gene expression during an acute-phase infection
(one day post-challenge). We then asked if previous pathogen exposure affects
chronic-phase pathogen persistence and longer-term survival (28 days post-challenge).
3. We predicted that previous exposure would increase host resistance to an early
stage bacterial infection while it might come at a cost to host fecundity tolerance.
We reasoned that resistance would be due in part to stronger immune gene expression
after challenge. We expected that previous exposure would improve long-term survival,
that it would reduce infection persistence, and we expected to find genetic variation
in these responses. 4. We found that previous exposure to P. entomophila weakened
host resistance to a second infection independent of genotype and had no effect
on immune gene expression. Fecundity tolerance showed genotypic variation but
was not influenced by previous exposure. However, L. lactis persisted as a chronic
infection, whereas survivors cleared the more pathogenic P. entomophila infection.
5. To our knowledge, this is the first study that addresses host tolerance to
bacteria in relation to previous exposure, taking a multi-faceted approach to
address the topic. Our results suggest that previous exposure comes with transient
costs to resistance during the early stage of infection in this host-pathogen
system and that infection persistence may be bacterium-specific.
article_processing_charge: No
author:
- first_name: Megan
full_name: Kutzer, Megan
id: 29D0B332-F248-11E8-B48F-1D18A9856A87
last_name: Kutzer
orcid: 0000-0002-8696-6978
- first_name: Joachim
full_name: Kurtz, Joachim
last_name: Kurtz
- first_name: Sophie A.O.
full_name: Armitage, Sophie A.O.
last_name: Armitage
citation:
ama: 'Kutzer M, Kurtz J, Armitage SAO. Data from: A multi-faceted approach testing
the effects of previous bacterial exposure on resistance and tolerance. 2019.
doi:10.5061/dryad.9kj41f0'
apa: 'Kutzer, M., Kurtz, J., & Armitage, S. A. O. (2019). Data from: A multi-faceted
approach testing the effects of previous bacterial exposure on resistance and
tolerance. Dryad. https://doi.org/10.5061/dryad.9kj41f0'
chicago: 'Kutzer, Megan, Joachim Kurtz, and Sophie A.O. Armitage. “Data from: A
Multi-Faceted Approach Testing the Effects of Previous Bacterial Exposure on Resistance
and Tolerance.” Dryad, 2019. https://doi.org/10.5061/dryad.9kj41f0.'
ieee: 'M. Kutzer, J. Kurtz, and S. A. O. Armitage, “Data from: A multi-faceted approach
testing the effects of previous bacterial exposure on resistance and tolerance.”
Dryad, 2019.'
ista: 'Kutzer M, Kurtz J, Armitage SAO. 2019. Data from: A multi-faceted approach
testing the effects of previous bacterial exposure on resistance and tolerance,
Dryad, 10.5061/dryad.9kj41f0.'
mla: 'Kutzer, Megan, et al. Data from: A Multi-Faceted Approach Testing the Effects
of Previous Bacterial Exposure on Resistance and Tolerance. Dryad, 2019, doi:10.5061/dryad.9kj41f0.'
short: M. Kutzer, J. Kurtz, S.A.O. Armitage, (2019).
date_created: 2021-08-06T12:06:40Z
date_published: 2019-02-05T00:00:00Z
date_updated: 2023-08-25T08:04:52Z
day: '05'
department:
- _id: SyCr
doi: 10.5061/dryad.9kj41f0
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.9kj41f0
month: '02'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '6105'
relation: used_in_publication
status: public
status: public
title: 'Data from: A multi-faceted approach testing the effects of previous bacterial
exposure on resistance and tolerance'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2019'
...
---
_id: '6086'
abstract:
- lang: eng
text: We show that linear analytic cocycles where all Lyapunov exponents are negative
infinite are nilpotent. For such one-frequency cocycles we show that they can
be analytically conjugated to an upper triangular cocycle or a Jordan normal form.
As a consequence, an arbitrarily small analytic perturbation leads to distinct
Lyapunov exponents. Moreover, in the one-frequency case where the th Lyapunov
exponent is finite and the st negative infinite, we obtain a simple criterion
for domination in which case there is a splitting into a nilpotent part and an
invertible part.
article_processing_charge: No
author:
- first_name: Christian
full_name: Sadel, Christian
id: 4760E9F8-F248-11E8-B48F-1D18A9856A87
last_name: Sadel
orcid: 0000-0001-8255-3968
- first_name: Disheng
full_name: Xu, Disheng
last_name: Xu
citation:
ama: Sadel C, Xu D. Singular analytic linear cocycles with negative infinite Lyapunov
exponents. Ergodic Theory and Dynamical Systems. 2019;39(4):1082-1098.
doi:10.1017/etds.2017.52
apa: Sadel, C., & Xu, D. (2019). Singular analytic linear cocycles with negative
infinite Lyapunov exponents. Ergodic Theory and Dynamical Systems. Cambridge
University Press. https://doi.org/10.1017/etds.2017.52
chicago: Sadel, Christian, and Disheng Xu. “Singular Analytic Linear Cocycles with
Negative Infinite Lyapunov Exponents.” Ergodic Theory and Dynamical Systems.
Cambridge University Press, 2019. https://doi.org/10.1017/etds.2017.52.
ieee: C. Sadel and D. Xu, “Singular analytic linear cocycles with negative infinite
Lyapunov exponents,” Ergodic Theory and Dynamical Systems, vol. 39, no.
4. Cambridge University Press, pp. 1082–1098, 2019.
ista: Sadel C, Xu D. 2019. Singular analytic linear cocycles with negative infinite
Lyapunov exponents. Ergodic Theory and Dynamical Systems. 39(4), 1082–1098.
mla: Sadel, Christian, and Disheng Xu. “Singular Analytic Linear Cocycles with Negative
Infinite Lyapunov Exponents.” Ergodic Theory and Dynamical Systems, vol.
39, no. 4, Cambridge University Press, 2019, pp. 1082–98, doi:10.1017/etds.2017.52.
short: C. Sadel, D. Xu, Ergodic Theory and Dynamical Systems 39 (2019) 1082–1098.
date_created: 2019-03-10T22:59:18Z
date_published: 2019-04-01T00:00:00Z
date_updated: 2023-08-25T08:03:30Z
day: '01'
department:
- _id: LaEr
doi: 10.1017/etds.2017.52
ec_funded: 1
external_id:
arxiv:
- '1601.06118'
isi:
- '000459725600012'
intvolume: ' 39'
isi: 1
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1601.06118
month: '04'
oa: 1
oa_version: Preprint
page: 1082-1098
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: Ergodic Theory and Dynamical Systems
publication_status: published
publisher: Cambridge University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Singular analytic linear cocycles with negative infinite Lyapunov exponents
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 39
year: '2019'
...
---
_id: '6102'
abstract:
- lang: eng
text: 'Light is a union of electric and magnetic fields, and nowhere is the complex
relationship between these fields more evident than in the near fields of nanophotonic
structures. There, complicated electric and magnetic fields varying over subwavelength
scales are generally present, which results in photonic phenomena such as extraordinary
optical momentum, superchiral fields, and a complex spatial evolution of optical
singularities. An understanding of such phenomena requires nanoscale measurements
of the complete optical field vector. Although the sensitivity of near- field
scanning optical microscopy to the complete electromagnetic field was recently
demonstrated, a separation of different components required a priori knowledge
of the sample. Here, we introduce a robust algorithm that can disentangle all
six electric and magnetic field components from a single near-field measurement
without any numerical modeling of the structure. As examples, we unravel the fields
of two prototypical nanophotonic structures: a photonic crystal waveguide and
a plasmonic nanowire. These results pave the way for new studies of complex photonic
phenomena at the nanoscale and for the design of structures that optimize their
optical behavior.'
article_number: '28'
article_processing_charge: No
author:
- first_name: B.
full_name: Le Feber, B.
last_name: Le Feber
- first_name: J. E.
full_name: Sipe, J. E.
last_name: Sipe
- first_name: Matthias
full_name: Wulf, Matthias
id: 45598606-F248-11E8-B48F-1D18A9856A87
last_name: Wulf
orcid: 0000-0001-6613-1378
- first_name: L.
full_name: Kuipers, L.
last_name: Kuipers
- first_name: N.
full_name: Rotenberg, N.
last_name: Rotenberg
citation:
ama: 'Le Feber B, Sipe JE, Wulf M, Kuipers L, Rotenberg N. A full vectorial mapping
of nanophotonic light fields. Light: Science and Applications. 2019;8(1).
doi:10.1038/s41377-019-0124-3'
apa: 'Le Feber, B., Sipe, J. E., Wulf, M., Kuipers, L., & Rotenberg, N. (2019).
A full vectorial mapping of nanophotonic light fields. Light: Science and Applications.
Springer Nature. https://doi.org/10.1038/s41377-019-0124-3'
chicago: 'Le Feber, B., J. E. Sipe, Matthias Wulf, L. Kuipers, and N. Rotenberg.
“A Full Vectorial Mapping of Nanophotonic Light Fields.” Light: Science and
Applications. Springer Nature, 2019. https://doi.org/10.1038/s41377-019-0124-3.'
ieee: 'B. Le Feber, J. E. Sipe, M. Wulf, L. Kuipers, and N. Rotenberg, “A full vectorial
mapping of nanophotonic light fields,” Light: Science and Applications,
vol. 8, no. 1. Springer Nature, 2019.'
ista: 'Le Feber B, Sipe JE, Wulf M, Kuipers L, Rotenberg N. 2019. A full vectorial
mapping of nanophotonic light fields. Light: Science and Applications. 8(1), 28.'
mla: 'Le Feber, B., et al. “A Full Vectorial Mapping of Nanophotonic Light Fields.”
Light: Science and Applications, vol. 8, no. 1, 28, Springer Nature, 2019,
doi:10.1038/s41377-019-0124-3.'
short: 'B. Le Feber, J.E. Sipe, M. Wulf, L. Kuipers, N. Rotenberg, Light: Science
and Applications 8 (2019).'
date_created: 2019-03-17T22:59:13Z
date_published: 2019-03-06T00:00:00Z
date_updated: 2023-08-25T08:06:10Z
day: '06'
ddc:
- '530'
department:
- _id: JoFi
doi: 10.1038/s41377-019-0124-3
external_id:
arxiv:
- '1803.10145'
isi:
- '000460470700004'
file:
- access_level: open_access
checksum: d71e528cff9c56f70ccc29dd7005257f
content_type: application/pdf
creator: dernst
date_created: 2019-03-18T08:08:22Z
date_updated: 2020-07-14T12:47:19Z
file_id: '6108'
file_name: 2019_Light_LeFeber.pdf
file_size: 1119947
relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
issue: '1'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: 'Light: Science and Applications'
publication_identifier:
eissn:
- '20477538'
issn:
- '20955545'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: A full vectorial mapping of nanophotonic light fields
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: 8
year: '2019'
...
---
_id: '6104'
abstract:
- lang: eng
text: Abiotic stress poses constant challenges for plant survival and is a serious
problem for global agricultural productivity. On a molecular level, stress conditions
result in elevation of reactive oxygen species (ROS) production causing oxidative
stress associated with oxidation of proteins and nucleic acids as well as impairment
of membrane functions. Adaptation of root growth to ROS accumulation is facilitated
through modification of auxin and cytokinin hormone homeostasis. Here, we report
that in Arabidopsis root meristem, ROS-induced changes of auxin levels correspond
to decreased abundance of PIN auxin efflux carriers at the plasma membrane (PM).
Specifically, increase in H2O2 levels affects PIN2 endocytic recycling. We show
that the PIN2 intracellular trafficking during adaptation to oxidative stress
requires the function of the ADP-ribosylation factor (ARF)-guanine-nucleotide
exchange factor (GEF) BEN1, an actin-associated regulator of the trafficking from
the PM to early endosomes and, presumably, indirectly, trafficking to the vacuoles.
We propose that H2O2 levels affect the actin dynamics thus modulating ARF-GEF-dependent
trafficking of PIN2. This mechanism provides a way how root growth acclimates
to stress and adapts to a changing environment.
article_processing_charge: No
author:
- first_name: Marta
full_name: Zwiewka, Marta
last_name: Zwiewka
- first_name: Agnieszka
full_name: Bielach, Agnieszka
last_name: Bielach
- first_name: Prashanth
full_name: Tamizhselvan, Prashanth
last_name: Tamizhselvan
- first_name: Sharmila
full_name: Madhavan, Sharmila
last_name: Madhavan
- first_name: Eman Elrefaay
full_name: Ryad, Eman Elrefaay
last_name: Ryad
- first_name: Shutang
full_name: Tan, Shutang
id: 2DE75584-F248-11E8-B48F-1D18A9856A87
last_name: Tan
orcid: 0000-0002-0471-8285
- first_name: Mónika
full_name: Hrtyan, Mónika
id: 45A71A74-F248-11E8-B48F-1D18A9856A87
last_name: Hrtyan
- first_name: Petre
full_name: Dobrev, Petre
last_name: Dobrev
- first_name: Radomira
full_name: Vanková, Radomira
last_name: Vanková
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Vanesa B.
full_name: Tognetti, Vanesa B.
last_name: Tognetti
citation:
ama: Zwiewka M, Bielach A, Tamizhselvan P, et al. Root adaptation to H2O2-induced
oxidative stress by ARF-GEF BEN1- and cytoskeleton-mediated PIN2 trafficking.
Plant and Cell Physiology. 2019;60(2):255-273. doi:10.1093/pcp/pcz001
apa: Zwiewka, M., Bielach, A., Tamizhselvan, P., Madhavan, S., Ryad, E. E., Tan,
S., … Tognetti, V. B. (2019). Root adaptation to H2O2-induced oxidative stress
by ARF-GEF BEN1- and cytoskeleton-mediated PIN2 trafficking. Plant and Cell
Physiology. Oxford University Press. https://doi.org/10.1093/pcp/pcz001
chicago: Zwiewka, Marta, Agnieszka Bielach, Prashanth Tamizhselvan, Sharmila Madhavan,
Eman Elrefaay Ryad, Shutang Tan, Mónika Hrtyan, et al. “Root Adaptation to H2O2-Induced
Oxidative Stress by ARF-GEF BEN1- and Cytoskeleton-Mediated PIN2 Trafficking.”
Plant and Cell Physiology. Oxford University Press, 2019. https://doi.org/10.1093/pcp/pcz001.
ieee: M. Zwiewka et al., “Root adaptation to H2O2-induced oxidative stress
by ARF-GEF BEN1- and cytoskeleton-mediated PIN2 trafficking,” Plant and Cell
Physiology, vol. 60, no. 2. Oxford University Press, pp. 255–273, 2019.
ista: Zwiewka M, Bielach A, Tamizhselvan P, Madhavan S, Ryad EE, Tan S, Hrtyan M,
Dobrev P, Vanková R, Friml J, Tognetti VB. 2019. Root adaptation to H2O2-induced
oxidative stress by ARF-GEF BEN1- and cytoskeleton-mediated PIN2 trafficking.
Plant and Cell Physiology. 60(2), 255–273.
mla: Zwiewka, Marta, et al. “Root Adaptation to H2O2-Induced Oxidative Stress by
ARF-GEF BEN1- and Cytoskeleton-Mediated PIN2 Trafficking.” Plant and Cell Physiology,
vol. 60, no. 2, Oxford University Press, 2019, pp. 255–73, doi:10.1093/pcp/pcz001.
short: M. Zwiewka, A. Bielach, P. Tamizhselvan, S. Madhavan, E.E. Ryad, S. Tan,
M. Hrtyan, P. Dobrev, R. Vanková, J. Friml, V.B. Tognetti, Plant and Cell Physiology
60 (2019) 255–273.
date_created: 2019-03-17T22:59:14Z
date_published: 2019-02-01T00:00:00Z
date_updated: 2023-08-25T08:05:28Z
day: '01'
department:
- _id: JiFr
doi: 10.1093/pcp/pcz001
external_id:
isi:
- '000459634300002'
pmid:
- '30668780'
intvolume: ' 60'
isi: 1
issue: '2'
language:
- iso: eng
month: '02'
oa_version: None
page: 255-273
pmid: 1
publication: Plant and Cell Physiology
publication_identifier:
eissn:
- 1471-9053
issn:
- 0032-0781
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Root adaptation to H2O2-induced oxidative stress by ARF-GEF BEN1- and cytoskeleton-mediated
PIN2 trafficking
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 60
year: '2019'
...
---
_id: '6191'
abstract:
- lang: eng
text: The formation of self-organized patterns is key to the morphogenesis of multicellular
organisms, although a comprehensive theory of biological pattern formation is
still lacking. Here, we propose a minimal model combining tissue mechanics with
morphogen turnover and transport to explore routes to patterning. Our active description
couples morphogen reaction and diffusion, which impact cell differentiation and
tissue mechanics, to a two-phase poroelastic rheology, where one tissue phase
consists of a poroelastic cell network and the other one of a permeating extracellular
fluid, which provides a feedback by actively transporting morphogens. While this
model encompasses previous theories approximating tissues to inert monophasic
media, such as Turing’s reaction–diffusion model, it overcomes some of their key
limitations permitting pattern formation via any two-species biochemical kinetics
due to mechanically induced cross-diffusion flows. Moreover, we describe a qualitatively
different advection-driven Keller–Segel instability which allows for the formation
of patterns with a single morphogen and whose fundamental mode pattern robustly
scales with tissue size. We discuss the potential relevance of these findings
for tissue morphogenesis.
article_processing_charge: No
author:
- first_name: Pierre
full_name: Recho, Pierre
last_name: Recho
- first_name: Adrien
full_name: Hallou, Adrien
last_name: Hallou
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
citation:
ama: Recho P, Hallou A, Hannezo EB. Theory of mechanochemical patterning in biphasic
biological tissues. Proceedings of the National Academy of Sciences of the
United States of America. 2019;116(12):5344-5349. doi:10.1073/pnas.1813255116
apa: Recho, P., Hallou, A., & Hannezo, E. B. (2019). Theory of mechanochemical
patterning in biphasic biological tissues. Proceedings of the National Academy
of Sciences of the United States of America. National Academy of Sciences.
https://doi.org/10.1073/pnas.1813255116
chicago: Recho, Pierre, Adrien Hallou, and Edouard B Hannezo. “Theory of Mechanochemical
Patterning in Biphasic Biological Tissues.” Proceedings of the National Academy
of Sciences of the United States of America. National Academy of Sciences,
2019. https://doi.org/10.1073/pnas.1813255116.
ieee: P. Recho, A. Hallou, and E. B. Hannezo, “Theory of mechanochemical patterning
in biphasic biological tissues,” Proceedings of the National Academy of Sciences
of the United States of America, vol. 116, no. 12. National Academy of Sciences,
pp. 5344–5349, 2019.
ista: Recho P, Hallou A, Hannezo EB. 2019. Theory of mechanochemical patterning
in biphasic biological tissues. Proceedings of the National Academy of Sciences
of the United States of America. 116(12), 5344–5349.
mla: Recho, Pierre, et al. “Theory of Mechanochemical Patterning in Biphasic Biological
Tissues.” Proceedings of the National Academy of Sciences of the United States
of America, vol. 116, no. 12, National Academy of Sciences, 2019, pp. 5344–49,
doi:10.1073/pnas.1813255116.
short: P. Recho, A. Hallou, E.B. Hannezo, Proceedings of the National Academy of
Sciences of the United States of America 116 (2019) 5344–5349.
date_created: 2019-03-31T21:59:13Z
date_published: 2019-03-19T00:00:00Z
date_updated: 2023-08-25T08:57:30Z
day: '19'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1073/pnas.1813255116
external_id:
isi:
- '000461679000027'
pmid:
- '30819884'
file:
- access_level: open_access
checksum: 8b67eee0ea8e5db61583e4d485215258
content_type: application/pdf
creator: dernst
date_created: 2019-04-03T14:10:30Z
date_updated: 2020-07-14T12:47:23Z
file_id: '6193'
file_name: 2019_PNAS_Recho.pdf
file_size: 3456045
relation: main_file
file_date_updated: 2020-07-14T12:47:23Z
has_accepted_license: '1'
intvolume: ' 116'
isi: 1
issue: '12'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 5344-5349
pmid: 1
project:
- _id: 268294B6-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P31639
name: Active mechano-chemical description of the cell cytoskeleton
publication: Proceedings of the National Academy of Sciences of the United States
of America
publication_identifier:
eissn:
- '10916490'
issn:
- '00278424'
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
related_material:
link:
- relation: supplementary_material
url: www.pnas.org/lookup/suppl/doi:10.1073/pnas.1813255116/-/DCSupplemental
scopus_import: '1'
status: public
title: Theory of mechanochemical patterning in biphasic biological tissues
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: 116
year: '2019'
...