---
_id: '14552'
abstract:
- lang: eng
text: Interactions between plants and herbivores are central in most ecosystems,
but their strength is highly variable. The amount of variability within a system
is thought to influence most aspects of plant-herbivore biology, from ecological
stability to plant defense evolution. Our understanding of what influences variability,
however, is limited by sparse data. We collected standardized surveys of herbivory
for 503 plant species at 790 sites across 116° of latitude. With these data, we
show that within-population variability in herbivory increases with latitude,
decreases with plant size, and is phylogenetically structured. Differences in
the magnitude of variability are thus central to how plant-herbivore biology varies
across macroscale gradients. We argue that increased focus on interaction variability
will advance understanding of patterns of life on Earth.
acknowledgement: The authors acknowledge funding for central project coordination
from NSF Research Coordination Network grant DEB-2203582; the Ecology, Evolution,
and Behavior Program at Michigan State University; and AgBioResearch at Michigan
State University. Site-specific funding is listed in the supplementary materials.
article_processing_charge: No
article_type: original
author:
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full_name: Robinson, M. L.
last_name: Robinson
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full_name: Hahn, P. G.
last_name: Hahn
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full_name: Inouye, B. D.
last_name: Inouye
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full_name: Underwood, N.
last_name: Underwood
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full_name: Whitehead, S. R.
last_name: Whitehead
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full_name: Abbott, K. C.
last_name: Abbott
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last_name: Bruna
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full_name: Cacho, N. I.
last_name: Cacho
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last_name: Dyer
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last_name: Abdala-Roberts
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last_name: Allen
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last_name: Angulo
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full_name: Barrett, S.
last_name: Barrett
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full_name: Baskett, Carina
id: 3B4A7CE2-F248-11E8-B48F-1D18A9856A87
last_name: Baskett
orcid: 0000-0002-7354-8574
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citation:
ama: Robinson ML, Hahn PG, Inouye BD, et al. Plant size, latitude, and phylogeny
explain within-population variability in herbivory. Science. 2023;382(6671):679-683.
doi:10.1126/science.adh8830
apa: Robinson, M. L., Hahn, P. G., Inouye, B. D., Underwood, N., Whitehead, S. R.,
Abbott, K. C., … Wetzel, W. C. (2023). Plant size, latitude, and phylogeny explain
within-population variability in herbivory. Science. AAAS. https://doi.org/10.1126/science.adh8830
chicago: Robinson, M. L., P. G. Hahn, B. D. Inouye, N. Underwood, S. R. Whitehead,
K. C. Abbott, E. M. Bruna, et al. “Plant Size, Latitude, and Phylogeny Explain
within-Population Variability in Herbivory.” Science. AAAS, 2023. https://doi.org/10.1126/science.adh8830.
ieee: M. L. Robinson et al., “Plant size, latitude, and phylogeny explain
within-population variability in herbivory,” Science, vol. 382, no. 6671.
AAAS, pp. 679–683, 2023.
ista: Robinson ML et al. 2023. Plant size, latitude, and phylogeny explain within-population
variability in herbivory. Science. 382(6671), 679–683.
mla: Robinson, M. L., et al. “Plant Size, Latitude, and Phylogeny Explain within-Population
Variability in Herbivory.” Science, vol. 382, no. 6671, AAAS, 2023, pp.
679–83, doi:10.1126/science.adh8830.
short: M.L. Robinson, P.G. Hahn, B.D. Inouye, N. Underwood, S.R. Whitehead, K.C.
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A. Yamawo, S. Yim, P.L. Zarnetske, L.N. Zehr, Z. Zhong, W.C. Wetzel, Science 382
(2023) 679–683.
date_created: 2023-11-19T23:00:54Z
date_published: 2023-11-09T00:00:00Z
date_updated: 2023-11-20T11:17:34Z
day: '09'
department:
- _id: NiBa
doi: 10.1126/science.adh8830
external_id:
pmid:
- '37943897'
intvolume: ' 382'
issue: '6671'
language:
- iso: eng
month: '11'
oa_version: None
page: 679-683
pmid: 1
publication: Science
publication_identifier:
eissn:
- 1095-9203
publication_status: published
publisher: AAAS
quality_controlled: '1'
related_material:
record:
- id: '14579'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Plant size, latitude, and phylogeny explain within-population variability in
herbivory
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 382
year: '2023'
...
---
_id: '14551'
abstract:
- lang: eng
text: Methylation of CG dinucleotides (mCGs), which regulates eukaryotic genome
functions, is epigenetically propagated by Dnmt1/MET1 methyltransferases. How
mCG is established and transmitted across generations despite imperfect enzyme
fidelity is unclear. Whether mCG variation in natural populations is governed
by genetic or epigenetic inheritance also remains mysterious. Here, we show that
MET1 de novo activity, which is enhanced by existing proximate methylation, seeds
and stabilizes mCG in Arabidopsis thaliana genes. MET1 activity is restricted
by active demethylation and suppressed by histone variant H2A.Z, producing localized
mCG patterns. Based on these observations, we develop a stochastic mathematical
model that precisely recapitulates mCG inheritance dynamics and predicts intragenic
mCG patterns and their population-scale variation given only CG site spacing.
Our results demonstrate that intragenic mCG establishment, inheritance, and variance
constitute a unified epigenetic process, revealing that intragenic mCG undergoes
large, millennia-long epigenetic fluctuations and can therefore mediate evolution
on this timescale.
acknowledgement: We would like to thank Xiaoqi Feng, Ander Movilla Miangolarra, and
Suzanne de Bruijn for discussions. This work was supported by BBSRC Institute Strategic
Programme GEN (BB/P013511/1) to M.H. and D.Z. and by a European Research Council
grant MaintainMeth (725746) to D.Z.
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Amy
full_name: Briffa, Amy
last_name: Briffa
- first_name: Elizabeth
full_name: Hollwey, Elizabeth
id: b8c4f54b-e484-11eb-8fdc-a54df64ef6dd
last_name: Hollwey
- first_name: Zaigham
full_name: Shahzad, Zaigham
last_name: Shahzad
- first_name: Jonathan D.
full_name: Moore, Jonathan D.
last_name: Moore
- first_name: David B.
full_name: Lyons, David B.
last_name: Lyons
- first_name: Martin
full_name: Howard, Martin
last_name: Howard
- first_name: Daniel
full_name: Zilberman, Daniel
id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
last_name: Zilberman
orcid: 0000-0002-0123-8649
citation:
ama: Briffa A, Hollwey E, Shahzad Z, et al. Millennia-long epigenetic fluctuations
generate intragenic DNA methylation variance in Arabidopsis populations. Cell
Systems. 2023;14(11):953-967. doi:10.1016/j.cels.2023.10.007
apa: Briffa, A., Hollwey, E., Shahzad, Z., Moore, J. D., Lyons, D. B., Howard, M.,
& Zilberman, D. (2023). Millennia-long epigenetic fluctuations generate intragenic
DNA methylation variance in Arabidopsis populations. Cell Systems. Elsevier.
https://doi.org/10.1016/j.cels.2023.10.007
chicago: Briffa, Amy, Elizabeth Hollwey, Zaigham Shahzad, Jonathan D. Moore, David
B. Lyons, Martin Howard, and Daniel Zilberman. “Millennia-Long Epigenetic Fluctuations
Generate Intragenic DNA Methylation Variance in Arabidopsis Populations.” Cell
Systems. Elsevier, 2023. https://doi.org/10.1016/j.cels.2023.10.007.
ieee: A. Briffa et al., “Millennia-long epigenetic fluctuations generate
intragenic DNA methylation variance in Arabidopsis populations,” Cell Systems,
vol. 14, no. 11. Elsevier, pp. 953–967, 2023.
ista: Briffa A, Hollwey E, Shahzad Z, Moore JD, Lyons DB, Howard M, Zilberman D.
2023. Millennia-long epigenetic fluctuations generate intragenic DNA methylation
variance in Arabidopsis populations. Cell Systems. 14(11), 953–967.
mla: Briffa, Amy, et al. “Millennia-Long Epigenetic Fluctuations Generate Intragenic
DNA Methylation Variance in Arabidopsis Populations.” Cell Systems, vol.
14, no. 11, Elsevier, 2023, pp. 953–67, doi:10.1016/j.cels.2023.10.007.
short: A. Briffa, E. Hollwey, Z. Shahzad, J.D. Moore, D.B. Lyons, M. Howard, D.
Zilberman, Cell Systems 14 (2023) 953–967.
date_created: 2023-11-19T23:00:54Z
date_published: 2023-11-15T00:00:00Z
date_updated: 2023-11-20T11:24:34Z
day: '15'
ddc:
- '570'
department:
- _id: DaZi
doi: 10.1016/j.cels.2023.10.007
ec_funded: 1
external_id:
pmid:
- '37944515'
file:
- access_level: open_access
checksum: 101fdac59e6f1102d68ef91f2b5bd51a
content_type: application/pdf
creator: dernst
date_created: 2023-11-20T11:22:52Z
date_updated: 2023-11-20T11:22:52Z
file_id: '14580'
file_name: 2023_CellSystems_Briffa.pdf
file_size: 5587897
relation: main_file
success: 1
file_date_updated: 2023-11-20T11:22:52Z
has_accepted_license: '1'
intvolume: ' 14'
issue: '11'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 953-967
pmid: 1
project:
- _id: 62935a00-2b32-11ec-9570-eff30fa39068
call_identifier: H2020
grant_number: '725746'
name: Quantitative analysis of DNA methylation maintenance with chromatin
publication: Cell Systems
publication_identifier:
eissn:
- 2405-4720
issn:
- 2405-4712
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Millennia-long epigenetic fluctuations generate intragenic DNA methylation
variance in Arabidopsis populations
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: 14
year: '2023'
...
---
_id: '14579'
abstract:
- lang: eng
text: "This is associated with our paper \"Plant size, latitude, and phylogeny explain
within-population variability in herbivory\" published in Science.\r\n"
article_processing_charge: No
author:
- first_name: William
full_name: Wetzel, William
last_name: Wetzel
citation:
ama: 'Wetzel W. HerbVar-Network/HV-Large-Patterns-MS-public: v1.0.0. 2023. doi:10.5281/ZENODO.8133117'
apa: 'Wetzel, W. (2023). HerbVar-Network/HV-Large-Patterns-MS-public: v1.0.0. Zenodo.
https://doi.org/10.5281/ZENODO.8133117'
chicago: 'Wetzel, William. “HerbVar-Network/HV-Large-Patterns-MS-Public: V1.0.0.”
Zenodo, 2023. https://doi.org/10.5281/ZENODO.8133117.'
ieee: 'W. Wetzel, “HerbVar-Network/HV-Large-Patterns-MS-public: v1.0.0.” Zenodo,
2023.'
ista: 'Wetzel W. 2023. HerbVar-Network/HV-Large-Patterns-MS-public: v1.0.0, Zenodo,
10.5281/ZENODO.8133117.'
mla: 'Wetzel, William. HerbVar-Network/HV-Large-Patterns-MS-Public: V1.0.0.
Zenodo, 2023, doi:10.5281/ZENODO.8133117.'
short: W. Wetzel, (2023).
date_created: 2023-11-20T11:07:45Z
date_published: 2023-07-11T00:00:00Z
date_updated: 2023-11-20T11:17:33Z
day: '11'
ddc:
- '570'
department:
- _id: NiBa
doi: 10.5281/ZENODO.8133117
main_file_link:
- open_access: '1'
url: https://doi.org/10.5281/zenodo.8133118
month: '07'
oa: 1
oa_version: Published Version
publisher: Zenodo
related_material:
record:
- id: '14552'
relation: used_in_publication
status: public
status: public
title: 'HerbVar-Network/HV-Large-Patterns-MS-public: v1.0.0'
type: research_data_reference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '12334'
abstract:
- lang: eng
text: Regulation of the Arp2/3 complex is required for productive nucleation of
branched actin networks. An emerging aspect of regulation is the incorporation
of subunit isoforms into the Arp2/3 complex. Specifically, both ArpC5 subunit
isoforms, ArpC5 and ArpC5L, have been reported to fine-tune nucleation activity
and branch junction stability. We have combined reverse genetics and cellular
structural biology to describe how ArpC5 and ArpC5L differentially affect cell
migration. Both define the structural stability of ArpC1 in branch junctions and,
in turn, by determining protrusion characteristics, affect protein dynamics and
actin network ultrastructure. ArpC5 isoforms also affect the positioning of members
of the Ena/Vasodilator-stimulated phosphoprotein (VASP) family of actin filament
elongators, which mediate ArpC5 isoform–specific effects on the actin assembly
level. Our results suggest that ArpC5 and Ena/VASP proteins are part of a signaling
pathway enhancing cell migration.
acknowledged_ssus:
- _id: ScienComp
- _id: LifeSc
- _id: Bio
- _id: EM-Fac
acknowledgement: "We would like to thank K. von Peinen and B. Denker (Helmholtz Centre
for Infection Research, Braunschweig, Germany) for experimental and technical assistance,
respectively.\r\nThis research was supported by the Scientific Service Units (SSUs)
of ISTA through resources provided by Scientific Computing (SciComp), the Life Science
Facility (LSF), the Imaging and Optics facility (IOF), and the Electron Microscopy
Facility (EMF). We acknowledge support from ISTA and from the Austrian Science Fund
(FWF) (P33367) to F.K.M.S., from the Research Training Group GRK2223 and the Helmholtz
Society to K.R,. and from the Deutsche Forschungsgemeinschaft (DFG) to J.F. and
K.R."
article_number: add6495
article_processing_charge: No
article_type: original
author:
- first_name: Florian
full_name: Fäßler, Florian
id: 404F5528-F248-11E8-B48F-1D18A9856A87
last_name: Fäßler
orcid: 0000-0001-7149-769X
- first_name: Manjunath
full_name: Javoor, Manjunath
id: 305ab18b-dc7d-11ea-9b2f-b58195228ea2
last_name: Javoor
- first_name: Julia
full_name: Datler, Julia
id: 3B12E2E6-F248-11E8-B48F-1D18A9856A87
last_name: Datler
orcid: 0000-0002-3616-8580
- first_name: Hermann
full_name: Döring, Hermann
last_name: Döring
- first_name: Florian
full_name: Hofer, Florian
id: b9d234ba-9e33-11ed-95b6-cd561df280e6
last_name: Hofer
- 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: Victor-Valentin
full_name: Hodirnau, Victor-Valentin
id: 3661B498-F248-11E8-B48F-1D18A9856A87
last_name: Hodirnau
- first_name: Jan
full_name: Faix, Jan
last_name: Faix
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Florian KM
full_name: Schur, Florian KM
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
citation:
ama: Fäßler F, Javoor M, Datler J, et al. ArpC5 isoforms regulate Arp2/3 complex–dependent
protrusion through differential Ena/VASP positioning. Science Advances.
2023;9(3). doi:10.1126/sciadv.add6495
apa: Fäßler, F., Javoor, M., Datler, J., Döring, H., Hofer, F., Dimchev, G. A.,
… Schur, F. K. (2023). ArpC5 isoforms regulate Arp2/3 complex–dependent protrusion
through differential Ena/VASP positioning. Science Advances. American Association
for the Advancement of Science. https://doi.org/10.1126/sciadv.add6495
chicago: Fäßler, Florian, Manjunath Javoor, Julia Datler, Hermann Döring, Florian
Hofer, Georgi A Dimchev, Victor-Valentin Hodirnau, Jan Faix, Klemens Rottner,
and Florian KM Schur. “ArpC5 Isoforms Regulate Arp2/3 Complex–Dependent Protrusion
through Differential Ena/VASP Positioning.” Science Advances. American
Association for the Advancement of Science, 2023. https://doi.org/10.1126/sciadv.add6495.
ieee: F. Fäßler et al., “ArpC5 isoforms regulate Arp2/3 complex–dependent
protrusion through differential Ena/VASP positioning,” Science Advances,
vol. 9, no. 3. American Association for the Advancement of Science, 2023.
ista: Fäßler F, Javoor M, Datler J, Döring H, Hofer F, Dimchev GA, Hodirnau V-V,
Faix J, Rottner K, Schur FK. 2023. ArpC5 isoforms regulate Arp2/3 complex–dependent
protrusion through differential Ena/VASP positioning. Science Advances. 9(3),
add6495.
mla: Fäßler, Florian, et al. “ArpC5 Isoforms Regulate Arp2/3 Complex–Dependent Protrusion
through Differential Ena/VASP Positioning.” Science Advances, vol. 9, no.
3, add6495, American Association for the Advancement of Science, 2023, doi:10.1126/sciadv.add6495.
short: F. Fäßler, M. Javoor, J. Datler, H. Döring, F. Hofer, G.A. Dimchev, V.-V.
Hodirnau, J. Faix, K. Rottner, F.K. Schur, Science Advances 9 (2023).
date_created: 2023-01-23T07:26:42Z
date_published: 2023-01-20T00:00:00Z
date_updated: 2023-11-21T08:05:35Z
day: '20'
ddc:
- '570'
department:
- _id: FlSc
- _id: EM-Fac
doi: 10.1126/sciadv.add6495
external_id:
isi:
- '000964550100015'
file:
- access_level: open_access
checksum: ce81a6d0b84170e5e8c62f6acfa15d9e
content_type: application/pdf
creator: dernst
date_created: 2023-01-23T07:45:54Z
date_updated: 2023-01-23T07:45:54Z
file_id: '12335'
file_name: 2023_ScienceAdvances_Faessler.pdf
file_size: 1756234
relation: main_file
success: 1
file_date_updated: 2023-01-23T07:45:54Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
issue: '3'
keyword:
- Multidisciplinary
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
project:
- _id: 9B954C5C-BA93-11EA-9121-9846C619BF3A
grant_number: P33367
name: Structure and isoform diversity of the Arp2/3 complex
publication: Science Advances
publication_identifier:
issn:
- 2375-2548
publication_status: published
publisher: American Association for the Advancement of Science
quality_controlled: '1'
related_material:
record:
- id: '14562'
relation: research_data
status: public
scopus_import: '1'
status: public
title: ArpC5 isoforms regulate Arp2/3 complex–dependent protrusion through differential
Ena/VASP positioning
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: 9
year: '2023'
...
---
_id: '14562'
abstract:
- lang: eng
text: "Regulation of the Arp2/3 complex is required for productive nucleation of
branched actin networks. An emerging aspect of regulation is the incorporation
of subunit isoforms into the Arp2/3 complex. Specifically, both ArpC5 subunit
isoforms, ArpC5 and ArpC5L, have been reported to fine-tune nucleation activity
and branch junction stability. We have combined reverse genetics and cellular
structural biology to describe how ArpC5 and ArpC5L differentially affect cell
migration. Both define the structural stability of ArpC1 in branch junctions and,
in turn, by determining protrusion characteristics, affect protein dynamics and
actin network ultrastructure. ArpC5 isoforms also affect the positioning of members
of the Ena/Vasodilator-stimulated phosphoprotein (VASP) family of actin filament
elongators, which mediate ArpC5 isoform–specific effects on the actin assembly
level. Our results suggest that ArpC5 and Ena/VASP proteins are part of a signaling
pathway enhancing cell migration.\r\n"
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
- _id: ScienComp
- _id: EM-Fac
acknowledgement: "We would like to thank K. von Peinen and B. Denker (Helmholtz Centre
for Infection Research, Braunschweig, Germany) for experimental and technical assistance,
respectively.\r\nFunding: This research was supported by the Scientific Service
Units (SSUs) of ISTA through resources provided by Scientific Computing (SciComp),
the Life Science Facility (LSF), the Imaging and Optics facility (IOF), and the
Electron Microscopy Facility (EMF). We acknowledge support from ISTA and from the
Austrian Science Fund (FWF) (P33367) to F.K.M.S., from the Research Training Group
GRK2223 and the Helmholtz Society to K.R,. and from the Deutsche Forschungsgemeinschaft
(DFG) to J.F. and K.R."
article_processing_charge: No
author:
- first_name: Florian KM
full_name: Schur, Florian KM
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
citation:
ama: Schur FK. Research data of the publication “ArpC5 isoforms regulate Arp2/3
complex-dependent protrusion through differential Ena/VASP positioning.” 2023.
doi:10.15479/AT:ISTA:14562
apa: Schur, F. K. (2023). Research data of the publication “ArpC5 isoforms regulate
Arp2/3 complex-dependent protrusion through differential Ena/VASP positioning.”
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:14562
chicago: Schur, Florian KM. “Research Data of the Publication ‘ArpC5 Isoforms Regulate
Arp2/3 Complex-Dependent Protrusion through Differential Ena/VASP Positioning.’”
Institute of Science and Technology Austria, 2023. https://doi.org/10.15479/AT:ISTA:14562.
ieee: F. K. Schur, “Research data of the publication ‘ArpC5 isoforms regulate Arp2/3
complex-dependent protrusion through differential Ena/VASP positioning.’” Institute
of Science and Technology Austria, 2023.
ista: Schur FK. 2023. Research data of the publication ‘ArpC5 isoforms regulate
Arp2/3 complex-dependent protrusion through differential Ena/VASP positioning’,
Institute of Science and Technology Austria, 10.15479/AT:ISTA:14562.
mla: Schur, Florian KM. Research Data of the Publication “ArpC5 Isoforms Regulate
Arp2/3 Complex-Dependent Protrusion through Differential Ena/VASP Positioning.”
Institute of Science and Technology Austria, 2023, doi:10.15479/AT:ISTA:14562.
short: F.K. Schur, (2023).
contributor:
- contributor_type: researcher
first_name: Florian
id: 404F5528-F248-11E8-B48F-1D18A9856A87
last_name: Fäßler
orcid: 0000-0001-7149-769X
- contributor_type: researcher
first_name: Manjunath
id: 305ab18b-dc7d-11ea-9b2f-b58195228ea2
last_name: Javoor
- contributor_type: researcher
first_name: Julia
id: 3B12E2E6-F248-11E8-B48F-1D18A9856A87
last_name: Datler
orcid: 0000-0002-3616-8580
- contributor_type: researcher
first_name: Hermann
last_name: Döring
- contributor_type: researcher
first_name: Florian
id: b9d234ba-9e33-11ed-95b6-cd561df280e6
last_name: Hofer
- contributor_type: researcher
first_name: Georgi A
id: 38C393BE-F248-11E8-B48F-1D18A9856A87
last_name: Dimchev
orcid: 0000-0001-8370-6161
- contributor_type: researcher
first_name: Victor-Valentin
id: 3661B498-F248-11E8-B48F-1D18A9856A87
last_name: Hodirnau
- contributor_type: researcher
first_name: Jan
last_name: Faix
- contributor_type: researcher
first_name: Klemens
last_name: Rottner
- contributor_type: researcher
first_name: Florian KM
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
date_created: 2023-11-20T09:22:33Z
date_published: 2023-11-21T00:00:00Z
date_updated: 2023-11-21T08:05:34Z
day: '21'
ddc:
- '570'
department:
- _id: FlSc
doi: 10.15479/AT:ISTA:14562
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month: '11'
oa: 1
oa_version: Published Version
project:
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grant_number: P33367
name: Structure and isoform diversity of the Arp2/3 complex
publisher: Institute of Science and Technology Austria
related_material:
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status: public
title: Research data of the publication "ArpC5 isoforms regulate Arp2/3 complex-dependent
protrusion through differential Ena/VASP positioning"
tmp:
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legal_code_url: https://creativecommons.org/licenses/by-sa/4.0/legalcode
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BY-SA 4.0)
short: CC BY-SA (4.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '14502'
abstract:
- lang: eng
text: A precise quantitative description of the ultrastructural characteristics
underlying biological mechanisms is often key to their understanding. This is
particularly true for dynamic extra- and intracellular filamentous assemblies,
playing a role in cell motility, cell integrity, cytokinesis, tissue formation
and maintenance. For example, genetic manipulation or modulation of actin regulatory
proteins frequently manifests in changes of the morphology, dynamics, and ultrastructural
architecture of actin filament-rich cell peripheral structures, such as lamellipodia
or filopodia. However, the observed ultrastructural effects often remain subtle
and require sufficiently large datasets for appropriate quantitative analysis.
The acquisition of such large datasets has been enabled by recent advances in
high-throughput cryo-electron tomography (cryo-ET) methods. This also necessitates
the development of complementary approaches to maximize the extraction of relevant
biological information. We have developed a computational toolbox for the semi-automatic
quantification of segmented and vectorized fila- mentous networks from pre-processed
cryo-electron tomograms, facilitating the analysis and cross-comparison of multiple
experimental conditions. GUI-based components simplify the processing of data
and allow users to obtain a large number of ultrastructural parameters describing
filamentous assemblies. We demonstrate the feasibility of this workflow by analyzing
cryo-ET data of untreated and chemically perturbed branched actin filament networks
and that of parallel actin filament arrays. In principle, the computational toolbox
presented here is applicable for data analysis comprising any type of filaments
in regular (i.e. parallel) or random arrangement. We show that it can ease the
identification of key differences between experimental groups and facilitate the
in-depth analysis of ultrastructural data in a time-efficient manner.
author:
- 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: Behnam
full_name: Amiri, Behnam
last_name: Amiri
- first_name: Florian
full_name: Fäßler, Florian
id: 404F5528-F248-11E8-B48F-1D18A9856A87
last_name: Fäßler
orcid: 0000-0001-7149-769X
- first_name: Martin
full_name: Falcke, Martin
last_name: Falcke
- first_name: Florian KM
full_name: Schur, Florian KM
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
citation:
ama: Dimchev GA, Amiri B, Fäßler F, Falcke M, Schur FK. Computational toolbox for
ultrastructural quantitative analysis of filament networks in cryo-ET data. 2023.
doi:10.15479/AT:ISTA:14502
apa: Dimchev, G. A., Amiri, B., Fäßler, F., Falcke, M., & Schur, F. K. (2023).
Computational toolbox for ultrastructural quantitative analysis of filament networks
in cryo-ET data. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:14502
chicago: Dimchev, Georgi A, Behnam Amiri, Florian Fäßler, Martin Falcke, and Florian
KM Schur. “Computational Toolbox for Ultrastructural Quantitative Analysis of
Filament Networks in Cryo-ET Data.” Institute of Science and Technology Austria,
2023. https://doi.org/10.15479/AT:ISTA:14502.
ieee: G. A. Dimchev, B. Amiri, F. Fäßler, M. Falcke, and F. K. Schur, “Computational
toolbox for ultrastructural quantitative analysis of filament networks in cryo-ET
data.” Institute of Science and Technology Austria, 2023.
ista: Dimchev GA, Amiri B, Fäßler F, Falcke M, Schur FK. 2023. Computational toolbox
for ultrastructural quantitative analysis of filament networks in cryo-ET data,
Institute of Science and Technology Austria, 10.15479/AT:ISTA:14502.
mla: Dimchev, Georgi A., et al. Computational Toolbox for Ultrastructural Quantitative
Analysis of Filament Networks in Cryo-ET Data. Institute of Science and Technology
Austria, 2023, doi:10.15479/AT:ISTA:14502.
short: G.A. Dimchev, B. Amiri, F. Fäßler, M. Falcke, F.K. Schur, (2023).
date_created: 2023-11-08T19:40:54Z
date_published: 2023-11-21T00:00:00Z
date_updated: 2023-11-21T08:36:02Z
day: '21'
ddc:
- '570'
department:
- _id: FlSc
doi: 10.15479/AT:ISTA:14502
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creator: dernst
date_created: 2023-11-21T08:20:23Z
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success: 1
file_date_updated: 2023-11-21T08:20:23Z
has_accepted_license: '1'
keyword:
- cryo-electron tomography
- actin cytoskeleton
- toolbox
license: https://choosealicense.com/licenses/agpl-3.0/
month: '11'
oa: 1
project:
- _id: 9B954C5C-BA93-11EA-9121-9846C619BF3A
grant_number: P33367
name: Structure and isoform diversity of the Arp2/3 complex
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '10290'
relation: used_for_analysis_in
status: public
status: public
title: Computational toolbox for ultrastructural quantitative analysis of filament
networks in cryo-ET data
tmp:
legal_code_url: https://www.gnu.org/licenses/agpl-3.0.html
name: GNU Affero General Public License v3.0
short: 'GNU AGPLv3 '
type: software
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '13342'
abstract:
- lang: eng
text: Motile cells moving in multicellular organisms encounter microenvironments
of locally heterogeneous mechanochemical composition. Individual compositional
parameters like chemotactic signals, adhesiveness, and pore sizes are well known
to be sensed by motile cells, providing individual guidance cues for cellular
pathfinding. However, motile cells encounter diverse mechanochemical signals at
the same time, raising the question of how cells respond to locally diverse and
potentially competing signals on their migration routes. Here, we reveal that
motile amoeboid cells require nuclear repositioning, termed nucleokinesis, for
adaptive pathfinding in heterogeneous mechanochemical microenvironments. Using
mammalian immune cells and the amoebaDictyostelium discoideum,
we discover that frequent, rapid and long-distance nucleokinesis is a basic component
of amoeboid pathfinding, enabling cells to reorientate quickly between locally
competing cues. Amoeboid nucleokinesis comprises a two-step cell polarity switch
and is driven by myosin II-forces, sliding the nucleus from a ‘losing’ to the
‘winning’ leading edge to re-adjust the nuclear to the cellular path. Impaired
nucleokinesis distorts fast path adaptions and causes cellular arrest in the microenvironment.
Our findings establish that nucleokinesis is required for amoeboid cell navigation.
Given that motile single-cell amoebae, many immune cells, and some cancer cells
utilize an amoeboid migration strategy, these results suggest that amoeboid nucleokinesis
underlies cellular navigation during unicellular biology, immunity, and disease.
acknowledgement: We thank Christoph Mayr and Bingzhi Wang for initial experiments
on amoeboid nucleokinesis, Ana-Maria Lennon-Duménil and Aline Yatim for bone marrow
from MyoIIA-Flox*CD11c-Cre mice, Michael Sixt and Aglaja Kopf for EMTB-mCherry,
EB3-mCherry, Lifeact-GFP, Lfc knockout, and Myh9-GFP expressing HoxB8 cells, Malte
Benjamin Braun, Mauricio Ruiz, and Madeleine T. Schmitt for critical reading of
the manuscript, and the Core Facility Bioimaging, the Core Facility Flow Cytometry,
and the Animal Core Facility of the Biomedical Center (BMC) for excellent support.
This study was supported by the Peter Hans Hofschneider Professorship of the foundation
“Stiftung Experimentelle Biomedizin” (to JR), the LMU Institutional Strategy LMU-Excellent
within the framework of the German Excellence Initiative (to JR), and the Deutsche
Forschungsgemeinschaft (DFG; German Research Foundation; SFB914 project A12, to
JR), and the CZI grant DAF2020-225401 (https://doi.org/10.37921/120055ratwvi) from
the Chan Zuckerberg Initiative DAF (to RH; an advised fund of Silicon Valley Community
Foundation (funder https://doi.org/10.13039/100014989)). Open Access funding enabled
and organized by Projekt DEAL.
article_number: e114557
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Janina
full_name: Kroll, Janina
last_name: Kroll
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Arthur
full_name: Kuznetcov, Arthur
last_name: Kuznetcov
- first_name: Kasia
full_name: Stefanowski, Kasia
last_name: Stefanowski
- first_name: Monika D.
full_name: Hermann, Monika D.
last_name: Hermann
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Lubuna B
full_name: Shafeek, Lubuna B
id: 3CD37A82-F248-11E8-B48F-1D18A9856A87
last_name: Shafeek
orcid: 0000-0001-7180-6050
- first_name: Annette
full_name: Müller-Taubenberger, Annette
last_name: Müller-Taubenberger
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
citation:
ama: Kroll J, Hauschild R, Kuznetcov A, et al. Adaptive pathfinding by nucleokinesis
during amoeboid migration. EMBO Journal. 2023. doi:10.15252/embj.2023114557
apa: Kroll, J., Hauschild, R., Kuznetcov, A., Stefanowski, K., Hermann, M. D., Merrin,
J., … Renkawitz, J. (2023). Adaptive pathfinding by nucleokinesis during amoeboid
migration. EMBO Journal. Embo Press. https://doi.org/10.15252/embj.2023114557
chicago: Kroll, Janina, Robert Hauschild, Arthur Kuznetcov, Kasia Stefanowski, Monika
D. Hermann, Jack Merrin, Lubuna B Shafeek, Annette Müller-Taubenberger, and Jörg
Renkawitz. “Adaptive Pathfinding by Nucleokinesis during Amoeboid Migration.”
EMBO Journal. Embo Press, 2023. https://doi.org/10.15252/embj.2023114557.
ieee: J. Kroll et al., “Adaptive pathfinding by nucleokinesis during amoeboid
migration,” EMBO Journal. Embo Press, 2023.
ista: Kroll J, Hauschild R, Kuznetcov A, Stefanowski K, Hermann MD, Merrin J, Shafeek
LB, Müller-Taubenberger A, Renkawitz J. 2023. Adaptive pathfinding by nucleokinesis
during amoeboid migration. EMBO Journal., e114557.
mla: Kroll, Janina, et al. “Adaptive Pathfinding by Nucleokinesis during Amoeboid
Migration.” EMBO Journal, e114557, Embo Press, 2023, doi:10.15252/embj.2023114557.
short: J. Kroll, R. Hauschild, A. Kuznetcov, K. Stefanowski, M.D. Hermann, J. Merrin,
L.B. Shafeek, A. Müller-Taubenberger, J. Renkawitz, EMBO Journal (2023).
date_created: 2023-08-01T08:59:06Z
date_published: 2023-11-21T00:00:00Z
date_updated: 2023-11-27T08:47:45Z
day: '21'
ddc:
- '570'
department:
- _id: NanoFab
- _id: Bio
doi: 10.15252/embj.2023114557
external_id:
pmid:
- '37987147'
file:
- access_level: open_access
checksum: 6261d0041c7e8d284c39712c40079730
content_type: application/pdf
creator: dernst
date_created: 2023-11-27T08:45:56Z
date_updated: 2023-11-27T08:45:56Z
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file_name: 2023_EmboJournal_Kroll.pdf
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file_date_updated: 2023-11-27T08:45:56Z
has_accepted_license: '1'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: 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: Adaptive pathfinding by nucleokinesis during amoeboid migration
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
year: '2023'
...
---
_id: '14610'
abstract:
- lang: eng
text: AbstractEndomembrane damage represents a
form of stress that is detrimental for eukaryotic cells1,2.
To cope with this threat, cells possess mechanisms that repair the damage and
restore cellular homeostasis3–7. Endomembrane damage also
results in organelle instability and the mechanisms by which cells stabilize damaged
endomembranes to enable membrane repair remains unknown. Here, by combining in
vitro and in cellulo studies with computational modelling we uncover a biological
function for stress granules whereby these biomolecular condensates form rapidly
at endomembrane damage sites and act as a plug that stabilizes the ruptured membrane.
Functionally, we demonstrate that stress granule formation and membrane stabilization
enable efficient repair of damaged endolysosomes, through both ESCRT (endosomal
sorting complex required for transport)-dependent and independent mechanisms.
We also show that blocking stress granule formation in human macrophages creates
a permissive environment for Mycobacterium tuberculosis,
a human pathogen that exploits endomembrane damage to survive within the host.
acknowledgement: "We thank the Human Embryonic Stem Cell Unit, Advanced Light Microscopy
and High-throughput Screening facilities at the Crick for their support in various
aspects of the work. We thank the laboratory of P. Anderson for providing the G3BP-DKO
U2OS cells. The authors thank N. Chen for providing the purified glycinin protein;
Z. Zhao for providing the microfluidic chip wafers; and M. Amaral and F. Frey for
helpful discussions and valuable input regarding analysis methods. This work was
supported by the Francis Crick Institute (to M.G.G.), which receives its core funding
from Cancer Research UK (FC001092), the UK Medical Research Council (FC001092) and
the Wellcome Trust (FC001092). This project has received funding from the European
Research Council (ERC) under the European Union’s Horizon 2020 research and innovation
programme (grant agreement no. 772022 to M.G.G.). C.B. has received funding from
the European Respiratory Society and the European Union’s H2020 research and innovation
programme under the Marie Sklodowska-Curie grant agreement no. 713406. A.M. acknowledges
support from Alexander von Humboldt Foundation and C.V.-C. acknowledges funding
by the Royal Society and the European Research Council under the European Union’s
Horizon 2020 Research and Innovation Programme (grant no. 802960 to A.S.). All simulations
were carried out on the high-performance computing cluster at the Institute of Science
and Technology Austria. For the purpose of Open Access, the author has applied a
CC BY public copyright licence to any Author Accepted Manuscript version arising
from this submission.\r\nOpen Access funding provided by The Francis Crick Institute."
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Claudio
full_name: Bussi, Claudio
last_name: Bussi
- first_name: Agustín
full_name: Mangiarotti, Agustín
last_name: Mangiarotti
- first_name: Christian Eduardo
full_name: Vanhille-Campos, Christian Eduardo
id: 3adeca52-9313-11ed-b1ac-c170b2505714
last_name: Vanhille-Campos
- first_name: Beren
full_name: Aylan, Beren
last_name: Aylan
- first_name: Enrica
full_name: Pellegrino, Enrica
last_name: Pellegrino
- first_name: Natalia
full_name: Athanasiadi, Natalia
last_name: Athanasiadi
- first_name: Antony
full_name: Fearns, Antony
last_name: Fearns
- first_name: Angela
full_name: Rodgers, Angela
last_name: Rodgers
- first_name: Titus M.
full_name: Franzmann, Titus M.
last_name: Franzmann
- first_name: Anđela
full_name: Šarić, Anđela
id: bf63d406-f056-11eb-b41d-f263a6566d8b
last_name: Šarić
orcid: 0000-0002-7854-2139
- first_name: Rumiana
full_name: Dimova, Rumiana
last_name: Dimova
- first_name: Maximiliano G.
full_name: Gutierrez, Maximiliano G.
last_name: Gutierrez
citation:
ama: Bussi C, Mangiarotti A, Vanhille-Campos CE, et al. Stress granules plug and
stabilize damaged endolysosomal membranes. Nature. 2023. doi:10.1038/s41586-023-06726-w
apa: Bussi, C., Mangiarotti, A., Vanhille-Campos, C. E., Aylan, B., Pellegrino,
E., Athanasiadi, N., … Gutierrez, M. G. (2023). Stress granules plug and stabilize
damaged endolysosomal membranes. Nature. Springer Nature. https://doi.org/10.1038/s41586-023-06726-w
chicago: Bussi, Claudio, Agustín Mangiarotti, Christian Eduardo Vanhille-Campos,
Beren Aylan, Enrica Pellegrino, Natalia Athanasiadi, Antony Fearns, et al. “Stress
Granules Plug and Stabilize Damaged Endolysosomal Membranes.” Nature. Springer
Nature, 2023. https://doi.org/10.1038/s41586-023-06726-w.
ieee: C. Bussi et al., “Stress granules plug and stabilize damaged endolysosomal
membranes,” Nature. Springer Nature, 2023.
ista: Bussi C, Mangiarotti A, Vanhille-Campos CE, Aylan B, Pellegrino E, Athanasiadi
N, Fearns A, Rodgers A, Franzmann TM, Šarić A, Dimova R, Gutierrez MG. 2023. Stress
granules plug and stabilize damaged endolysosomal membranes. Nature.
mla: Bussi, Claudio, et al. “Stress Granules Plug and Stabilize Damaged Endolysosomal
Membranes.” Nature, Springer Nature, 2023, doi:10.1038/s41586-023-06726-w.
short: C. Bussi, A. Mangiarotti, C.E. Vanhille-Campos, B. Aylan, E. Pellegrino,
N. Athanasiadi, A. Fearns, A. Rodgers, T.M. Franzmann, A. Šarić, R. Dimova, M.G.
Gutierrez, Nature (2023).
date_created: 2023-11-27T07:56:37Z
date_published: 2023-11-15T00:00:00Z
date_updated: 2023-11-27T09:05:08Z
day: '15'
department:
- _id: AnSa
doi: 10.1038/s41586-023-06726-w
external_id:
pmid:
- '37968398'
keyword:
- Multidisciplinary
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1038/s41586-023-06726-w
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: epub_ahead
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1038/s41586-023-06882-z
record:
- id: '14472'
relation: research_data
status: public
status: public
title: Stress granules plug and stabilize damaged endolysosomal membranes
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '14472'
abstract:
- lang: eng
text: "Data related to the following paper:\r\n\"Stress granules plug and stabilize
damaged endolysosomal membranes\" (https://doi.org/10.1038/s41586-023-06726-w)\r\n\r\nAbstract:
\r\nEndomembrane damage represents a form of stress that is detrimental for eukaryotic
cells. To cope with this threat, cells possess mechanisms that repair the damage
and restore cellular homeostasis. Endomembrane damage also results in organelle
instability and the mechanisms by which cells stabilize damaged endomembranes
to enable membrane repair remains unknown. In this work we use a minimal coarse-grained
molecular dynamics system to explore how lipid vesicles undergoing poration in
a protein-rich medium can be plugged and stabilised by condensate formation. The
solution of proteins in and out of the vesicle is described by beads dispersed
in implicit solvent. The membrane is described as a one-bead-thick fluid elastic
layer of mechanical properties that mimic biological membranes. We tune the interactions
between solution beads in the different compartments to capture the differences
between the cytoplasmic and endosomal protein solutions and explore how the system
responds to different degrees of membrane poration. We find that, in the right
interaction regime, condensates form rapidly at the damage site upon solution
mixing and act as a plug that prevents futher mixing and destabilisation of the
vesicle. Further, when the condensate can interact with the membrane (wetting
interactions) we find that it mediates pore sealing and membrane repair. This
research is part of the work published in \"Stress granules plug and stabilize
damaged endolysosomal membranes\", Bussi et al, Nature, 2023 - 10.1038/s41586-023-06726-w."
article_processing_charge: No
author:
- first_name: Christian Eduardo
full_name: Vanhille-Campos, Christian Eduardo
id: 3adeca52-9313-11ed-b1ac-c170b2505714
last_name: Vanhille-Campos
- first_name: Anđela
full_name: Šarić, Anđela
id: bf63d406-f056-11eb-b41d-f263a6566d8b
last_name: Šarić
orcid: 0000-0002-7854-2139
citation:
ama: Vanhille-Campos CE, Šarić A. Stress granules plug and stabilize damaged endolysosomal
membranes. 2023. doi:10.15479/AT:ISTA:14472
apa: Vanhille-Campos, C. E., & Šarić, A. (2023). Stress granules plug and stabilize
damaged endolysosomal membranes. Institute of Science and Technology Austria.
https://doi.org/10.15479/AT:ISTA:14472
chicago: Vanhille-Campos, Christian Eduardo, and Anđela Šarić. “Stress Granules
Plug and Stabilize Damaged Endolysosomal Membranes.” Institute of Science and
Technology Austria, 2023. https://doi.org/10.15479/AT:ISTA:14472.
ieee: C. E. Vanhille-Campos and A. Šarić, “Stress granules plug and stabilize damaged
endolysosomal membranes.” Institute of Science and Technology Austria, 2023.
ista: Vanhille-Campos CE, Šarić A. 2023. Stress granules plug and stabilize damaged
endolysosomal membranes, Institute of Science and Technology Austria, 10.15479/AT:ISTA:14472.
mla: Vanhille-Campos, Christian Eduardo, and Anđela Šarić. Stress Granules Plug
and Stabilize Damaged Endolysosomal Membranes. Institute of Science and Technology
Austria, 2023, doi:10.15479/AT:ISTA:14472.
short: C.E. Vanhille-Campos, A. Šarić, (2023).
date_created: 2023-10-30T16:38:32Z
date_published: 2023-10-31T00:00:00Z
date_updated: 2023-11-27T09:05:07Z
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month: '10'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
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record:
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relation: used_in_publication
status: public
status: public
title: Stress granules plug and stabilize damaged endolysosomal membranes
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '12747'
abstract:
- lang: eng
text: Muscle degeneration is the most prevalent cause for frailty and dependency
in inherited diseases and ageing. Elucidation of pathophysiological mechanisms,
as well as effective treatments for muscle diseases, represents an important goal
in improving human health. Here, we show that the lipid synthesis enzyme phosphatidylethanolamine
cytidyltransferase (PCYT2/ECT) is critical to muscle health. Human deficiency
in PCYT2 causes a severe disease with failure to thrive and progressive weakness.
pcyt2-mutant zebrafish and muscle-specific Pcyt2-knockout mice recapitulate the
participant phenotypes, with failure to thrive, progressive muscle weakness and
accelerated ageing. Mechanistically, muscle Pcyt2 deficiency affects cellular
bioenergetics and membrane lipid bilayer structure and stability. PCYT2 activity
declines in ageing muscles of mice and humans, and adeno-associated virus-based
delivery of PCYT2 ameliorates muscle weakness in Pcyt2-knockout and old mice,
offering a therapy for individuals with a rare disease and muscle ageing. Thus,
PCYT2 plays a fundamental and conserved role in vertebrate muscle health, linking
PCYT2 and PCYT2-synthesized lipids to severe muscle dystrophy and ageing.
acknowledgement: 'The authors thank the participants and their families for participating
in the study. We thank all members of our laboratories for helpful discussions.
We are grateful to Vienna BioCenter Core Facilities: Mouse Phenotyping Unit, Histopathology
Unit, Bioinformatics Unit, BioOptics Unit, Electron Microscopy Unit and Comparative
Medicine Unit. We are grateful to the Lipidomics Facility, and K. Klavins and T.
Hannich at the CeMM Research Center for Molecular Medicine of the Austrian Academy
of Sciences for assistance with lipidomics analysis. We also thank T. Huan and A.
Hui (UBC Vancouver) for mouse tissue and mitochondria lipidomics analysis. We thank
A. Klymchenko (Laboratoire de Bioimagerie et Pathologies Université de Strasbourg,
Strasbourg, France) for providing the NR12S probe. We are thankful to the Sen. Paul
D. Wellstone Muscular Dystrophy Cooperative Specialized Research Center Viral Vector
Core Facility for AAV6 production. We also thank K. P. Campbell and M. E. Anderson
(University of Iowa, Carver College of Medicine) for advice on muscle tissue handling.
We thank A. Al-Qassabi from the Sultan Qaboos University for the clinical assessment
of the participants. D.C. and J.M.P. are supported by the Austrian Federal Ministry
of Education, Science and Research, the Austrian Academy of Sciences, and the City
of Vienna, and grants from the Austrian Science Fund (FWF) Wittgenstein award (Z
271-B19), the T. von Zastrow Foundation, and a Canada 150 Research Chairs Program
(F18-01336). J.S.C. is supported by grants RO1AR44533 and P50AR065139 from the US
National Institutes of Health. C.K. is supported by a grant from the Agence Nationale
de la Recherche (ANR-18-CE14-0007-01). A.V.K. is supported by European Union’s Horizon
2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement
no. 67544, and an Austrian Science Fund (FWF; no P-33799). A.W. is supported by
Austrian Research Promotion Agency (FFG) project no 867674. E.S. is supported by
a SciLifeLab fellowship and Karolinska Institutet Foundation Grants. Work in the
laboratory of G.S.-F. is supported by the Austrian Academy of Sciences, the European
Research Council (ERC AdG 695214 GameofGates) and the Innovative Medicines Initiative
2 Joint Undertaking (grant agreement no. 777372, ReSOLUTE). S.B., M.L. and R.Y.
acknowledge the support of the Spastic Paraplegia Foundation.'
article_processing_charge: No
article_type: original
author:
- first_name: Domagoj
full_name: Cikes, Domagoj
last_name: Cikes
- first_name: Kareem
full_name: Elsayad, Kareem
last_name: Elsayad
- first_name: Erdinc
full_name: Sezgin, Erdinc
last_name: Sezgin
- first_name: Erika
full_name: Koitai, Erika
last_name: Koitai
- first_name: Torma
full_name: Ferenc, Torma
last_name: Ferenc
- first_name: Michael
full_name: Orthofer, Michael
last_name: Orthofer
- first_name: Rebecca
full_name: Yarwood, Rebecca
last_name: Yarwood
- first_name: Leonhard X.
full_name: Heinz, Leonhard X.
last_name: Heinz
- first_name: Vitaly
full_name: Sedlyarov, Vitaly
last_name: Sedlyarov
- first_name: Nasser
full_name: Darwish-Miranda, Nasser
id: 39CD9926-F248-11E8-B48F-1D18A9856A87
last_name: Darwish-Miranda
orcid: 0000-0002-8821-8236
- first_name: Adrian
full_name: Taylor, Adrian
last_name: Taylor
- first_name: Sophie
full_name: Grapentine, Sophie
last_name: Grapentine
- first_name: Fathiya
full_name: al-Murshedi, Fathiya
last_name: al-Murshedi
- first_name: Anne
full_name: Abot, Anne
last_name: Abot
- first_name: Adelheid
full_name: Weidinger, Adelheid
last_name: Weidinger
- first_name: Candice
full_name: Kutchukian, Candice
last_name: Kutchukian
- first_name: Colline
full_name: Sanchez, Colline
last_name: Sanchez
- first_name: Shane J. F.
full_name: Cronin, Shane J. F.
last_name: Cronin
- first_name: Maria
full_name: Novatchkova, Maria
last_name: Novatchkova
- first_name: Anoop
full_name: Kavirayani, Anoop
last_name: Kavirayani
- first_name: Thomas
full_name: Schuetz, Thomas
last_name: Schuetz
- first_name: Bernhard
full_name: Haubner, Bernhard
last_name: Haubner
- first_name: Lisa
full_name: Haas, Lisa
last_name: Haas
- first_name: Astrid
full_name: Hagelkruys, Astrid
last_name: Hagelkruys
- first_name: Suzanne
full_name: Jackowski, Suzanne
last_name: Jackowski
- first_name: Andrey
full_name: Kozlov, Andrey
last_name: Kozlov
- first_name: Vincent
full_name: Jacquemond, Vincent
last_name: Jacquemond
- first_name: Claude
full_name: Knauf, Claude
last_name: Knauf
- first_name: Giulio
full_name: Superti-Furga, Giulio
last_name: Superti-Furga
- first_name: Eric
full_name: Rullman, Eric
last_name: Rullman
- first_name: Thomas
full_name: Gustafsson, Thomas
last_name: Gustafsson
- first_name: John
full_name: McDermot, John
last_name: McDermot
- first_name: Martin
full_name: Lowe, Martin
last_name: Lowe
- first_name: Zsolt
full_name: Radak, Zsolt
last_name: Radak
- first_name: Jeffrey S.
full_name: Chamberlain, Jeffrey S.
last_name: Chamberlain
- first_name: Marica
full_name: Bakovic, Marica
last_name: Bakovic
- first_name: Siddharth
full_name: Banka, Siddharth
last_name: Banka
- first_name: Josef M.
full_name: Penninger, Josef M.
last_name: Penninger
citation:
ama: Cikes D, Elsayad K, Sezgin E, et al. PCYT2-regulated lipid biosynthesis is
critical to muscle health and ageing. Nature Metabolism. 2023;5:495-515.
doi:10.1038/s42255-023-00766-2
apa: Cikes, D., Elsayad, K., Sezgin, E., Koitai, E., Ferenc, T., Orthofer, M., …
Penninger, J. M. (2023). PCYT2-regulated lipid biosynthesis is critical to muscle
health and ageing. Nature Metabolism. Springer Nature. https://doi.org/10.1038/s42255-023-00766-2
chicago: Cikes, Domagoj, Kareem Elsayad, Erdinc Sezgin, Erika Koitai, Torma Ferenc,
Michael Orthofer, Rebecca Yarwood, et al. “PCYT2-Regulated Lipid Biosynthesis
Is Critical to Muscle Health and Ageing.” Nature Metabolism. Springer Nature,
2023. https://doi.org/10.1038/s42255-023-00766-2.
ieee: D. Cikes et al., “PCYT2-regulated lipid biosynthesis is critical to
muscle health and ageing,” Nature Metabolism, vol. 5. Springer Nature,
pp. 495–515, 2023.
ista: Cikes D, Elsayad K, Sezgin E, Koitai E, Ferenc T, Orthofer M, Yarwood R, Heinz
LX, Sedlyarov V, Darwish-Miranda N, Taylor A, Grapentine S, al-Murshedi F, Abot
A, Weidinger A, Kutchukian C, Sanchez C, Cronin SJF, Novatchkova M, Kavirayani
A, Schuetz T, Haubner B, Haas L, Hagelkruys A, Jackowski S, Kozlov A, Jacquemond
V, Knauf C, Superti-Furga G, Rullman E, Gustafsson T, McDermot J, Lowe M, Radak
Z, Chamberlain JS, Bakovic M, Banka S, Penninger JM. 2023. PCYT2-regulated lipid
biosynthesis is critical to muscle health and ageing. Nature Metabolism. 5, 495–515.
mla: Cikes, Domagoj, et al. “PCYT2-Regulated Lipid Biosynthesis Is Critical to Muscle
Health and Ageing.” Nature Metabolism, vol. 5, Springer Nature, 2023, pp.
495–515, doi:10.1038/s42255-023-00766-2.
short: D. Cikes, K. Elsayad, E. Sezgin, E. Koitai, T. Ferenc, M. Orthofer, R. Yarwood,
L.X. Heinz, V. Sedlyarov, N. Darwish-Miranda, A. Taylor, S. Grapentine, F. al-Murshedi,
A. Abot, A. Weidinger, C. Kutchukian, C. Sanchez, S.J.F. Cronin, M. Novatchkova,
A. Kavirayani, T. Schuetz, B. Haubner, L. Haas, A. Hagelkruys, S. Jackowski, A.
Kozlov, V. Jacquemond, C. Knauf, G. Superti-Furga, E. Rullman, T. Gustafsson,
J. McDermot, M. Lowe, Z. Radak, J.S. Chamberlain, M. Bakovic, S. Banka, J.M. Penninger,
Nature Metabolism 5 (2023) 495–515.
date_created: 2023-03-23T12:58:43Z
date_published: 2023-03-20T00:00:00Z
date_updated: 2023-11-28T07:31:33Z
day: '20'
department:
- _id: Bio
doi: 10.1038/s42255-023-00766-2
external_id:
isi:
- '000992064000002'
pmid:
- '36941451'
intvolume: ' 5'
isi: 1
keyword:
- Cell Biology
- Physiology (medical)
- Endocrinology
- Diabetes and Metabolism
- Internal Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2022.03.02.482658
month: '03'
oa: 1
oa_version: Preprint
page: 495-515
pmid: 1
publication: Nature Metabolism
publication_identifier:
issn:
- 2522-5812
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1038/s42255-023-00791-1
scopus_import: '1'
status: public
title: PCYT2-regulated lipid biosynthesis is critical to muscle health and ageing
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2023'
...