---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
PlanS_conform: '1'
_id: '21384'
abstract:
- lang: eng
text: 'Cell migration in vivo is often guided by chemical signaling, i.e., chemotaxis.
For immune cells performing chemotaxis in the organism, this process is influenced
by the complex geometry of the tissue environment. In this study, we use a theoretical
model of branched cell migration on a network to explore the cellular response
to chemical gradients. The model predicts the response of a branched cell to a
chemical gradient: how the cell reorients its internal polarity and how it navigates
through a complex environment up a chemical gradient. We then compare the model’s
predictions with experimental observations of neutrophils migrating to the site
of a laser-inflicted wound in a zebrafish larva fin, and neutrophils migrating
in vitro inside a regular lattice of pillars. We find that the model captures
the details of the subcellular response to the chemokine gradient, as well as
qualitative characteristics of the large-scale migration, suggesting that the
neutrophils behave as fast cells, which explains the functionality of these immune
cells.'
acknowledgement: "N.S.G. is the incumbent of the Lee and William Abramowitz Professorial
Chair of Biophysics (Weizmann Institute), and acknowledges support from the Royal
Society Wolfson Visiting Fellowship, and Human Frontier Science Program grant RGP0032/2022.
Work by M.S., I.W., G.R. and A.G. was supported by the Leverhulme Trust (grant RPG-2021-226)
and the European Research Council (ERC) under the Horizon 2020 program and UKRI,
Grant agreement No.\r\nEP/Y02799X/1. M.S. and I.d.V acknowledge support by the European
Research Council (grant ERC-SyG 101071793 to M.S). The funders had no role in study
design, data collection and\r\nanalysis, decision to publish, or preparation of
the manuscript."
article_number: e1013934
article_processing_charge: Yes
article_type: original
author:
- first_name: Jiayi
full_name: Liu, Jiayi
last_name: Liu
- first_name: Jonathan E.
full_name: Ron, Jonathan E.
last_name: Ron
- first_name: Giulia
full_name: Rinaldi, Giulia
last_name: Rinaldi
- first_name: Ivanna
full_name: Williantarra, Ivanna
last_name: Williantarra
- first_name: Antonios
full_name: Georgantzoglou, Antonios
last_name: Georgantzoglou
- first_name: Ingrid
full_name: de Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: de Vries
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Milka
full_name: Sarris, Milka
last_name: Sarris
- first_name: Nir S.
full_name: Gov, Nir S.
last_name: Gov
citation:
ama: Liu J, Ron JE, Rinaldi G, et al. Modelling chemotaxis of branched cells in
complex environments provides insights into immune cell navigation. PLOS Computational
Biology. 2026;22(2). doi:10.1371/journal.pcbi.1013934
apa: Liu, J., Ron, J. E., Rinaldi, G., Williantarra, I., Georgantzoglou, A., de
Vries, I., … Gov, N. S. (2026). Modelling chemotaxis of branched cells in complex
environments provides insights into immune cell navigation. PLOS Computational
Biology. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1013934
chicago: Liu, Jiayi, Jonathan E. Ron, Giulia Rinaldi, Ivanna Williantarra, Antonios
Georgantzoglou, Ingrid de Vries, Michael K Sixt, Milka Sarris, and Nir S. Gov.
“Modelling Chemotaxis of Branched Cells in Complex Environments Provides Insights
into Immune Cell Navigation.” PLOS Computational Biology. Public Library
of Science, 2026. https://doi.org/10.1371/journal.pcbi.1013934.
ieee: J. Liu et al., “Modelling chemotaxis of branched cells in complex environments
provides insights into immune cell navigation,” PLOS Computational Biology,
vol. 22, no. 2. Public Library of Science, 2026.
ista: Liu J, Ron JE, Rinaldi G, Williantarra I, Georgantzoglou A, de Vries I, Sixt
MK, Sarris M, Gov NS. 2026. Modelling chemotaxis of branched cells in complex
environments provides insights into immune cell navigation. PLOS Computational
Biology. 22(2), e1013934.
mla: Liu, Jiayi, et al. “Modelling Chemotaxis of Branched Cells in Complex Environments
Provides Insights into Immune Cell Navigation.” PLOS Computational Biology,
vol. 22, no. 2, e1013934, Public Library of Science, 2026, doi:10.1371/journal.pcbi.1013934.
short: J. Liu, J.E. Ron, G. Rinaldi, I. Williantarra, A. Georgantzoglou, I. de Vries,
M.K. Sixt, M. Sarris, N.S. Gov, PLOS Computational Biology 22 (2026).
date_created: 2026-03-02T10:08:38Z
date_published: 2026-02-03T00:00:00Z
date_updated: 2026-03-02T14:12:22Z
day: '03'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1371/journal.pcbi.1013934
external_id:
pmid:
- '41632822'
file:
- access_level: open_access
checksum: 564041089e7334804ad3cade973f80b4
content_type: application/pdf
creator: dernst
date_created: 2026-03-02T14:11:14Z
date_updated: 2026-03-02T14:11:14Z
file_id: '21388'
file_name: 2026_PloSCompBio_.pdf
file_size: 20688452
relation: main_file
success: 1
file_date_updated: 2026-03-02T14:11:14Z
has_accepted_license: '1'
intvolume: ' 22'
issue: '2'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: bd91e723-d553-11ed-ba76-fe7eeb2185fd
grant_number: '101071793'
name: 'Pushing from within: Control of cell shape, integrity and motility by cytoskeletal
pushing forces'
publication: PLOS Computational Biology
publication_identifier:
eissn:
- 1553-7358
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: Modelling chemotaxis of branched cells in complex environments provides insights
into immune cell navigation
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: 22
year: '2026'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '21707'
abstract:
- lang: eng
text: Structural and functional differences between brain hemispheres are a common
feature of animal nervous systems with reduced bilateral asymmetry often linked
to impaired cognitive performance. How neuronal left-right asymmetry is initiated
and integrated into a bilaterally symmetrical ground pattern is poorly understood.
Here, we show that the directional asymmetry of a Drosophila central brain circuit
originates from axonal interactions of two types of bilateral pioneer neurons.
Subsequent recruitment of neighboring neurons into the asymmetric neuropil primordium
results in hemisphere-specific microcircuits. Circuit lateralization requires
dynamic expression of the cell adhesion molecule Fasciclin 2 to maintain structural
plasticity in axonal remodeling. Reduced circuit asymmetry following cell type–specific
Fasciclin 2 manipulation affects adult brain function. These results reveal an
unexpected degree of developmental plasticity of late-born Drosophila neurons
in the formation of a circuit node via the lateralized recruitment of symmetric
circuit components.
acknowledgement: "We thank I. Salecker (Flybow), B. Altenhein (Fas2-Gal4Mz507), A.
Nose (UAS-intra- and extra-Fas2::YFP), and C. S. Goodman (UAS-Fas2PEST+/−), as well
as the Bloomington Stock Center for providing materials and fly stocks. We thank
S. Waddell and the lab, especially B. Senapati, for providing the opportunity to
conduct memory experiments at the CNCB, University of Oxford, and for supervision
and discussions during this period. We also thank W. Kallina, S. Ilgerl, D. Bartel,
A. Grimm, and A. Litin for technical support and the Hummel Lab for stimulating
discussions and critical comments on the manuscript. We acknowledge the early exploratory
work of A. Mattia, S. Trkulja, C. Schönherr, S. Bogner, B. Simpson, L. Tomasek,
H. Roth, H. Vokač, R. Gredler, F. Kapelari, T. Kolarova, C. Ignitsch, Á. Bautista-Soldevila,
and M. Kassem.\r\nThis research was funded by the University of Vienna, the Vienna
Doctoral School Cognition, Behaviour and Neuroscience (uni:docs fellowship) (to
J.W.M.) and by the Austrian Science Fund (FWF) (Cluster of Excellence Neuronal Circuits
in Health and Disease, grant DOI 10.55776/COE16; https://www.fwf.ac.at/en/research-radar/10.55776/COE16)
(to T.H.). For open access purposes, the author has applied a CC BY public copyright
license to any author-accepted manuscript version arising from this submission."
article_number: eaea6020
article_processing_charge: Yes
article_type: original
author:
- first_name: Johann W.
full_name: Markovitsch, Johann W.
last_name: Markovitsch
- first_name: Daniel
full_name: Mitić, Daniel
last_name: Mitić
- first_name: Alisa
full_name: Del Pilar Jiménez García, Alisa
last_name: Del Pilar Jiménez García
- first_name: Alsberga
full_name: Zane, Alsberga
id: 60f7509a-f652-11ea-9d86-b963d6490d7c
last_name: Zane
orcid: 0009-0003-0415-7603
- first_name: Sarah
full_name: Kainz, Sarah
last_name: Kainz
- first_name: Rashmit
full_name: Kaur, Rashmit
last_name: Kaur
- first_name: Thomas
full_name: Hummel, Thomas
last_name: Hummel
citation:
ama: Markovitsch JW, Mitić D, Del Pilar Jiménez García A, et al. Sequential formation
of Drosophila circuit asymmetry via prolonged structural plasticity. Science
Advances. 2026;12(13). doi:10.1126/sciadv.aea6020
apa: Markovitsch, J. W., Mitić, D., Del Pilar Jiménez García, A., Zane, A., Kainz,
S., Kaur, R., & Hummel, T. (2026). Sequential formation of Drosophila circuit
asymmetry via prolonged structural plasticity. Science Advances. American
Association for the Advancement of Science. https://doi.org/10.1126/sciadv.aea6020
chicago: Markovitsch, Johann W., Daniel Mitić, Alisa Del Pilar Jiménez García, Alsberga
Zane, Sarah Kainz, Rashmit Kaur, and Thomas Hummel. “Sequential Formation of Drosophila
Circuit Asymmetry via Prolonged Structural Plasticity.” Science Advances.
American Association for the Advancement of Science, 2026. https://doi.org/10.1126/sciadv.aea6020.
ieee: J. W. Markovitsch et al., “Sequential formation of Drosophila circuit
asymmetry via prolonged structural plasticity,” Science Advances, vol.
12, no. 13. American Association for the Advancement of Science, 2026.
ista: Markovitsch JW, Mitić D, Del Pilar Jiménez García A, Zane A, Kainz S, Kaur
R, Hummel T. 2026. Sequential formation of Drosophila circuit asymmetry via prolonged
structural plasticity. Science Advances. 12(13), eaea6020.
mla: Markovitsch, Johann W., et al. “Sequential Formation of Drosophila Circuit
Asymmetry via Prolonged Structural Plasticity.” Science Advances, vol.
12, no. 13, eaea6020, American Association for the Advancement of Science, 2026,
doi:10.1126/sciadv.aea6020.
short: J.W. Markovitsch, D. Mitić, A. Del Pilar Jiménez García, A. Zane, S. Kainz,
R. Kaur, T. Hummel, Science Advances 12 (2026).
date_created: 2026-04-12T22:01:48Z
date_published: 2026-03-27T00:00:00Z
date_updated: 2026-05-04T09:18:06Z
day: '27'
ddc:
- '570'
department:
- _id: MiSi
- _id: GradSch
doi: 10.1126/sciadv.aea6020
file:
- access_level: open_access
checksum: 3eed470fe73e53d2a8d55d6fba6934e3
content_type: application/pdf
creator: dernst
date_created: 2026-05-04T09:16:36Z
date_updated: 2026-05-04T09:16:36Z
file_id: '21786'
file_name: 2026_ScienceAdv_Markovitsch.pdf
file_size: 11101140
relation: main_file
success: 1
file_date_updated: 2026-05-04T09:16:36Z
has_accepted_license: '1'
intvolume: ' 12'
issue: '13'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: Science Advances
publication_identifier:
eissn:
- 2375-2548
publication_status: published
publisher: American Association for the Advancement of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: Sequential formation of Drosophila circuit asymmetry via prolonged structural
plasticity
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: 12
year: '2026'
...
---
OA_place: publisher
OA_type: hybrid
_id: '19928'
abstract:
- lang: eng
text: 'Patho-mechanistic origins of ulcerative colitis are still poorly understood.
The actin cross-linker filamin A (FLNA) impacts cellular responses through interaction
with cytosolic proteins. Posttranscriptional A-to-I editing generates two forms
of FLNA: genome-encoded FLNAQ and FLNAR. FLNA is edited in colon fibroblasts,
smooth muscle cells, and endothelial cells. We found that the FLNA editing status
determines colitis severity. Editing was highest in healthy colons and reduced
during murine and human colitis. Mice that exclusively express FLNAR were highly
resistant to DSS-induced colitis, whereas fully FLNAQ animals developed severe
inflammation. While the genetic induction of FLNA editing influenced transcriptional
states of structural cells and microbiome composition, we found that FLNAR exerts
protection specifically via myeloid cells, which are physiologically unedited.
Introducing fixed FLNAR did not hamper cell migration but reduced macrophage inflammation
and rendered neutrophils less prone to NETosis. Thus, loss of FLNA editing correlates
with colitis severity, and targeted editing of myeloid cells serves as a novel
therapeutic approach in intestinal inflammation.'
acknowledgement: "Sequencing was performed by the Vienna BioCenter Core Facilities
(Medical University of Vienna Core Facility) and the Biomedical Sequencing Facility
at CeMM, Vienna. Cell sorting and flow cytometry were performed at the Core Facility
Flow Cytometry and Imaging (Medical University of Vienna). We thank Jasmin Schwarz,
Gudrun Kohl, Petra Pjevac, and Joana Seneca Silva from the Joint Microbiome Facility
of the Medical University of Vienna and the University of Vienna for assisting with
amplicon and metagenomic sequencing, as well as repositing of sequencing data. We
thank Sophia Derdak and Michael Schuster for initial data analysis, Robert Vilvoi
and Stephan Hemm for animal handling, Marcel Kertesz for mouse genotyping, and Salwan
Roumaia for next generation sequencing sample preparation. Treatment schemes and
graphical abstracts were created with https://BioRender.com.\r\n\r\nThis work was
supported by the Austrian Science Fund, grant number ZK 57-B28 to C. Vesely, R.
Gawish, and F.C. Pereira; grant number V 1025-B to R. Gawish; grant number DOC32-B28
to R. Varada and M.F. Jantsch; and F8007 and P32678 to M.F. Jantsch. Open Access
funding provided by Medical University of Vienna."
article_number: e20240109
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Riem
full_name: Gawish, Riem
last_name: Gawish
- first_name: Rajagopal
full_name: Varada, Rajagopal
last_name: Varada
- first_name: Florian
full_name: Deckert, Florian
last_name: Deckert
- first_name: Anastasiya
full_name: Hladik, Anastasiya
last_name: Hladik
- first_name: Linda
full_name: Steinbichl, Linda
last_name: Steinbichl
- first_name: Laura
full_name: Cimatti, Laura
last_name: Cimatti
- first_name: Katarina
full_name: Milanovic, Katarina
last_name: Milanovic
- first_name: Mamta
full_name: Jain, Mamta
last_name: Jain
- first_name: Natalya
full_name: Torgasheva, Natalya
last_name: Torgasheva
- first_name: Andrea
full_name: Tanzer, Andrea
last_name: Tanzer
- first_name: Kim
full_name: De Paepe, Kim
last_name: De Paepe
- first_name: Tom
full_name: Van De Wiele, Tom
last_name: Van De Wiele
- first_name: Bela
full_name: Hausmann, Bela
last_name: Hausmann
- first_name: Michaela
full_name: Lang, Michaela
last_name: Lang
- first_name: Martin
full_name: Pechhacker, Martin
last_name: Pechhacker
- first_name: Nahla
full_name: Ibrahim, Nahla
last_name: Ibrahim
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Christine
full_name: Brostjan, Christine
last_name: Brostjan
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Christoph
full_name: Gasche, Christoph
last_name: Gasche
- first_name: Louis
full_name: Boon, Louis
last_name: Boon
- first_name: David
full_name: Berry, David
last_name: Berry
- first_name: Michael F.
full_name: Jantsch, Michael F.
last_name: Jantsch
- first_name: Fatima C.
full_name: Pereira, Fatima C.
last_name: Pereira
- first_name: Cornelia
full_name: Vesely, Cornelia
last_name: Vesely
citation:
ama: Gawish R, Varada R, Deckert F, et al. Filamin A editing in myeloid cells reduces
intestinal inflammation and protects from colitis. Journal of Experimental
Medicine. 2025;222(9). doi:10.1084/jem.20240109
apa: Gawish, R., Varada, R., Deckert, F., Hladik, A., Steinbichl, L., Cimatti, L.,
… Vesely, C. (2025). Filamin A editing in myeloid cells reduces intestinal inflammation
and protects from colitis. Journal of Experimental Medicine. Rockefeller
University Press. https://doi.org/10.1084/jem.20240109
chicago: Gawish, Riem, Rajagopal Varada, Florian Deckert, Anastasiya Hladik, Linda
Steinbichl, Laura Cimatti, Katarina Milanovic, et al. “Filamin A Editing in Myeloid
Cells Reduces Intestinal Inflammation and Protects from Colitis.” Journal of
Experimental Medicine. Rockefeller University Press, 2025. https://doi.org/10.1084/jem.20240109.
ieee: R. Gawish et al., “Filamin A editing in myeloid cells reduces intestinal
inflammation and protects from colitis,” Journal of Experimental Medicine,
vol. 222, no. 9. Rockefeller University Press, 2025.
ista: Gawish R, Varada R, Deckert F, Hladik A, Steinbichl L, Cimatti L, Milanovic
K, Jain M, Torgasheva N, Tanzer A, De Paepe K, Van De Wiele T, Hausmann B, Lang
M, Pechhacker M, Ibrahim N, de Vries I, Brostjan C, Sixt MK, Gasche C, Boon L,
Berry D, Jantsch MF, Pereira FC, Vesely C. 2025. Filamin A editing in myeloid
cells reduces intestinal inflammation and protects from colitis. Journal of Experimental
Medicine. 222(9), e20240109.
mla: Gawish, Riem, et al. “Filamin A Editing in Myeloid Cells Reduces Intestinal
Inflammation and Protects from Colitis.” Journal of Experimental Medicine,
vol. 222, no. 9, e20240109, Rockefeller University Press, 2025, doi:10.1084/jem.20240109.
short: R. Gawish, R. Varada, F. Deckert, A. Hladik, L. Steinbichl, L. Cimatti, K.
Milanovic, M. Jain, N. Torgasheva, A. Tanzer, K. De Paepe, T. Van De Wiele, B.
Hausmann, M. Lang, M. Pechhacker, N. Ibrahim, I. de Vries, C. Brostjan, M.K. Sixt,
C. Gasche, L. Boon, D. Berry, M.F. Jantsch, F.C. Pereira, C. Vesely, Journal of
Experimental Medicine 222 (2025).
date_created: 2025-06-29T22:01:15Z
date_published: 2025-09-01T00:00:00Z
date_updated: 2025-12-30T09:00:42Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1084/jem.20240109
external_id:
isi:
- '001502896900001'
pmid:
- '40471139'
file:
- access_level: open_access
checksum: 708d61fb8cf1d83ee1e33ddcfde0857e
content_type: application/pdf
creator: dernst
date_created: 2025-12-30T09:00:04Z
date_updated: 2025-12-30T09:00:04Z
file_id: '20899'
file_name: 2025_JEM_Gawish.pdf
file_size: 9349311
relation: main_file
success: 1
file_date_updated: 2025-12-30T09:00:04Z
has_accepted_license: '1'
intvolume: ' 222'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Experimental Medicine
publication_identifier:
eissn:
- 1540-9538
issn:
- 0022-1007
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Filamin A editing in myeloid cells reduces intestinal inflammation and protects
from colitis
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: 222
year: '2025'
...
---
OA_type: closed access
_id: '20427'
abstract:
- lang: eng
text: Animal cells migrating up chemotactic gradients often show speed oscillations.
A new study describes a molecular circuit that switches zebrafish germ cells between
phases of straight runs, tumbling and directional reorientation.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Ziqiang
full_name: Li, Ziqiang
id: 922e68bb-1727-11ee-857c-966e8cc1b6c3
last_name: Li
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'LI Z, Sixt MK. Cell migration: How animal cells run and tumble. Current
Biology. 2025;35(18):R890-R892. doi:10.1016/j.cub.2025.08.016'
apa: 'LI, Z., & Sixt, M. K. (2025). Cell migration: How animal cells run and
tumble. Current Biology. Elsevier. https://doi.org/10.1016/j.cub.2025.08.016'
chicago: 'LI, ZIQIANG, and Michael K Sixt. “Cell Migration: How Animal Cells Run
and Tumble.” Current Biology. Elsevier, 2025. https://doi.org/10.1016/j.cub.2025.08.016.'
ieee: 'Z. LI and M. K. Sixt, “Cell migration: How animal cells run and tumble,”
Current Biology, vol. 35, no. 18. Elsevier, pp. R890–R892, 2025.'
ista: 'LI Z, Sixt MK. 2025. Cell migration: How animal cells run and tumble. Current
Biology. 35(18), R890–R892.'
mla: 'LI, ZIQIANG, and Michael K. Sixt. “Cell Migration: How Animal Cells Run and
Tumble.” Current Biology, vol. 35, no. 18, Elsevier, 2025, pp. R890–92,
doi:10.1016/j.cub.2025.08.016.'
short: Z. LI, M.K. Sixt, Current Biology 35 (2025) R890–R892.
corr_author: '1'
date_created: 2025-10-05T22:01:35Z
date_published: 2025-09-22T00:00:00Z
date_updated: 2025-12-01T12:54:02Z
day: '22'
department:
- _id: MiSi
doi: 10.1016/j.cub.2025.08.016
external_id:
isi:
- '001592664700001'
pmid:
- '40987270'
intvolume: ' 35'
isi: 1
issue: '18'
language:
- iso: eng
month: '09'
oa_version: None
page: R890-R892
pmid: 1
publication: Current Biology
publication_identifier:
eissn:
- 1879-0445
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Cell migration: How animal cells run and tumble'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 35
year: '2025'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '19404'
abstract:
- lang: eng
text: Cell migration is a fundamental process during embryonic development. Most
studies in vivo have focused on the migration of cells using the extracellular
matrix (ECM) as their substrate for migration. In contrast, much less is known
about how cells migrate on other cells, as found in early embryos when the ECM
has not yet formed. Here, we show that lateral mesendoderm (LME) cells in the
early zebrafish gastrula use the ectoderm as their substrate for migration. We
show that the lateral ectoderm is permissive for the animal-pole-directed migration
of LME cells, while the ectoderm at the animal pole halts it. These differences
in permissiveness depend on the lateral ectoderm being more cohesive than the
animal ectoderm, a property controlled by bone morphogenetic protein (BMP) signaling
within the ectoderm. Collectively, these findings identify ectoderm tissue cohesion
as one critical factor in regulating LME migration during zebrafish gastrulation.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: ScienComp
acknowledgement: 'We are grateful to the colleagues who contributed to this work with
discussions, technical advice, and feedback on the manuscript: Irene Steccari, David
Labrousse Arias and the other members of the Heisenberg lab, Nicole Amberg, Florian
Pauler, Nicoletta Petridou, Elena Scarpa, and Edouard Hannezo. We also thank the
Imaging and Optics Facility, the Life Science Facility, and the Scientific Computing
Unit at ISTA for support. The Next Generation Sequencing Facility at Vienna BioCenter
Core Facilities performed the RNA-seq for animal and lateral ectoderm. D.B.B. was
supported by the NOMIS Foundation as a NOMIS Fellow and by an EMBO Postdoctoral
Fellowship (ALTF 343-2022). S. Tavano was supported by an EMBO Postdoctoral Fellowship
(ALTF 1159-2018).'
article_number: '115387'
article_processing_charge: Yes
article_type: original
author:
- first_name: Ste
full_name: Tavano, Ste
id: 2F162F0C-F248-11E8-B48F-1D18A9856A87
last_name: Tavano
orcid: 0000-0001-9970-7804
- first_name: David
full_name: Brückner, David
id: e1e86031-6537-11eb-953a-f7ab92be508d
last_name: Brückner
orcid: 0000-0001-7205-2975
- first_name: Saren
full_name: Tasciyan, Saren
id: 4323B49C-F248-11E8-B48F-1D18A9856A87
last_name: Tasciyan
orcid: 0000-0003-1671-393X
- first_name: Xin
full_name: Tong, Xin
id: 50F65CDC-AA30-11E9-A72B-8A12E6697425
last_name: Tong
- first_name: Roland
full_name: Kardos, Roland
id: 4039350E-F248-11E8-B48F-1D18A9856A87
last_name: Kardos
- first_name: Alexandra
full_name: Schauer, Alexandra
id: 30A536BA-F248-11E8-B48F-1D18A9856A87
last_name: Schauer
orcid: 0000-0001-7659-9142
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- 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: Tavano S, Brückner D, Tasciyan S, et al. BMP-dependent patterning of ectoderm
tissue material properties modulates lateral mesendoderm cell migration during
early zebrafish gastrulation. Cell Reports. 2025;44(3). doi:10.1016/j.celrep.2025.115387
apa: Tavano, S., Brückner, D., Tasciyan, S., Tong, X., Kardos, R., Schauer, A.,
… Heisenberg, C.-P. J. (2025). BMP-dependent patterning of ectoderm tissue material
properties modulates lateral mesendoderm cell migration during early zebrafish
gastrulation. Cell Reports. Elsevier. https://doi.org/10.1016/j.celrep.2025.115387
chicago: Tavano, Ste, David Brückner, Saren Tasciyan, Xin Tong, Roland Kardos, Alexandra
Schauer, Robert Hauschild, and Carl-Philipp J Heisenberg. “BMP-Dependent Patterning
of Ectoderm Tissue Material Properties Modulates Lateral Mesendoderm Cell Migration
during Early Zebrafish Gastrulation.” Cell Reports. Elsevier, 2025. https://doi.org/10.1016/j.celrep.2025.115387.
ieee: S. Tavano et al., “BMP-dependent patterning of ectoderm tissue material
properties modulates lateral mesendoderm cell migration during early zebrafish
gastrulation,” Cell Reports, vol. 44, no. 3. Elsevier, 2025.
ista: Tavano S, Brückner D, Tasciyan S, Tong X, Kardos R, Schauer A, Hauschild R,
Heisenberg C-PJ. 2025. BMP-dependent patterning of ectoderm tissue material properties
modulates lateral mesendoderm cell migration during early zebrafish gastrulation.
Cell Reports. 44(3), 115387.
mla: Tavano, Ste, et al. “BMP-Dependent Patterning of Ectoderm Tissue Material Properties
Modulates Lateral Mesendoderm Cell Migration during Early Zebrafish Gastrulation.”
Cell Reports, vol. 44, no. 3, 115387, Elsevier, 2025, doi:10.1016/j.celrep.2025.115387.
short: S. Tavano, D. Brückner, S. Tasciyan, X. Tong, R. Kardos, A. Schauer, R. Hauschild,
C.-P.J. Heisenberg, Cell Reports 44 (2025).
corr_author: '1'
date_created: 2025-03-16T23:01:24Z
date_published: 2025-03-25T00:00:00Z
date_updated: 2025-10-22T07:00:04Z
day: '25'
ddc:
- '570'
department:
- _id: CaHe
- _id: EdHa
- _id: MiSi
- _id: Bio
doi: 10.1016/j.celrep.2025.115387
external_id:
isi:
- '001443652700001'
pmid:
- '40057955'
file:
- access_level: open_access
checksum: 57e05dd1598c807af0afdb32cec039d3
content_type: application/pdf
creator: dernst
date_created: 2025-03-17T10:26:54Z
date_updated: 2025-03-17T10:26:54Z
file_id: '19413'
file_name: 2025_CellReports_Tavano.pdf
file_size: 9067797
relation: main_file
success: 1
file_date_updated: 2025-03-17T10:26:54Z
has_accepted_license: '1'
intvolume: ' 44'
isi: 1
issue: '3'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 34e2a5b5-11ca-11ed-8bc3-b2265616ef0b
grant_number: ALTF 343-2022
name: A mechano-chemical theory for stem cell fate decisions in organoid development
- _id: 269CD5C4-B435-11E9-9278-68D0E5697425
grant_number: ALTF 1159-2018
name: 'Mechanosensation in cell migration: the role of friction forces in cell polarization
and directed migration'
publication: Cell Reports
publication_identifier:
eissn:
- 2211-1247
issn:
- 2639-1856
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: BMP-dependent patterning of ectoderm tissue material properties modulates lateral
mesendoderm cell migration during early zebrafish gastrulation
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 44
year: '2025'
...
---
OA_place: publisher
OA_type: hybrid
_id: '17459'
abstract:
- lang: eng
text: Atopic dermatitis (AD) is the most common chronic inflammatory skin disease
worldwide. AD is a highly complex disease with different subtypes. Many elements
of AD pathophysiology have been described, but if/how they interact with each
other or which mechanisms are important in which patients is still unclear. Langerhans
cells (LCs) are antigen-presenting cells (APCs) in the epidermis. Depending on
the context, they can act either pro- or anti-inflammatory. Many different studies
have investigated LCs in the context of AD and found them to be connected to all
major mechanisms of AD pathophysiology. As APCs, LCs recruit other immune cells
and shape the immune response, especially adaptive immunity via polarization of
T cells. As sentinel cells, LCs are primary sensors of the skin microbiome and
are important for the decision of immunity versus tolerance. LCs are also involved
with the integrity of the skin barrier by influencing tight junctions. Finally,
LCs are important cells in the neuro-immune crosstalk in the skin. In this review,
we provide an overview about the many different roles of LCs in AD. Understanding
LCs might bring us closer to a more complete understanding of this highly complex
disease. Potentially, modulating LCs might offer new options for targeted therapies
for AD patients.
acknowledgement: This work was supported by the CK-CARE of the KühneFoundation, Switzerland;
the China Scholarship Counciland Shanghai Biocelline Enterprise Co. Ltd, China.
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Yi
full_name: Pan, Yi
last_name: Pan
- first_name: Mathias
full_name: Hochgerner, Mathias
last_name: Hochgerner
- first_name: Malgorzata Anna
full_name: Cichon, Malgorzata Anna
id: d63197a3-c188-11ed-9387-8d33a3f13871
last_name: Cichon
- first_name: Theresa
full_name: Benezeder, Theresa
last_name: Benezeder
- first_name: Thomas
full_name: Bieber, Thomas
last_name: Bieber
- first_name: Peter
full_name: Wolf, Peter
last_name: Wolf
citation:
ama: 'Pan Y, Hochgerner M, Cichon MA, Benezeder T, Bieber T, Wolf P. Langerhans
cells: Central players in the pathophysiology of atopic dermatitis. Journal
of the European Academy of Dermatology and Venereology. 2025;39(2):278-289.
doi:10.1111/jdv.20291'
apa: 'Pan, Y., Hochgerner, M., Cichon, M. A., Benezeder, T., Bieber, T., & Wolf,
P. (2025). Langerhans cells: Central players in the pathophysiology of atopic
dermatitis. Journal of the European Academy of Dermatology and Venereology.
Wiley. https://doi.org/10.1111/jdv.20291'
chicago: 'Pan, Yi, Mathias Hochgerner, Malgorzata Anna Cichon, Theresa Benezeder,
Thomas Bieber, and Peter Wolf. “Langerhans Cells: Central Players in the Pathophysiology
of Atopic Dermatitis.” Journal of the European Academy of Dermatology and Venereology.
Wiley, 2025. https://doi.org/10.1111/jdv.20291.'
ieee: 'Y. Pan, M. Hochgerner, M. A. Cichon, T. Benezeder, T. Bieber, and P. Wolf,
“Langerhans cells: Central players in the pathophysiology of atopic dermatitis,”
Journal of the European Academy of Dermatology and Venereology, vol. 39,
no. 2. Wiley, pp. 278–289, 2025.'
ista: 'Pan Y, Hochgerner M, Cichon MA, Benezeder T, Bieber T, Wolf P. 2025. Langerhans
cells: Central players in the pathophysiology of atopic dermatitis. Journal of
the European Academy of Dermatology and Venereology. 39(2), 278–289.'
mla: 'Pan, Yi, et al. “Langerhans Cells: Central Players in the Pathophysiology
of Atopic Dermatitis.” Journal of the European Academy of Dermatology and Venereology,
vol. 39, no. 2, Wiley, 2025, pp. 278–89, doi:10.1111/jdv.20291.'
short: Y. Pan, M. Hochgerner, M.A. Cichon, T. Benezeder, T. Bieber, P. Wolf, Journal
of the European Academy of Dermatology and Venereology 39 (2025) 278–289.
date_created: 2024-08-25T22:01:07Z
date_published: 2025-02-01T00:00:00Z
date_updated: 2025-05-19T13:58:50Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1111/jdv.20291
external_id:
isi:
- '001292894900001'
pmid:
- '39157943'
file:
- access_level: open_access
checksum: 12555ddb3490daf10b8d44e334e7312e
content_type: application/pdf
creator: dernst
date_created: 2025-04-16T09:59:37Z
date_updated: 2025-04-16T09:59:37Z
file_id: '19583'
file_name: 2025_JEADV_Pan.pdf
file_size: 457698
relation: main_file
success: 1
file_date_updated: 2025-04-16T09:59:37Z
has_accepted_license: '1'
intvolume: ' 39'
isi: 1
issue: '2'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 278-289
pmid: 1
publication: Journal of the European Academy of Dermatology and Venereology
publication_identifier:
eissn:
- 1468-3083
issn:
- 0926-9959
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Langerhans cells: Central players in the pathophysiology of atopic dermatitis'
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: 39
year: '2025'
...
---
OA_place: repository
_id: '21427'
abstract:
- lang: eng
text: While tumor malignancy has been extensively studied under the prism of genetic
and epigenetic heterogeneity, tumor cell states also critically depend on reciprocal
interactions with the microenvironment. This raises the hitherto untested possibility
that heterogeneity of the untransformed tumor stroma can actively fuel malignant
progression. As biological heterogeneity is inherently difficult to control, we
adopted a reductionist approach and let tumor cells invade micro-engineered environments
harboring obstacles with precision-controlled geometry. We find that not only
the presence of obstacles, but more surprisingly their spatial disorder, causes
a drastic shift from a collective to a single-cell mode of invasion – comparable
in strength to cadherin loss. Combining live-imaging and perturbation experiments
with minimal biophysical modeling, we demonstrate that cell detachments result
both from local geometrical constraints and a global integration of spatial disorder
over time. We show that different types of microenvironments map onto different
universality classes of invasion dynamics - homogeneous substrates follow Kardar–Parisi–Zhang
(KPZ) scaling, while disordered ones exhibit exponents consistent with KPZ with
quenched disorder (KPZq). Our findings highlight generic physical principles for
how the mode of cancer cell invasion depends on environmental heterogeneity, with
potential implications to understand tumor evolution in vivo.
acknowledgement: "European Research Council, https://ror.org/0472cxd90, 101071793\r\nAustrian
Academy of Sciences, 26360"
article_processing_charge: No
author:
- first_name: Zuzana
full_name: Dunajova, Zuzana
id: 4B39F286-F248-11E8-B48F-1D18A9856A87
last_name: Dunajova
- first_name: Saren
full_name: Tasciyan, Saren
id: 4323B49C-F248-11E8-B48F-1D18A9856A87
last_name: Tasciyan
orcid: 0000-0003-1671-393X
- first_name: Juraj
full_name: Majek, Juraj
id: 3e6d9473-f38e-11ec-8ae0-c4e05a8aa9e1
last_name: Majek
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Erik
full_name: Sahai, Erik
last_name: Sahai
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
citation:
ama: Dunajova Z, Tasciyan S, Majek J, et al. Substrate heterogeneity promotes cancer
cell dissemination through interface roughening. doi:10.1101/2025.05.20.655037
apa: Dunajova, Z., Tasciyan, S., Majek, J., Merrin, J., Sahai, E., Sixt, M. K.,
& Hannezo, E. B. (n.d.). Substrate heterogeneity promotes cancer cell dissemination
through interface roughening. bioRxiv. https://doi.org/10.1101/2025.05.20.655037
chicago: Dunajova, Zuzana, Saren Tasciyan, Juraj Majek, Jack Merrin, Erik Sahai,
Michael K Sixt, and Edouard B Hannezo. “Substrate Heterogeneity Promotes Cancer
Cell Dissemination through Interface Roughening.” bioRxiv, n.d. https://doi.org/10.1101/2025.05.20.655037.
ieee: Z. Dunajova et al., “Substrate heterogeneity promotes cancer cell dissemination
through interface roughening.” bioRxiv.
ista: Dunajova Z, Tasciyan S, Majek J, Merrin J, Sahai E, Sixt MK, Hannezo EB. Substrate
heterogeneity promotes cancer cell dissemination through interface roughening.
10.1101/2025.05.20.655037.
mla: Dunajova, Zuzana, et al. Substrate Heterogeneity Promotes Cancer Cell Dissemination
through Interface Roughening. bioRxiv, doi:10.1101/2025.05.20.655037.
short: Z. Dunajova, S. Tasciyan, J. Majek, J. Merrin, E. Sahai, M.K. Sixt, E.B.
Hannezo, (n.d.).
corr_author: '1'
date_created: 2026-03-11T08:40:06Z
date_published: 2025-09-25T00:00:00Z
date_updated: 2026-03-18T14:11:35Z
day: '25'
ddc:
- '539'
- '570'
department:
- _id: GradSch
- _id: EdHa
- _id: MiSi
- _id: NanoFab
- _id: AnSa
doi: 10.1101/2025.05.20.655037
has_accepted_license: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2025.05.20.655037
month: '09'
oa: 1
oa_version: Preprint
project:
- _id: bd91e723-d553-11ed-ba76-fe7eeb2185fd
grant_number: '101071793'
name: 'Pushing from within: Control of cell shape, integrity and motility by cytoskeletal
pushing forces'
- _id: 34d75525-11ca-11ed-8bc3-89b6307fee9d
grant_number: '26360'
name: Motile active matter models of migrating cells and chiral filaments
publication_status: draft
publisher: bioRxiv
related_material:
record:
- id: '21423'
relation: dissertation_contains
status: public
- id: '21439'
relation: research_data
status: public
status: public
title: Substrate heterogeneity promotes cancer cell dissemination through interface
roughening
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: preprint
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2025'
...
---
OA_place: publisher
OA_type: hybrid
PlanS_conform: '1'
_id: '20082'
abstract:
- lang: eng
text: Efficient immune responses rely on the capacity of leukocytes to traverse
diverse and complex tissues. To meet such changing environmental conditions, leukocytes
usually adopt an ameboid configuration, using their forward-positioned nucleus
as a probe to identify and follow the path of least resistance among pre-existing
pores. We show that, in dense environments where even the largest pores preclude
free passage, leukocytes position their nucleus behind the centrosome and organelles.
The local compression imposed on the cell body by its surroundings triggers assembly
of a central F-actin pool, located between cell front and nucleus. Central actin
pushes outward to transiently dilate a path for organelles and nucleus. Pools
of central and front actin are tightly coupled and experimental depletion of the
central pool enhances actin accumulation and protrusion formation at the cell
front. Although this shifted balance speeds up cells in permissive environments,
migration in restrictive environments is impaired, as the unleashed leading edge
dissociates from the trapped cell body. Our findings establish an actin regulatory
loop that balances path dilation with advancement of the leading edge to maintain
cellular coherence.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
acknowledgement: This research was supported by the Scientific Service Units of ISTA
through resources provided by the Imaging and Optics, Preclinical and Lab Support
Facilities. In particular, we thank M. A. Symth and F. G. G. Leite, from the Virus
Service Team, who helped generating the lentiviral particles used in this study.
We thank all the members of the Sixt group for valuable discussions and feedback,
in particular, I. Mayer, for helping with T cell isolation and Z. (P.) Li for providing
the Actin–GFP DC line. We are also thankful to J. Mandl and C. Shen for their feedback
during the writing of this manuscript. This work was supported by a European Research
Council grant ERC-SyG 101071793 to M.S. M.J.A. was supported by an HFSP Postdoctoral
Fellowship LTF 177 2021 and A.J.G. by a Lise Meitner Fellowship of the FWF (Austrian
Science Fund). Y.F. was supported by the AMED-CREST (JP19gm1310005), the Medical
Research Center Initiative for High Depth Omics and CURE:JPMXP1323015486 for MIB,
Kyushu University. Open access funding provided by Institute of Science and Technology
(IST Austria).
article_processing_charge: Yes (via OA deal)
article_type: letter_note
author:
- first_name: Patricia
full_name: Dos Reis Rodrigues, Patricia
id: 26E95904-5160-11E9-9C0B-C5B0DC97E90F
last_name: Dos Reis Rodrigues
orcid: 0000-0003-1681-508X
- first_name: Mario
full_name: Avellaneda Sarrió, Mario
id: DC4BA84C-56E6-11EA-AD5D-348C3DDC885E
last_name: Avellaneda Sarrió
orcid: 0000-0001-6406-524X
- first_name: Nikola
full_name: Canigova, Nikola
id: 3795523E-F248-11E8-B48F-1D18A9856A87
last_name: Canigova
orcid: 0000-0002-8518-5926
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Michael
full_name: Riedl, Michael
id: 3BE60946-F248-11E8-B48F-1D18A9856A87
last_name: Riedl
orcid: 0000-0003-4844-6311
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Yoshinori
full_name: Fukui, Yoshinori
last_name: Fukui
- first_name: Alba
full_name: Juanes Garcia, Alba
id: 40F05888-F248-11E8-B48F-1D18A9856A87
last_name: Juanes Garcia
orcid: 0000-0002-1009-9652
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Dos Reis Rodrigues P, Avellaneda Sarrió M, Canigova N, et al. Migrating immune
cells globally coordinate protrusive forces. Nature Immunology. 2025;26:1258–1266.
doi:10.1038/s41590-025-02211-w
apa: Dos Reis Rodrigues, P., Avellaneda Sarrió, M., Canigova, N., Gärtner, F. R.,
Vaahtomeri, K., Riedl, M., … Sixt, M. K. (2025). Migrating immune cells globally
coordinate protrusive forces. Nature Immunology. Springer Nature. https://doi.org/10.1038/s41590-025-02211-w
chicago: Dos Reis Rodrigues, Patricia, Mario Avellaneda Sarrió, Nikola Canigova,
Florian R Gärtner, Kari Vaahtomeri, Michael Riedl, Ingrid de Vries, et al. “Migrating
Immune Cells Globally Coordinate Protrusive Forces.” Nature Immunology.
Springer Nature, 2025. https://doi.org/10.1038/s41590-025-02211-w.
ieee: P. Dos Reis Rodrigues et al., “Migrating immune cells globally coordinate
protrusive forces,” Nature Immunology, vol. 26. Springer Nature, pp. 1258–1266,
2025.
ista: Dos Reis Rodrigues P, Avellaneda Sarrió M, Canigova N, Gärtner FR, Vaahtomeri
K, Riedl M, de Vries I, Merrin J, Hauschild R, Fukui Y, Juanes Garcia A, Sixt
MK. 2025. Migrating immune cells globally coordinate protrusive forces. Nature
Immunology. 26, 1258–1266.
mla: Dos Reis Rodrigues, Patricia, et al. “Migrating Immune Cells Globally Coordinate
Protrusive Forces.” Nature Immunology, vol. 26, Springer Nature, 2025,
pp. 1258–1266, doi:10.1038/s41590-025-02211-w.
short: P. Dos Reis Rodrigues, M. Avellaneda Sarrió, N. Canigova, F.R. Gärtner, K.
Vaahtomeri, M. Riedl, I. de Vries, J. Merrin, R. Hauschild, Y. Fukui, A. Juanes
Garcia, M.K. Sixt, Nature Immunology 26 (2025) 1258–1266.
corr_author: '1'
date_created: 2025-07-27T22:01:26Z
date_published: 2025-08-01T00:00:00Z
date_updated: 2026-04-28T13:26:50Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
- _id: NanoFab
- _id: Bio
doi: 10.1038/s41590-025-02211-w
external_id:
isi:
- '001529134300001'
pmid:
- '40664976'
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language:
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month: '08'
oa: 1
oa_version: Published Version
page: 1258–1266
pmid: 1
project:
- _id: bd91e723-d553-11ed-ba76-fe7eeb2185fd
grant_number: '101071793'
name: 'Pushing from within: Control of cell shape, integrity and motility by cytoskeletal
pushing forces'
- _id: c092d618-5a5b-11eb-8a69-f92e1e843fc8
grant_number: 944-2020
name: 'Bioelectric patrolling: the role of the local membrane potential in immune
cell migration'
publication: Nature Immunology
publication_identifier:
eissn:
- 1529-2916
issn:
- 1529-2908
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on ISTA website
relation: press_release
url: https://ista.ac.at/en/news/bench-pressing-cells/
record:
- id: '20149'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Migrating immune cells globally coordinate protrusive forces
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 26
year: '2025'
...
---
OA_place: publisher
_id: '20149'
abstract:
- lang: eng
text: "Immune responses depend on the coordinated and efficient migration of leukocytes.
These\r\ncells, which are embedded and tightly confined within tissues, must navigate
and traverse\r\ndiverse and complex three-dimensional environments. Leukocytes
adapt their locomotory\r\nbehavior to the mechanical, geometrical, and biochemical
characteristics of their\r\nsurroundings. In low-density environments, where the
pore size of the interstitial matrix\r\nallows free passage, these cells position
the nucleus directly behind the lamellipodium, the\r\nprotrusive actin structure
that forms the leading front of the cell. In this configuration, they\r\nuse the
nucleus as a gauge to identify the path of least resistance.\r\nHere, we show
that in high-density environments, where the pore size precludes free passage\r\nof
the cell body, leukocytes reposition the microtubule-organizing center (MTOC)
and\r\nassociated organelles in front of the nucleus. In this configuration, they
use actin structures\r\nprotruding orthogonally to the direction of migration
in order to open a path for the cell body.\r\nWe identify two distinct actin populations
that serve this purpose at different subcellular\r\nlocalizations. At the leading
edge, local indentation of the plasma membrane leads to\r\nrecruitment of the
Wiskott-Aldrich syndrome protein (WASp), which, via Arp2/3, results in\r\nthe
formation of individual actin foci. At the cell body, actin polymerization is
triggered by\r\nDOCK8, a Cdc42 exchange factor, resulting in the formation of
a central actin pool.\r\nWe demonstrate that the central and peripheral actin
pools are functionally communicating\r\nand that depletion of the central actin
pool leads to increased actin accumulation at the cell\r\nfront, resulting in
excessive extension of the leading edge."
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: M-Shop
- _id: NanoFab
acknowledgement: "I would like to acknowledge the\r\nfinancial support of the European
Research Council through the ERC-SyG grant “Pushing from\r\nwithin: Control of cell
shape, integrity and motility by cytoskeletal pushing forces”\r\n(01071793), which
made this research possible. "
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Patricia
full_name: Dos Reis Rodrigues, Patricia
id: 26E95904-5160-11E9-9C0B-C5B0DC97E90F
last_name: Dos Reis Rodrigues
orcid: 0000-0003-1681-508X
citation:
ama: Dos Reis Rodrigues P. Coordination of protrusive forces in immune cell migration
. 2025. doi:10.15479/AT-ISTA-20149
apa: Dos Reis Rodrigues, P. (2025). Coordination of protrusive forces in immune
cell migration . Institute of Science and Technology Austria. https://doi.org/10.15479/AT-ISTA-20149
chicago: Dos Reis Rodrigues, Patricia. “Coordination of Protrusive Forces in Immune
Cell Migration .” Institute of Science and Technology Austria, 2025. https://doi.org/10.15479/AT-ISTA-20149.
ieee: P. Dos Reis Rodrigues, “Coordination of protrusive forces in immune cell migration
,” Institute of Science and Technology Austria, 2025.
ista: Dos Reis Rodrigues P. 2025. Coordination of protrusive forces in immune cell
migration . Institute of Science and Technology Austria.
mla: Dos Reis Rodrigues, Patricia. Coordination of Protrusive Forces in Immune
Cell Migration . Institute of Science and Technology Austria, 2025, doi:10.15479/AT-ISTA-20149.
short: P. Dos Reis Rodrigues, Coordination of Protrusive Forces in Immune Cell Migration
, Institute of Science and Technology Austria, 2025.
corr_author: '1'
date_created: 2025-08-08T09:18:02Z
date_published: 2025-08-08T00:00:00Z
date_updated: 2026-04-28T13:26:50Z
day: '08'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
- _id: MiSi
doi: 10.15479/AT-ISTA-20149
file:
- access_level: open_access
checksum: fda8a1070667c3562263f4867609b41b
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date_created: 2025-08-27T13:00:30Z
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file_date_updated: 2025-08-27T13:02:28Z
has_accepted_license: '1'
language:
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month: '08'
oa: 1
oa_version: Published Version
page: '114'
project:
- _id: bd91e723-d553-11ed-ba76-fe7eeb2185fd
grant_number: '101071793'
name: 'Pushing from within: Control of cell shape, integrity and motility by cytoskeletal
pushing forces'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '10703'
relation: part_of_dissertation
status: public
- id: '20082'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: 'Coordination of protrusive forces in immune cell 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: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2025'
...
---
APC_amount: 5766,07 EUR
OA_place: publisher
OA_type: hybrid
PlanS_conform: '1'
_id: '20289'
abstract:
- lang: eng
text: Cell and tissue movement in development, cancer invasion, and immune response
relies on chemical or mechanical guidance cues. In many systems, this behavior
is locally directed by self-generated signaling gradients rather than long-range,
prepatterned cues. However, how heterogeneous mixtures of cells interact nonreciprocally
and navigate through self-generated gradients remains largely unexplored. Here,
we introduce a theoretical framework for the self-organized chemotaxis of heterogeneous
cell populations. We find that the relative chemotactic sensitivities of different
cell populations control their long-time coupling and comigration dynamics, with
boundary conditions such as external cell and attractant reservoirs substantially
influencing the migration patterns. Our model predicts an optimal parameter regime
that enables robust and colocalized migration. We test our theoretical predictions
with in vitro experiments demonstrating the comigration of distinct immune cell
populations, and quantitatively reproduce observed migration patterns under wild-type
and perturbed conditions. Interestingly, immune cell comigration occurs close
to the predicted optimal regime. Finally, we incorporate mechanical interactions
into our framework, revealing a nontrivial interplay between chemotactic and mechanical
nonreciprocity in driving collective migration. Together, our findings suggest
that self-generated chemotaxis is a robust strategy for the navigation of mixed
cell populations.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
- _id: LifeSc
- _id: NanoFab
acknowledgement: We thank all members of the M.S. and E.H. groups for stimulating
discussions.We thank the Imaging and Optics facility, the Pre-clinical and Lab Support
facility of the Institute of Science and Technology Austria for their excellent
support and provided resources for the experimental research. In particular, we
thank Jack Merrin from the Nanofabrication facility who generated the microfabricated
channel used in this study. This work received funding fromt he European Research
Council under the European Union’s Horizon 2020 research and innovation program
(grant agreement No. 851288 to E.H.). M.C.U.is funded by a University of Sheffield
Strategic Research Fellowship in the Physics of Life and Quantitative Biology.
article_number: e2504064122
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Mehmet C
full_name: Ucar, Mehmet C
id: 50B2A802-6007-11E9-A42B-EB23E6697425
last_name: Ucar
orcid: 0000-0003-0506-4217
- first_name: Alsberga
full_name: Zane, Alsberga
id: 60f7509a-f652-11ea-9d86-b963d6490d7c
last_name: Zane
orcid: 0009-0003-0415-7603
- first_name: Jonna H
full_name: Alanko, Jonna H
id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87
last_name: Alanko
orcid: 0000-0002-7698-3061
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- 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: Ucar MC, Zane A, Alanko JH, Sixt MK, Hannezo EB. Self-generated chemotaxis
of mixed cell populations. Proceedings of the National Academy of Sciences.
2025;122(34). doi:10.1073/pnas.2504064122
apa: Ucar, M. C., Zane, A., Alanko, J. H., Sixt, M. K., & Hannezo, E. B. (2025).
Self-generated chemotaxis of mixed cell populations. Proceedings of the National
Academy of Sciences. National Academy of Sciences. https://doi.org/10.1073/pnas.2504064122
chicago: Ucar, Mehmet C, Alsberga Zane, Jonna H Alanko, Michael K Sixt, and Edouard
B Hannezo. “Self-Generated Chemotaxis of Mixed Cell Populations.” Proceedings
of the National Academy of Sciences. National Academy of Sciences, 2025. https://doi.org/10.1073/pnas.2504064122.
ieee: M. C. Ucar, A. Zane, J. H. Alanko, M. K. Sixt, and E. B. Hannezo, “Self-generated
chemotaxis of mixed cell populations,” Proceedings of the National Academy
of Sciences, vol. 122, no. 34. National Academy of Sciences, 2025.
ista: Ucar MC, Zane A, Alanko JH, Sixt MK, Hannezo EB. 2025. Self-generated chemotaxis
of mixed cell populations. Proceedings of the National Academy of Sciences. 122(34),
e2504064122.
mla: Ucar, Mehmet C., et al. “Self-Generated Chemotaxis of Mixed Cell Populations.”
Proceedings of the National Academy of Sciences, vol. 122, no. 34, e2504064122,
National Academy of Sciences, 2025, doi:10.1073/pnas.2504064122.
short: M.C. Ucar, A. Zane, J.H. Alanko, M.K. Sixt, E.B. Hannezo, Proceedings of
the National Academy of Sciences 122 (2025).
corr_author: '1'
date_created: 2025-09-07T22:01:32Z
date_published: 2025-08-26T00:00:00Z
date_updated: 2026-05-20T08:59:54Z
day: '26'
ddc:
- '570'
department:
- _id: EdHa
- _id: MiSi
doi: 10.1073/pnas.2504064122
ec_funded: 1
external_id:
isi:
- '001562181600001'
pmid:
- '40838890'
file:
- access_level: open_access
checksum: b36abd92673b6d76376fc9434bad52cc
content_type: application/pdf
creator: dernst
date_created: 2025-09-08T07:23:29Z
date_updated: 2025-09-08T07:23:29Z
file_id: '20307'
file_name: 2025_PNAS_Ucar.pdf
file_size: 16069140
relation: main_file
success: 1
file_date_updated: 2025-09-08T07:23:29Z
has_accepted_license: '1'
intvolume: ' 122'
isi: 1
issue: '34'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 05943252-7A3F-11EA-A408-12923DDC885E
call_identifier: H2020
grant_number: '851288'
name: Design Principles of Branching Morphogenesis
publication: Proceedings of the National Academy of Sciences
publication_identifier:
eissn:
- 1091-6490
issn:
- 0027-8424
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
related_material:
link:
- relation: software
url: https://github.com/mehmetcanucar/Self-generated-chemotaxis
scopus_import: '1'
status: public
title: Self-generated chemotaxis of mixed cell 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: 122
year: '2025'
...
---
OA_embargo: '6'
OA_place: publisher
_id: '19745'
abstract:
- lang: eng
text: "Cell migration is a crucial process in animal development and maintenance.
It is incredibly\r\nheterogeneous, with different cell types utilizing fundamentally
distinct migration strategies.\r\nThe strategies also depend on the cellular microenvironment,
where cells can switch between\r\nmigration modes as they encounter new environmental
cues. In this thesis, we investigated\r\nhow dendritic cells adapt their migration
strategy when encountering geometrically,\r\nmechanically and chemically distinct
environments.\r\nWhen dendritic cells are embedded in a homogeneous fibrous network,
they migrate in a fast\r\nand directional amoeboid manner. In this migration strategy,
extracellular proteolysis and\r\nintegrin-mediated adhesions are dispensable.
Instead, the cells use topography of the\r\nenvironment to propel their cell body
forward. To migrate efficiently in the maze of different\r\npore sizes, they position
the nucleus ahead of the microtubule organizing center (MTOC) and\r\nuse it to
gauge the pores to identify the path of least resistance. Our aim was to identify\r\nwhether
dendritic cells adapt their migration strategy when encountering asymmetrical\r\ntransitions
into much denser environments with limited choice of large pores. In such invasive\r\ntransitions
it is unclear if the cells can cross tight pores without the use of adhesions
and\r\nextracellular proteolysis and whether they maintain the nucleus in the
cell front.\r\nUsing various cell migration assays such as fibrous 3D collagen
gels, geometrically defined\r\nmicrochannels with constrictions and simplistic
under agarose migration assay, we provide\r\na comprehensive characterization
of invasive migration of dendritic cells. We show that\r\nduring invasion the
cells stall and stretch, reflecting the difficulty to translocate the bulky cell\r\nbody
into the dense environment. In collagen gels, we show that dendritic cells can
invade\r\nwithout proteolysis and adhesions. Instead, they utilize contractility,
which can lead to largescale collagen compressions. During invasion, the nucleus
stalls at tight constrictions, leading\r\nto a transient organelle reorientation.
To resolve the stalling, upregulated rear contractility is\r\nrequired. This contractile
force is simultaneously necessary for reverting the nucleus back to\r\nthe cell
front after invasion and maintaining this positioning during permissive migration.\r\nA
functional role of the reorientation was uncovered in the first collaboration
project.\r\nA prominent central actin pool was identified around the MTOC, especially
pronounced in\r\ndense and compressive environments. The actin pool was shown
to generate pushing forces\r\nto dilate the space for cell translocation. These
forces are only necessary in non-permissive\r\nenvironments, where the nucleus
reorients to the cell rear, allowing the actin pool to\r\ngenerate space. In permissive
environments where space generation is dispensable, the\r\nMTOC is located behind
the nucleus and the actin cloud has reduced intensity, allowing more\r\nactin
to be incorporated into the lamellipodium, speeding up migration.\r\nIn the second
collaboration project, we investigated the effects of distinct chemical\r\nenvironments
on dendritic cell migration. The strikingly persistent migration of these cells\r\nwas
explained by their ability to modulate and even self-generate chemokine gradients.
This\r\nallows the cells to migrate faster and more persistent in uniform chemokine
fields compared\r\nto imposed chemokine gradients. The chemokine receptor CCR7
was identified as a crucial\r\nplayer in this process, both sensing the signal
and internalizing the chemokine to create a sink."
acknowledgement: "This project has received funding from the Austrian Science Fund
(FWF) via the doctorate\r\ncollege DK NanoCell and from the European Union’s Horizon
2020 research and innovation\r\nprogramme under the Marie Skłodowska-Curie Grant
Agreement No. 665385.\r\n"
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Nikola
full_name: Canigova, Nikola
id: 3795523E-F248-11E8-B48F-1D18A9856A87
last_name: Canigova
orcid: 0000-0002-8518-5926
citation:
ama: Canigova N. Adaptive strategies of dendritic cell migration in response to
environmental cues. 2025. doi:10.15479/AT-ISTA-19745
apa: Canigova, N. (2025). Adaptive strategies of dendritic cell migration in
response to environmental cues. Institute of Science and Technology Austria.
https://doi.org/10.15479/AT-ISTA-19745
chicago: Canigova, Nikola. “Adaptive Strategies of Dendritic Cell Migration in Response
to Environmental Cues.” Institute of Science and Technology Austria, 2025. https://doi.org/10.15479/AT-ISTA-19745.
ieee: N. Canigova, “Adaptive strategies of dendritic cell migration in response
to environmental cues,” Institute of Science and Technology Austria, 2025.
ista: Canigova N. 2025. Adaptive strategies of dendritic cell migration in response
to environmental cues. Institute of Science and Technology Austria.
mla: Canigova, Nikola. Adaptive Strategies of Dendritic Cell Migration in Response
to Environmental Cues. Institute of Science and Technology Austria, 2025,
doi:10.15479/AT-ISTA-19745.
short: N. Canigova, Adaptive Strategies of Dendritic Cell Migration in Response
to Environmental Cues, Institute of Science and Technology Austria, 2025.
corr_author: '1'
date_created: 2025-05-26T08:49:00Z
date_published: 2025-05-27T00:00:00Z
date_updated: 2026-04-07T12:38:44Z
day: '27'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: MiSi
- _id: GradSch
doi: 10.15479/AT-ISTA-19745
ec_funded: 1
file:
- access_level: closed
checksum: 1a2d1525d19347fbb879ef57c02951bf
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: cchlebak
date_created: 2025-05-28T07:38:17Z
date_updated: 2025-11-27T23:30:02Z
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relation: source_file
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date_created: 2025-05-28T07:39:53Z
date_updated: 2025-11-27T23:30:02Z
embargo: 2025-11-27
file_id: '19749'
file_name: NikolaCanigova_Thesis_final_PDFA2a_fixed.pdf
file_size: 194530600
relation: main_file
file_date_updated: 2025-11-27T23:30:02Z
has_accepted_license: '1'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: '133'
project:
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
- _id: 265E2996-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W01250-B20
name: Nano-Analytics of Cellular Systems
publication_identifier:
isbn:
- 978-3-99078-058-9
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '14274'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: Adaptive strategies of dendritic cell migration in response to environmental
cues
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2025'
...
---
_id: '18109'
abstract:
- lang: eng
text: Venous thromboembolism (VTE) is a common, deadly disease with an increasing
incidence despite preventive efforts. Clinical observations have associated elevated
antibody concentrations or antibody-based therapies with thrombotic events. However,
how antibodies contribute to thrombosis is unknown. Here, we show that reduced
blood flow enabled immunoglobulin M (IgM) to bind to FcμR and the polymeric immunoglobulin
receptor (pIgR), initiating endothelial activation and platelet recruitment. Subsequently,
the procoagulant surface of activated platelets accommodated antigen- and FcγR-independent
IgG deposition. This leads to classical complement activation, setting in motion
a prothrombotic vicious circle. Key elements of this mechanism were present in
humans in the setting of venous stasis as well as in the dysregulated immunothrombosis
of COVID-19. This antibody-driven thrombosis can be prevented by pharmacologically
targeting complement. Hence, our results uncover antibodies as previously unrecognized
central regulators of thrombosis. These findings carry relevance for therapeutic
application of antibodies and open innovative avenues to target thrombosis without
compromising hemostasis.
acknowledgement: "We thank Michael Carroll (Harvard Medical School, Boston) for providing
Ighmtm1Che, C4−/−, and C3−/− mice; Mark Suter (University of Zurich, Zurich) for
providing Aicda−/− mice; Marina Botto (Imperial College London, London) for providing
C1q−/− and fB−/− mice; Craig Gerard (Harvard Medical School, Boston) for providing
C3aR−/− mice; Falk Nimmerjahn (University Erlangen-Nuernberg, Erlangen) for providing
Fcgr−/−Fcgr2b−/− mice; Karl Lang (University of Duisburg-Essen, Essen) for providing
Fcmr−/− mice; Hans Hengartner and Rolf Zinkernagel (ETH Zurich, Zurich) for providing
KL25 mice; Mark Zabel (University Hospital of Zurich, Zurich) for providing CR2−/−
mice; Christie Ballantyne (Baylor College of Medicine, Houston) for providing CD11c−/−
mice; and Siamon Gordon (University of Oxford, Oxford) for providing CD11b−/− mice.
A.V. wishes to thank Michael Grünaug and dedicates this work to Annette, Rita, and
Hans.\r\nThis project has received funding from the European Research Council (ERC)
under the European Union’s Horizon 2020 research and innovation programme (grant
agreement no. \r\n947611) (K.S.). This study was supported by the Deutsche Forschungsgemeinschaft
through the collaborative research center 914 project B02 (K.S. and S.M.), project
B04 (A.V.), project A01 (M.M.), project B01 (M.S.), the collaborative research center
1123 project B07 (K.S. and S.M.), the collaborative research center 359 (project
A03 [K.S.] and B02 [M.S.]), the international research training group 1911 project
B09 (A.V.), the clinical research unit 303 project 7 (A.V.), cluster of excellence
2167 (A.V.), collaborative research center 1526 project 05 (A.V.), the ANR-DFG project
JAKPOT (K.S.), LMUexcellent (K.S.), and the Deutsche Zentrum für Herz-Kreislauf-Forschung
(PostDoc Grant and partner site project [K.S. and S.M.]). M.I. is supported by the
European Research Council (ERC) Advanced Grant 101141363, ERC Proof of Concept Grant
101138728, Italian Association for Cancer Research (AIRC) Grants 19891 and \r\n22737,
Italian Ministry for University and Research Grants PE00000007 (INF-ACT) and PRIN
\r\n2022FMESXL, Funded Research Agreement from Asher Biotherapeutics, VIR Biotechnology,
and BlueJay Therapeutics. V.F. is supported by the Italian Ministry for University
and Research Grants PE00000007 (INF-ACT) and Fondazione Prossimo Mio."
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Konstantin
full_name: Stark, Konstantin
last_name: Stark
- first_name: Badr
full_name: Kilani, Badr
last_name: Kilani
- first_name: Sven
full_name: Stockhausen, Sven
last_name: Stockhausen
- first_name: Johanna
full_name: Busse, Johanna
last_name: Busse
- first_name: Irene
full_name: Schubert, Irene
last_name: Schubert
- first_name: Thuy Duong
full_name: Tran, Thuy Duong
last_name: Tran
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Alexander
full_name: Leunig, Alexander
last_name: Leunig
- first_name: Kami
full_name: Pekayvaz, Kami
last_name: Pekayvaz
- first_name: Leo
full_name: Nicolai, Leo
last_name: Nicolai
- first_name: Valeria
full_name: Fumagalli, Valeria
last_name: Fumagalli
- first_name: Julia
full_name: Stermann, Julia
last_name: Stermann
- first_name: Felix
full_name: Stephan, Felix
last_name: Stephan
- first_name: Christian
full_name: David, Christian
last_name: David
- first_name: Martin B.
full_name: Müller, Martin B.
last_name: Müller
- first_name: Birgitta
full_name: Heyman, Birgitta
last_name: Heyman
- first_name: Anja
full_name: Lux, Anja
last_name: Lux
- first_name: Alexandra
full_name: Da Palma Guerreiro, Alexandra
last_name: Da Palma Guerreiro
- first_name: Lukas P.
full_name: Frenzel, Lukas P.
last_name: Frenzel
- first_name: Christoph Q.
full_name: Schmidt, Christoph Q.
last_name: Schmidt
- first_name: Arthur
full_name: Dopler, Arthur
last_name: Dopler
- first_name: Markus
full_name: Moser, Markus
last_name: Moser
- first_name: Sue
full_name: Chandraratne, Sue
last_name: Chandraratne
- first_name: Marie Luise
full_name: Von Brühl, Marie Luise
last_name: Von Brühl
- first_name: Michael
full_name: Lorenz, Michael
last_name: Lorenz
- first_name: Thomas
full_name: Korff, Thomas
last_name: Korff
- first_name: Martina
full_name: Rudelius, Martina
last_name: Rudelius
- first_name: Oliver
full_name: Popp, Oliver
last_name: Popp
- first_name: Marieluise
full_name: Kirchner, Marieluise
last_name: Kirchner
- first_name: Philipp
full_name: Mertins, Philipp
last_name: Mertins
- first_name: Falk
full_name: Nimmerjahn, Falk
last_name: Nimmerjahn
- first_name: Matteo
full_name: Iannacone, Matteo
last_name: Iannacone
- first_name: Markus
full_name: Sperandio, Markus
last_name: Sperandio
- first_name: Bernd
full_name: Engelmann, Bernd
last_name: Engelmann
- first_name: Admar
full_name: Verschoor, Admar
last_name: Verschoor
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
citation:
ama: Stark K, Kilani B, Stockhausen S, et al. Antibodies and complement are key
drivers of thrombosis. Immunity. 2024;57(9):2140-2156. doi:10.1016/j.immuni.2024.08.007
apa: Stark, K., Kilani, B., Stockhausen, S., Busse, J., Schubert, I., Tran, T. D.,
… Massberg, S. (2024). Antibodies and complement are key drivers of thrombosis.
Immunity. Elsevier. https://doi.org/10.1016/j.immuni.2024.08.007
chicago: Stark, Konstantin, Badr Kilani, Sven Stockhausen, Johanna Busse, Irene
Schubert, Thuy Duong Tran, Florian R Gärtner, et al. “Antibodies and Complement
Are Key Drivers of Thrombosis.” Immunity. Elsevier, 2024. https://doi.org/10.1016/j.immuni.2024.08.007.
ieee: K. Stark et al., “Antibodies and complement are key drivers of thrombosis,”
Immunity, vol. 57, no. 9. Elsevier, pp. 2140–2156, 2024.
ista: Stark K, Kilani B, Stockhausen S, Busse J, Schubert I, Tran TD, Gärtner FR,
Leunig A, Pekayvaz K, Nicolai L, Fumagalli V, Stermann J, Stephan F, David C,
Müller MB, Heyman B, Lux A, Da Palma Guerreiro A, Frenzel LP, Schmidt CQ, Dopler
A, Moser M, Chandraratne S, Von Brühl ML, Lorenz M, Korff T, Rudelius M, Popp
O, Kirchner M, Mertins P, Nimmerjahn F, Iannacone M, Sperandio M, Engelmann B,
Verschoor A, Massberg S. 2024. Antibodies and complement are key drivers of thrombosis.
Immunity. 57(9), 2140–2156.
mla: Stark, Konstantin, et al. “Antibodies and Complement Are Key Drivers of Thrombosis.”
Immunity, vol. 57, no. 9, Elsevier, 2024, pp. 2140–56, doi:10.1016/j.immuni.2024.08.007.
short: K. Stark, B. Kilani, S. Stockhausen, J. Busse, I. Schubert, T.D. Tran, F.R.
Gärtner, A. Leunig, K. Pekayvaz, L. Nicolai, V. Fumagalli, J. Stermann, F. Stephan,
C. David, M.B. Müller, B. Heyman, A. Lux, A. Da Palma Guerreiro, L.P. Frenzel,
C.Q. Schmidt, A. Dopler, M. Moser, S. Chandraratne, M.L. Von Brühl, M. Lorenz,
T. Korff, M. Rudelius, O. Popp, M. Kirchner, P. Mertins, F. Nimmerjahn, M. Iannacone,
M. Sperandio, B. Engelmann, A. Verschoor, S. Massberg, Immunity 57 (2024) 2140–2156.
date_created: 2024-09-22T22:01:42Z
date_published: 2024-09-10T00:00:00Z
date_updated: 2025-09-08T09:50:13Z
day: '10'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.immuni.2024.08.007
external_id:
isi:
- '001317438500001'
pmid:
- '39226900'
file:
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checksum: 4683de43d06a8fd8e3fc91af4ddc1ba2
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creator: dernst
date_created: 2024-09-30T09:16:03Z
date_updated: 2024-09-30T09:16:03Z
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file_name: 2024_Immunity_Stark.pdf
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file_date_updated: 2024-09-30T09:16:03Z
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intvolume: ' 57'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: 2140-2156
pmid: 1
publication: Immunity
publication_identifier:
eissn:
- 1097-4180
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Antibodies and complement are key drivers of thrombosis
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 57
year: '2024'
...
---
_id: '14846'
abstract:
- lang: eng
text: Contraction and flow of the actin cell cortex have emerged as a common principle
by which cells reorganize their cytoplasm and take shape. However, how these cortical
flows interact with adjacent cytoplasmic components, changing their form and localization,
and how this affects cytoplasmic organization and cell shape remains unclear.
Here we show that in ascidian oocytes, the cooperative activities of cortical
actomyosin flows and deformation of the adjacent mitochondria-rich myoplasm drive
oocyte cytoplasmic reorganization and shape changes following fertilization. We
show that vegetal-directed cortical actomyosin flows, established upon oocyte
fertilization, lead to both the accumulation of cortical actin at the vegetal
pole of the zygote and compression and local buckling of the adjacent elastic
solid-like myoplasm layer due to friction forces generated at their interface.
Once cortical flows have ceased, the multiple myoplasm buckles resolve into one
larger buckle, which again drives the formation of the contraction pole—a protuberance
of the zygote’s vegetal pole where maternal mRNAs accumulate. Thus, our findings
reveal a mechanism where cortical actomyosin network flows determine cytoplasmic
reorganization and cell shape by deforming adjacent cytoplasmic components through
friction forces.
acknowledged_ssus:
- _id: EM-Fac
- _id: Bio
- _id: NanoFab
acknowledgement: We would like to thank A. McDougall, E. Hannezo and the Heisenberg
lab for fruitful discussions and reagents. We also thank E. Munro for the iMyo-YFP
and Bra>iMyo-mScarlet constructs. This research was supported by the Scientific
Service Units of the Institute of Science and Technology Austria through resources
provided by the Electron Microscopy Facility, Imaging and Optics Facility and the
Nanofabrication Facility. This work was supported by a Joint Project Grant from
the FWF (I 3601-B27).
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Silvia
full_name: Caballero Mancebo, Silvia
id: 2F1E1758-F248-11E8-B48F-1D18A9856A87
last_name: Caballero Mancebo
orcid: 0000-0002-5223-3346
- first_name: Rushikesh
full_name: Shinde, Rushikesh
last_name: Shinde
- first_name: Madison
full_name: Bolger-Munro, Madison
id: 516F03FA-93A3-11EA-A7C5-D6BE3DDC885E
last_name: Bolger-Munro
orcid: 0000-0002-8176-4824
- first_name: Matilda
full_name: Peruzzo, Matilda
id: 3F920B30-F248-11E8-B48F-1D18A9856A87
last_name: Peruzzo
orcid: 0000-0002-3415-4628
- first_name: Gregory
full_name: Szep, Gregory
id: 4BFB7762-F248-11E8-B48F-1D18A9856A87
last_name: Szep
- first_name: Irene
full_name: Steccari, Irene
id: 2705C766-9FE2-11EA-B224-C6773DDC885E
last_name: Steccari
- first_name: David
full_name: Labrousse Arias, David
id: CD573DF4-9ED3-11E9-9D77-3223E6697425
last_name: Labrousse Arias
- first_name: Vanessa
full_name: Zheden, Vanessa
id: 39C5A68A-F248-11E8-B48F-1D18A9856A87
last_name: Zheden
orcid: 0000-0002-9438-4783
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Andrew
full_name: Callan-Jones, Andrew
last_name: Callan-Jones
- first_name: Raphaël
full_name: Voituriez, Raphaël
last_name: Voituriez
- 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: Caballero Mancebo S, Shinde R, Bolger-Munro M, et al. Friction forces determine
cytoplasmic reorganization and shape changes of ascidian oocytes upon fertilization.
Nature Physics. 2024;20:310-321. doi:10.1038/s41567-023-02302-1
apa: Caballero Mancebo, S., Shinde, R., Bolger-Munro, M., Peruzzo, M., Szep, G.,
Steccari, I., … Heisenberg, C.-P. J. (2024). Friction forces determine cytoplasmic
reorganization and shape changes of ascidian oocytes upon fertilization. Nature
Physics. Springer Nature. https://doi.org/10.1038/s41567-023-02302-1
chicago: Caballero Mancebo, Silvia, Rushikesh Shinde, Madison Bolger-Munro, Matilda
Peruzzo, Gregory Szep, Irene Steccari, David Labrousse Arias, et al. “Friction
Forces Determine Cytoplasmic Reorganization and Shape Changes of Ascidian Oocytes
upon Fertilization.” Nature Physics. Springer Nature, 2024. https://doi.org/10.1038/s41567-023-02302-1.
ieee: S. Caballero Mancebo et al., “Friction forces determine cytoplasmic
reorganization and shape changes of ascidian oocytes upon fertilization,” Nature
Physics, vol. 20. Springer Nature, pp. 310–321, 2024.
ista: Caballero Mancebo S, Shinde R, Bolger-Munro M, Peruzzo M, Szep G, Steccari
I, Labrousse Arias D, Zheden V, Merrin J, Callan-Jones A, Voituriez R, Heisenberg
C-PJ. 2024. Friction forces determine cytoplasmic reorganization and shape changes
of ascidian oocytes upon fertilization. Nature Physics. 20, 310–321.
mla: Caballero Mancebo, Silvia, et al. “Friction Forces Determine Cytoplasmic Reorganization
and Shape Changes of Ascidian Oocytes upon Fertilization.” Nature Physics,
vol. 20, Springer Nature, 2024, pp. 310–21, doi:10.1038/s41567-023-02302-1.
short: S. Caballero Mancebo, R. Shinde, M. Bolger-Munro, M. Peruzzo, G. Szep, I.
Steccari, D. Labrousse Arias, V. Zheden, J. Merrin, A. Callan-Jones, R. Voituriez,
C.-P.J. Heisenberg, Nature Physics 20 (2024) 310–321.
corr_author: '1'
date_created: 2024-01-21T23:00:57Z
date_published: 2024-02-01T00:00:00Z
date_updated: 2025-09-04T11:48:28Z
day: '01'
ddc:
- '530'
department:
- _id: CaHe
- _id: JoFi
- _id: MiSi
- _id: EM-Fac
- _id: NanoFab
doi: 10.1038/s41567-023-02302-1
external_id:
isi:
- '001138880800005'
pmid:
- '38370025'
file:
- access_level: open_access
checksum: 7891ebe7c900ae47469ab127031dd1ec
content_type: application/pdf
creator: dernst
date_created: 2024-07-16T12:12:43Z
date_updated: 2024-07-16T12:12:43Z
file_id: '17267'
file_name: 2024_NaturePhysics_CaballeroMancebo.pdf
file_size: 9897883
relation: main_file
success: 1
file_date_updated: 2024-07-16T12:12:43Z
has_accepted_license: '1'
intvolume: ' 20'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 310-321
pmid: 1
project:
- _id: 2646861A-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I03601
name: Control of embryonic cleavage pattern
publication: Nature Physics
publication_identifier:
eissn:
- 1745-2481
issn:
- 1745-2473
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on ISTA Website
relation: press_release
url: https://ista.ac.at/en/news/stranger-than-friction-a-force-initiating-life/
scopus_import: '1'
status: public
title: Friction forces determine cytoplasmic reorganization and shape changes of ascidian
oocytes upon fertilization
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 20
year: '2024'
...
---
_id: '14933'
abstract:
- lang: eng
text: Centrioles are part of centrosomes and cilia, which are microtubule organising
centres (MTOC) with diverse functions. Despite their stability, centrioles can
disappear during differentiation, such as in oocytes, but little is known about
the regulation of their structural integrity. Our previous research revealed that
the pericentriolar material (PCM) that surrounds centrioles and its recruiter,
Polo kinase, are downregulated in oogenesis and sufficient for maintaining both
centrosome structural integrity and MTOC activity. We now show that the expression
of specific components of the centriole cartwheel and wall, including ANA1/CEP295,
is essential for maintaining centrosome integrity. We find that Polo kinase requires
ANA1 to promote centriole stability in cultured cells and eggs. In addition, ANA1
expression prevents the loss of centrioles observed upon PCM-downregulation. However,
the centrioles maintained by overexpressing and tethering ANA1 are inactive, unlike
the MTOCs observed upon tethering Polo kinase. These findings demonstrate that
several centriole components are needed to maintain centrosome structure. Our
study also highlights that centrioles are more dynamic than previously believed,
with their structural stability relying on the continuous expression of multiple
components.
acknowledgement: We thank all members of the Cell Cycle and Regulation Lab for the
discussions and for the critical reading of the manuscript. We thank Tomer Avidor-Reiss
(University of Toledo, Toledo, OH), Daniel St. Johnston (The Gurdon Institute, Cambridge,
UK), David Glover (University of Cambridge, Cambridge, UK), Jingyan Fu (Agricultural
University, Beijing, China) Jordan Raff (University of Oxford, Oxford, UK) and Timothy
Megraw (Florida State University, Tallahassee, FL) for sharing tools. We acknowledge
the technical support of Instituto Gulbenkian de Ciência (IGC)‘s Advanced Imaging
Facility, in particular Gabriel Martins, Nuno Pimpão Martins and José Marques. We
also thank Tiago Paixão from the IGC’s Quantitative & Digital Science Unit and Marco
Louro from the CCR lab for the support provided on statistical analysis. IGC’s Advanced
Imaging Facility (AIF-UIC) is supported by the national Portuguese funding ref#
PPBI-POCI-01-0145-FEDER -022122. We thank the IGC’s Fly Facility, supported by CONGENTO
(LISBOA-01-0145-FEDER-022170). This work was supported by an ERC grant (ERC-2015-CoG-683258)
awarded to MBD and a grant from the Portuguese Research Council (FCT) awarded to
APM (PTDC/BIA-BID/32225/2017).
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Ana
full_name: Pimenta-Marques, Ana
last_name: Pimenta-Marques
- first_name: Tania
full_name: Perestrelo, Tania
last_name: Perestrelo
- first_name: Patricia
full_name: Dos Reis Rodrigues, Patricia
id: 26E95904-5160-11E9-9C0B-C5B0DC97E90F
last_name: Dos Reis Rodrigues
orcid: 0000-0003-1681-508X
- first_name: Paulo
full_name: Duarte, Paulo
last_name: Duarte
- first_name: Ana
full_name: Ferreira-Silva, Ana
last_name: Ferreira-Silva
- first_name: Mariana
full_name: Lince-Faria, Mariana
last_name: Lince-Faria
- first_name: Mónica
full_name: Bettencourt-Dias, Mónica
last_name: Bettencourt-Dias
citation:
ama: Pimenta-Marques A, Perestrelo T, Dos Reis Rodrigues P, et al. Ana1/CEP295 is
an essential player in the centrosome maintenance program regulated by Polo kinase
and the PCM. EMBO Reports. 2024;25(1):102-127. doi:10.1038/s44319-023-00020-6
apa: Pimenta-Marques, A., Perestrelo, T., Dos Reis Rodrigues, P., Duarte, P., Ferreira-Silva,
A., Lince-Faria, M., & Bettencourt-Dias, M. (2024). Ana1/CEP295 is an essential
player in the centrosome maintenance program regulated by Polo kinase and the
PCM. EMBO Reports. Embo Press. https://doi.org/10.1038/s44319-023-00020-6
chicago: Pimenta-Marques, Ana, Tania Perestrelo, Patricia Dos Reis Rodrigues, Paulo
Duarte, Ana Ferreira-Silva, Mariana Lince-Faria, and Mónica Bettencourt-Dias.
“Ana1/CEP295 Is an Essential Player in the Centrosome Maintenance Program Regulated
by Polo Kinase and the PCM.” EMBO Reports. Embo Press, 2024. https://doi.org/10.1038/s44319-023-00020-6.
ieee: A. Pimenta-Marques et al., “Ana1/CEP295 is an essential player in the
centrosome maintenance program regulated by Polo kinase and the PCM,” EMBO
Reports, vol. 25, no. 1. Embo Press, pp. 102–127, 2024.
ista: Pimenta-Marques A, Perestrelo T, Dos Reis Rodrigues P, Duarte P, Ferreira-Silva
A, Lince-Faria M, Bettencourt-Dias M. 2024. Ana1/CEP295 is an essential player
in the centrosome maintenance program regulated by Polo kinase and the PCM. EMBO
Reports. 25(1), 102–127.
mla: Pimenta-Marques, Ana, et al. “Ana1/CEP295 Is an Essential Player in the Centrosome
Maintenance Program Regulated by Polo Kinase and the PCM.” EMBO Reports,
vol. 25, no. 1, Embo Press, 2024, pp. 102–27, doi:10.1038/s44319-023-00020-6.
short: A. Pimenta-Marques, T. Perestrelo, P. Dos Reis Rodrigues, P. Duarte, A. Ferreira-Silva,
M. Lince-Faria, M. Bettencourt-Dias, EMBO Reports 25 (2024) 102–127.
date_created: 2024-02-04T23:00:53Z
date_published: 2024-01-10T00:00:00Z
date_updated: 2025-04-23T07:39:52Z
day: '10'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1038/s44319-023-00020-6
external_id:
pmid:
- '38200359'
file:
- access_level: open_access
checksum: 53c3ef43d9bd6d7bff3ffcf57d763cac
content_type: application/pdf
creator: dernst
date_created: 2024-02-05T12:35:03Z
date_updated: 2024-02-05T12:35:03Z
file_id: '14941'
file_name: 2023_EmboReports_PimentaMarques.pdf
file_size: 9645056
relation: main_file
success: 1
file_date_updated: 2024-02-05T12:35:03Z
has_accepted_license: '1'
intvolume: ' 25'
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 102-127
pmid: 1
publication: EMBO Reports
publication_identifier:
eissn:
- 1469-3178
publication_status: published
publisher: Embo Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Ana1/CEP295 is an essential player in the centrosome maintenance program regulated
by Polo kinase and the PCM
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: 25
year: '2024'
...
---
_id: '15146'
abstract:
- lang: eng
text: The extracellular matrix (ECM) serves as a scaffold for cells and plays an
essential role in regulating numerous cellular processes, including cell migration
and proliferation. Due to limitations in specimen preparation for conventional
room-temperature electron microscopy, we lack structural knowledge on how ECM
components are secreted, remodeled, and interact with surrounding cells. We have
developed a 3D-ECM platform compatible with sample thinning by cryo-focused ion
beam milling, the lift-out extraction procedure, and cryo-electron tomography.
Our workflow implements cell-derived matrices (CDMs) grown on EM grids, resulting
in a versatile tool closely mimicking ECM environments. This allows us to visualize
ECM for the first time in its hydrated, native context. Our data reveal an intricate
network of extracellular fibers, their positioning relative to matrix-secreting
cells, and previously unresolved structural entities. Our workflow and results
add to the structural atlas of the ECM, providing novel insights into its secretion
and assembly.
acknowledged_ssus:
- _id: LifeSc
- _id: ScienComp
- _id: EM-Fac
- _id: M-Shop
acknowledgement: "Open Access funding provided by IST Austria. We thank Armel Nicolas
and his team at the ISTA proteomics facility, Alois Schloegl, Stefano Elefante,
and colleagues at the ISTA Scientific Computing facility, Tommaso Constanzo and
Ludek Lovicar at the Electron Microsocpy Facility (EMF), and Thomas Menner at the
Miba Machine shop for their support. We also thank Wanda Kukulski (University of
Bern) as well as Darío Porley, Andreas Thader, and other members of the Schur group
for helpful discussions. Matt Swulius and Jessica Heebner provided great support
in using Dragonfly. We thank Dorotea Fracciolla (Art & Science) for support in figure
illustration.\r\n\r\nThis research was supported by the Scientific Service Units
of ISTA through resources provided by Scientific Computing, the Lab Support Facility,
and the Electron Microscopy Facility. We acknowledge funding support from the following
sources: Austrian Science Fund (FWF) grant P33367 (to F.K.M. Schur), the Federation
of European Biochemical Societies (to F.K.M. Schur), Niederösterreich (NÖ) Fonds
(to B. Zens), FWF grant E435 (to J.M. Hansen), European Research Council under the
European Union’s Horizon 2020 research (grant agreement No. 724373) (to M. Sixt),
and Jenny and Antti Wihuri Foundation (to J. Alanko). This publication has been
made possible in part by CZI grant DAF2021-234754 and grant DOI https://doi.org/10.37921/812628ebpcwg
from the Chan Zuckerberg Initiative DAF, an advised fund of Silicon Valley Community
Foundation (to F.K.M. Schur)."
article_number: e202309125
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Bettina
full_name: Zens, Bettina
id: 45FD126C-F248-11E8-B48F-1D18A9856A87
last_name: Zens
orcid: 0000-0002-9561-1239
- first_name: Florian
full_name: Fäßler, Florian
id: 404F5528-F248-11E8-B48F-1D18A9856A87
last_name: Fäßler
orcid: 0000-0001-7149-769X
- first_name: Jesse
full_name: Hansen, Jesse
id: 1063c618-6f9b-11ec-9123-f912fccded63
last_name: Hansen
orcid: 0000-0001-7967-2085
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Julia
full_name: Datler, Julia
id: 3B12E2E6-F248-11E8-B48F-1D18A9856A87
last_name: Datler
orcid: 0000-0002-3616-8580
- first_name: Victor-Valentin
full_name: Hodirnau, Victor-Valentin
id: 3661B498-F248-11E8-B48F-1D18A9856A87
last_name: Hodirnau
orcid: 0000-0003-3904-947X
- first_name: Vanessa
full_name: Zheden, Vanessa
id: 39C5A68A-F248-11E8-B48F-1D18A9856A87
last_name: Zheden
orcid: 0000-0002-9438-4783
- first_name: Jonna H
full_name: Alanko, Jonna H
id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87
last_name: Alanko
orcid: 0000-0002-7698-3061
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- 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: Zens B, Fäßler F, Hansen J, et al. Lift-out cryo-FIBSEM and cryo-ET reveal
the ultrastructural landscape of extracellular matrix. Journal of Cell Biology.
2024;223(6). doi:10.1083/jcb.202309125
apa: Zens, B., Fäßler, F., Hansen, J., Hauschild, R., Datler, J., Hodirnau, V.-V.,
… Schur, F. K. (2024). Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural
landscape of extracellular matrix. Journal of Cell Biology. Rockefeller
University Press. https://doi.org/10.1083/jcb.202309125
chicago: Zens, Bettina, Florian Fäßler, Jesse Hansen, Robert Hauschild, Julia Datler,
Victor-Valentin Hodirnau, Vanessa Zheden, Jonna H Alanko, Michael K Sixt, and
Florian KM Schur. “Lift-out Cryo-FIBSEM and Cryo-ET Reveal the Ultrastructural
Landscape of Extracellular Matrix.” Journal of Cell Biology. Rockefeller
University Press, 2024. https://doi.org/10.1083/jcb.202309125.
ieee: B. Zens et al., “Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural
landscape of extracellular matrix,” Journal of Cell Biology, vol. 223,
no. 6. Rockefeller University Press, 2024.
ista: Zens B, Fäßler F, Hansen J, Hauschild R, Datler J, Hodirnau V-V, Zheden V,
Alanko JH, Sixt MK, Schur FK. 2024. Lift-out cryo-FIBSEM and cryo-ET reveal the
ultrastructural landscape of extracellular matrix. Journal of Cell Biology. 223(6),
e202309125.
mla: Zens, Bettina, et al. “Lift-out Cryo-FIBSEM and Cryo-ET Reveal the Ultrastructural
Landscape of Extracellular Matrix.” Journal of Cell Biology, vol. 223,
no. 6, e202309125, Rockefeller University Press, 2024, doi:10.1083/jcb.202309125.
short: B. Zens, F. Fäßler, J. Hansen, R. Hauschild, J. Datler, V.-V. Hodirnau, V.
Zheden, J.H. Alanko, M.K. Sixt, F.K. Schur, Journal of Cell Biology 223 (2024).
corr_author: '1'
date_created: 2024-03-21T06:45:51Z
date_published: 2024-03-20T00:00:00Z
date_updated: 2025-09-04T13:17:16Z
day: '20'
ddc:
- '570'
department:
- _id: FlSc
- _id: MiSi
- _id: Bio
- _id: EM-Fac
doi: 10.1083/jcb.202309125
ec_funded: 1
external_id:
isi:
- '001264190100001'
pmid:
- '38506714'
file:
- access_level: open_access
checksum: 90d1984a93660735e506c2a304bc3f73
content_type: application/pdf
creator: dernst
date_created: 2024-03-25T12:52:04Z
date_updated: 2024-03-25T12:52:04Z
file_id: '15188'
file_name: 2024_JCB_Zens.pdf
file_size: 11907016
relation: main_file
success: 1
file_date_updated: 2024-03-25T12:52:04Z
has_accepted_license: '1'
intvolume: ' 223'
isi: 1
issue: '6'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 9B954C5C-BA93-11EA-9121-9846C619BF3A
grant_number: P33367
name: Structure and isoform diversity of the Arp2/3 complex
- _id: 7bd318a1-9f16-11ee-852c-cc9217763180
grant_number: E435
name: In Situ Actin Structures via Hybrid Cryo-electron Microscopy
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular Navigation Along Spatial Gradients
- _id: 059B463C-7A3F-11EA-A408-12923DDC885E
name: "NÃ\x96-Fonds Preis für die Jungforscherin des Jahres am IST Austria"
- _id: 2615199A-B435-11E9-9278-68D0E5697425
grant_number: '21317'
name: Spatiotemporal regulation of chemokine-induced signalling in leukocyte chemotaxis
- _id: 62909c6f-2b32-11ec-9570-e1476aab5308
grant_number: CZI01
name: CryoMinflux-guided in-situ visual proteomics and structure determination
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural landscape of extracellular
matrix
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 223
year: '2024'
...
---
OA_place: publisher
OA_type: hybrid
_id: '15408'
abstract:
- lang: eng
text: "Background: IgE-mediated degranulation of mast cells (MCs) provides rapid
protection against environmental hazards, including animal venoms. A fraction
of tissue-resident MCs intimately associates with blood vessels. These perivascular
MCs were reported to extend projections into the vessel lumen and to be the first
MCs to acquire intravenously injected IgE, suggesting that IgE loading of MCs
depends on their vascular association.\r\nObjective: We sought to elucidate the
molecular basis of the MC–blood vessel interaction and to determine its relevance
for IgE-mediated immune responses.\r\nMethods: We selectively inactivated the
Itgb1 gene, encoding the β1 chain of integrin adhesion molecules (ITGB1), in MCs
by conditional gene targeting in mice. We analyzed skin MCs for blood vessel association,
surface IgE density, and capability to bind circulating antibody specific for
MC surface molecules, as well as in vivo responses to antigen administered via
different routes.\r\nResults: Lack of ITGB1 expression severely compromised MC–blood
vessel association. ITGB1-deficient MCs showed normal densities of surface IgE
but reduced binding of intravenously injected antibodies. While their capacity
to degranulate in response to IgE ligation in vivo was unimpaired, anaphylactic
responses to antigen circulating in the vasculature were largely abolished.\r\nConclusions:
ITGB1-mediated association of MCs with blood vessels is key for MC immune surveillance
of blood vessel content, but is dispensable for slow steady-state loading of endogenous
IgE onto tissue-resident MCs."
acknowledgement: "This work was funded by Deutsche Forschungsgemeinschaft, Germany,
grants RO2133/ 9-1 and RO2133/ 9-2 in the setting of FOR2599 and TR156 project C11
(Project-ID 246807620–TRR 156) to A. Roers and Springboard-to-Postdoc grant of the
Dresden International Graduate School for Biomedicine and Bioengineering (DIGS-BB),
Dresden, Germany, and Fond zur Förderung der Wissenschaftlichen Forschung (FWF),
Austria, Hertha Firnberg grant (project number T-1219) to A. Polikarpova.\r\nWe
thank Dr Michael Gerlach, Core Facility Cellular Imaging, Faculty of Medicine Carl
Gustav Carus, TU Dresden, for expert support of in vivo imaging experiments; Grace
Wurigamule for help with 2-photon imaging and flow cytometric analysis of mouse
skin; and Christina Hiller, Livia Schulze, Madelaine Rickauer, and Christa Haase
for providing expert technical assistance."
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Kristina
full_name: Link, Kristina
last_name: Link
- first_name: Lina
full_name: Muhandes, Lina
last_name: Muhandes
- first_name: Anastasia
full_name: Polikarpova, Anastasia
last_name: Polikarpova
- first_name: Tim
full_name: Lämmermann, Tim
last_name: Lämmermann
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Reinhard
full_name: Fässler, Reinhard
last_name: Fässler
- first_name: Axel
full_name: Roers, Axel
last_name: Roers
citation:
ama: Link K, Muhandes L, Polikarpova A, et al. Integrin β1–mediated mast cell immune-surveillance
of blood vessel content. Journal of Allergy and Clinical Immunology. 2024;154(3):745-753.
doi:10.1016/j.jaci.2024.03.022
apa: Link, K., Muhandes, L., Polikarpova, A., Lämmermann, T., Sixt, M. K., Fässler,
R., & Roers, A. (2024). Integrin β1–mediated mast cell immune-surveillance
of blood vessel content. Journal of Allergy and Clinical Immunology. Elsevier.
https://doi.org/10.1016/j.jaci.2024.03.022
chicago: Link, Kristina, Lina Muhandes, Anastasia Polikarpova, Tim Lämmermann, Michael
K Sixt, Reinhard Fässler, and Axel Roers. “Integrin Β1–Mediated Mast Cell Immune-Surveillance
of Blood Vessel Content.” Journal of Allergy and Clinical Immunology. Elsevier,
2024. https://doi.org/10.1016/j.jaci.2024.03.022.
ieee: K. Link et al., “Integrin β1–mediated mast cell immune-surveillance
of blood vessel content,” Journal of Allergy and Clinical Immunology, vol.
154, no. 3. Elsevier, pp. 745–753, 2024.
ista: Link K, Muhandes L, Polikarpova A, Lämmermann T, Sixt MK, Fässler R, Roers
A. 2024. Integrin β1–mediated mast cell immune-surveillance of blood vessel content.
Journal of Allergy and Clinical Immunology. 154(3), 745–753.
mla: Link, Kristina, et al. “Integrin Β1–Mediated Mast Cell Immune-Surveillance
of Blood Vessel Content.” Journal of Allergy and Clinical Immunology, vol.
154, no. 3, Elsevier, 2024, pp. 745–53, doi:10.1016/j.jaci.2024.03.022.
short: K. Link, L. Muhandes, A. Polikarpova, T. Lämmermann, M.K. Sixt, R. Fässler,
A. Roers, Journal of Allergy and Clinical Immunology 154 (2024) 745–753.
date_created: 2024-05-19T22:01:13Z
date_published: 2024-09-01T00:00:00Z
date_updated: 2025-09-08T07:28:25Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.jaci.2024.03.022
external_id:
isi:
- '001308886700001'
pmid:
- '38636606'
file:
- access_level: open_access
checksum: 6a5af05082e1869d7cad6406fa4eb76c
content_type: application/pdf
creator: dernst
date_created: 2025-01-13T10:55:28Z
date_updated: 2025-01-13T10:55:28Z
file_id: '18840'
file_name: 2024_JourAllergyClinicalImm_Link.pdf
file_size: 1792425
relation: main_file
success: 1
file_date_updated: 2025-01-13T10:55:28Z
has_accepted_license: '1'
intvolume: ' 154'
isi: 1
issue: '3'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: 745-753
pmid: 1
publication: Journal of Allergy and Clinical Immunology
publication_identifier:
eissn:
- 1097-6825
issn:
- 0091-6749
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Integrin β1–mediated mast cell immune-surveillance of blood vessel content
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 154
year: '2024'
...
---
_id: '17191'
abstract:
- lang: eng
text: Dendritic cells migrate to and from lymph nodes in response to chemokine gradients.Data
now show that steady-state migration of these cells can be triggered by a mechanosensitive
pathway.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Sergio
full_name: Lembo, Sergio
id: d993a7b2-292f-11ed-aaac-fb045a912e31
last_name: Lembo
orcid: 0000-0002-2253-8771
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Lembo S, Sixt MK. Nuclear squeezing wakes up dendritic cells. Nature Immunology.
2024;25:1131–1132. doi:10.1038/s41590-024-01881-2
apa: Lembo, S., & Sixt, M. K. (2024). Nuclear squeezing wakes up dendritic cells.
Nature Immunology. Springer Nature. https://doi.org/10.1038/s41590-024-01881-2
chicago: Lembo, Sergio, and Michael K Sixt. “Nuclear Squeezing Wakes up Dendritic
Cells.” Nature Immunology. Springer Nature, 2024. https://doi.org/10.1038/s41590-024-01881-2.
ieee: S. Lembo and M. K. Sixt, “Nuclear squeezing wakes up dendritic cells,” Nature
Immunology, vol. 25. Springer Nature, pp. 1131–1132, 2024.
ista: Lembo S, Sixt MK. 2024. Nuclear squeezing wakes up dendritic cells. Nature
Immunology. 25, 1131–1132.
mla: Lembo, Sergio, and Michael K. Sixt. “Nuclear Squeezing Wakes up Dendritic Cells.”
Nature Immunology, vol. 25, Springer Nature, 2024, pp. 1131–1132, doi:10.1038/s41590-024-01881-2.
short: S. Lembo, M.K. Sixt, Nature Immunology 25 (2024) 1131–1132.
corr_author: '1'
date_created: 2024-06-30T22:01:05Z
date_published: 2024-06-21T00:00:00Z
date_updated: 2025-09-08T08:06:56Z
day: '21'
department:
- _id: MiSi
doi: 10.1038/s41590-024-01881-2
external_id:
isi:
- '001251509300001'
pmid:
- '38907047'
intvolume: ' 25'
isi: 1
language:
- iso: eng
month: '06'
oa_version: None
page: '1131–1132 '
pmid: 1
publication: Nature Immunology
publication_identifier:
eissn:
- 1529-2916
issn:
- 1529-2908
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nuclear squeezing wakes up dendritic cells
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 25
year: '2024'
...
---
_id: '17233'
abstract:
- lang: eng
text: CRISPR-Cas9 technology has become an essential tool for plant genome editing.
Recent advancements have significantly improved the ability to target multiple
genes simultaneously within the same genetic background through various strategies.
Additionally, there has been significant progress in developing methods for inducible
or tissue-specific editing. These advancements offer numerous possibilities for
tailored genome modifications. Building upon existing research, we have developed
an optimized and modular strategy allowing the targeting of several genes simultaneously
in combination with the synchronized expression of the Cas9 endonuclease in the
egg cell. This system allows significant editing efficiency while avoiding mosaicism.
In addition, the versatile system we propose allows adaptation to inducible and/or
tissue-specific edition according to the promoter chosen to drive the expression
of the Cas9 gene. Here, we describe a step-by-step protocol for generating the
binary vector necessary for establishing Arabidopsis edited lines using a versatile
cloning strategy that combines Gateway® and Golden Gate technologies. We describe
a versatile system that allows the cloning of as many guides as needed to target
DNA, which can be multiplexed into a polycistronic gene and combined in the same
construct with sequences for the expression of the Cas9 endonuclease. The expression
of Cas9 is controlled by selecting from among a collection of promoters, including
constitutive, inducible, ubiquitous, or tissue-specific promoters. Only one vector
containing the polycistronic gene (tRNA-sgRNA) needs to be constructed. For that,
sgRNA (composed of protospacers chosen to target the gene of interest and sgRNA
scaffold) is cloned in tandem with the pre-tRNA sequence. Then, a single recombination
reaction is required to assemble the promoter, the zCas9 coding sequence, and
the tRNA-gRNA polycistronic gene. Each element is cloned in an entry vector and
finally assembled according to the Multisite Gateway® Technology. Here, we detail
the process to express zCas9 under the control of egg cell promoter fused to enhancer
sequence (EC1.2en-EC1.1p) and to simultaneously target two multiple C2 domains
and transmembrane region protein genes (MCTP3 and MCTP4, respectively at3g57880
and at1g51570), using one or two sgRNA per gene.
acknowledgement: This work was supported by the European Research Council (ERC) under
the European Union’s Horizon 2020 research and innovation program (project 772103-BRIDGING
to E.M.B.).
article_number: e5029
article_processing_charge: Yes
article_type: original
author:
- first_name: Ziqiang
full_name: Li, Ziqiang
id: 922e68bb-1727-11ee-857c-966e8cc1b6c3
last_name: Li
- first_name: Jennifer
full_name: Huard, Jennifer
last_name: Huard
- first_name: Emmanuelle M.
full_name: Bayer, Emmanuelle M.
last_name: Bayer
- first_name: Valérie
full_name: Wattelet-Boyer, Valérie
last_name: Wattelet-Boyer
citation:
ama: LI Z, Huard J, Bayer EM, Wattelet-Boyer V. Versatile cloning strategy for efficient
multigene editing in Arabidopsis. Bio-protocol. 2024;14(13). doi:10.21769/BioProtoc.5029
apa: LI, Z., Huard, J., Bayer, E. M., & Wattelet-Boyer, V. (2024). Versatile
cloning strategy for efficient multigene editing in Arabidopsis. Bio-Protocol.
Bio-Protocol. https://doi.org/10.21769/BioProtoc.5029
chicago: LI, ZIQIANG, Jennifer Huard, Emmanuelle M. Bayer, and Valérie Wattelet-Boyer.
“Versatile Cloning Strategy for Efficient Multigene Editing in Arabidopsis.” Bio-Protocol.
Bio-Protocol, 2024. https://doi.org/10.21769/BioProtoc.5029.
ieee: Z. LI, J. Huard, E. M. Bayer, and V. Wattelet-Boyer, “Versatile cloning strategy
for efficient multigene editing in Arabidopsis,” Bio-protocol, vol. 14,
no. 13. Bio-Protocol, 2024.
ista: LI Z, Huard J, Bayer EM, Wattelet-Boyer V. 2024. Versatile cloning strategy
for efficient multigene editing in Arabidopsis. Bio-protocol. 14(13), e5029.
mla: LI, ZIQIANG, et al. “Versatile Cloning Strategy for Efficient Multigene Editing
in Arabidopsis.” Bio-Protocol, vol. 14, no. 13, e5029, Bio-Protocol, 2024,
doi:10.21769/BioProtoc.5029.
short: Z. LI, J. Huard, E.M. Bayer, V. Wattelet-Boyer, Bio-Protocol 14 (2024).
date_created: 2024-07-14T22:01:11Z
date_published: 2024-07-05T00:00:00Z
date_updated: 2025-03-06T10:28:18Z
day: '05'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.21769/BioProtoc.5029
external_id:
pmid:
- '39007160'
file:
- access_level: open_access
checksum: c8671c0ad483da6407cb16cc3fef1990
content_type: application/pdf
creator: dernst
date_created: 2024-07-16T06:16:11Z
date_updated: 2024-07-16T06:16:11Z
file_id: '17242'
file_name: 2024_BioProtocol_Li.pdf
file_size: 2896048
relation: main_file
success: 1
file_date_updated: 2024-07-16T06:16:11Z
has_accepted_license: '1'
intvolume: ' 14'
issue: '13'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: Bio-protocol
publication_identifier:
eissn:
- 2331-8325
publication_status: published
publisher: Bio-Protocol
quality_controlled: '1'
scopus_import: '1'
status: public
title: Versatile cloning strategy for efficient multigene editing in Arabidopsis
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: '2024'
...
---
_id: '17279'
abstract:
- lang: eng
text: In a recent issue of Cell, Zhang et al.1 demonstrate that mechanical features
of a solid tumor can drive T cells into dysfunctionality and identify pathways
that revert this “exhausted” state.
article_processing_charge: No
article_type: review
author:
- first_name: Mario
full_name: Avellaneda Sarrió, Mario
id: DC4BA84C-56E6-11EA-AD5D-348C3DDC885E
last_name: Avellaneda Sarrió
orcid: 0000-0001-6406-524X
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Avellaneda Sarrió M, Sixt MK. Rescuing T cells from stiff tumors. Cell Chemical
Biology. 2024;31(7):1242-1243. doi:10.1016/j.chembiol.2024.06.011
apa: Avellaneda Sarrió, M., & Sixt, M. K. (2024). Rescuing T cells from stiff
tumors. Cell Chemical Biology. Elsevier. https://doi.org/10.1016/j.chembiol.2024.06.011
chicago: Avellaneda Sarrió, Mario, and Michael K Sixt. “Rescuing T Cells from Stiff
Tumors.” Cell Chemical Biology. Elsevier, 2024. https://doi.org/10.1016/j.chembiol.2024.06.011.
ieee: M. Avellaneda Sarrió and M. K. Sixt, “Rescuing T cells from stiff tumors,”
Cell Chemical Biology, vol. 31, no. 7. Elsevier, pp. 1242–1243, 2024.
ista: Avellaneda Sarrió M, Sixt MK. 2024. Rescuing T cells from stiff tumors. Cell
Chemical Biology. 31(7), 1242–1243.
mla: Avellaneda Sarrió, Mario, and Michael K. Sixt. “Rescuing T Cells from Stiff
Tumors.” Cell Chemical Biology, vol. 31, no. 7, Elsevier, 2024, pp. 1242–43,
doi:10.1016/j.chembiol.2024.06.011.
short: M. Avellaneda Sarrió, M.K. Sixt, Cell Chemical Biology 31 (2024) 1242–1243.
corr_author: '1'
date_created: 2024-07-21T22:01:00Z
date_published: 2024-07-18T00:00:00Z
date_updated: 2025-09-08T08:27:03Z
day: '18'
department:
- _id: MiSi
doi: 10.1016/j.chembiol.2024.06.011
external_id:
isi:
- '001275725000001'
pmid:
- '39029454'
intvolume: ' 31'
isi: 1
issue: '7'
language:
- iso: eng
month: '07'
oa_version: None
page: 1242-1243
pmid: 1
publication: Cell Chemical Biology
publication_identifier:
eissn:
- 2451-9448
issn:
- 2451-9456
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Rescuing T cells from stiff tumors
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 31
year: '2024'
...
---
_id: '17284'
abstract:
- lang: eng
text: Platelet homeostasis is essential for vascular integrity and immune defence1,2.
Although the process of platelet formation by fragmenting megakaryocytes (MKs;
thrombopoiesis) has been extensively studied, the cellular and molecular mechanisms
required to constantly replenish the pool of MKs by their progenitor cells (megakaryopoiesis)
remains unclear3,4. Here we use intravital imaging to track the cellular dynamics
of megakaryopoiesis over days. We identify plasmacytoid dendritic cells (pDCs)
as homeostatic sensors that monitor the bone marrow for apoptotic MKs and deliver
IFNα to the MK niche triggering local on-demand proliferation and maturation of
MK progenitors. This pDC-dependent feedback loop is crucial for MK and platelet
homeostasis at steady state and under stress. pDCs are best known for their ability
to function as vigilant detectors of viral infection5. We show that virus-induced
activation of pDCs interferes with their function as homeostatic sensors of megakaryopoiesis.
Consequently, activation of pDCs by SARS-CoV-2 leads to excessive megakaryopoiesis.
Together, we identify a pDC-dependent homeostatic circuit that involves innate
immune sensing and demand-adapted release of inflammatory mediators to maintain
homeostasis of the megakaryocytic lineage.
acknowledgement: 'We thank S. Helmer, N. Blount, E. Raatz and Z. Sisic for technical
assistance. This work was funded by the Deutsche Forschungsgemeinschaft (DFG, German
Research Foundation) SFB 1123 (S.M. project B06); SFB 914 (S.M. projects B02 and
Z01, H.I.-A. project Z01, S.S. project A06, K.S. project B02, C. Schulz project
A10, B.W. project A02, C. Scheiermann project B09); SFB 1054 (T.B. project B03);
FOR2033 (F.G., R.A.J.O., S.M.); Individual research grant project ID: 514478744
(F.G.); Heisenberg Programme project ID: 514477451 (F.G.); the DZHK (German Center
for Cardiovascular Research) (MHA 1.4VD (S.M.), Postdoc Start-up Grant, 81×3600213
(F.G.)); and LMUexcellence NFF (F.G.). W.F. received funding from China Scholarship
Council (CSC, no. 201306270012). P.B. is supported by the German Research Foundation
(DFG, project IDs 322900939, 432698239 and 445703531), European Research Council
(ERC Consolidator grant no. 101001791) and the Federal Ministry of Education and
Research (BMBF, STOP-FSGS-01GM2202C and NATON within the framework of the Network
of University Medicine, no. 01KX2121). S.v.S. is supported by the START-Program
of the Faculty of Medicine of the RWTH Aachen University (AZ 125/17). A.D. and S.E.
are supported by the German Research Foundation (SFB TRR 267); S.E. by the BMBF
in the framework of the Cluster4future program (CNATM—Cluster for Nucleic Acid Therapeutics
Munich). 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. 833440 to S.M.). F.G. received funding from the European Union’s Horizon
2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement
no. 747687. The project is funded by the European Union (ERC, MEKanics, 101078110).
Views and opinions expressed are those of the author(s) only and do not necessarily
reflect those of the European Union or the European Research Council Executive Agency.
Neither the European Union nor the granting authority can be held responsible for
them.'
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Hellen
full_name: Ishikawa-Ankerhold, Hellen
last_name: Ishikawa-Ankerhold
- first_name: Susanne
full_name: Stutte, Susanne
last_name: Stutte
- first_name: Wenwen
full_name: Fu, Wenwen
last_name: Fu
- first_name: Jutta
full_name: Weitz, Jutta
last_name: Weitz
- first_name: Anne
full_name: Dueck, Anne
last_name: Dueck
- first_name: Bhavishya
full_name: Nelakuditi, Bhavishya
last_name: Nelakuditi
- first_name: Valeria
full_name: Fumagalli, Valeria
last_name: Fumagalli
- first_name: Dominic
full_name: Van Den Heuvel, Dominic
last_name: Van Den Heuvel
- first_name: Larissa
full_name: Belz, Larissa
last_name: Belz
- first_name: Gulnoza
full_name: Sobirova, Gulnoza
last_name: Sobirova
- first_name: Zhe
full_name: Zhang, Zhe
last_name: Zhang
- first_name: Anna
full_name: Titova, Anna
last_name: Titova
- first_name: Alejandro Martinez
full_name: Navarro, Alejandro Martinez
last_name: Navarro
- first_name: Kami
full_name: Pekayvaz, Kami
last_name: Pekayvaz
- first_name: Michael
full_name: Lorenz, Michael
last_name: Lorenz
- first_name: Louisa
full_name: Von Baumgarten, Louisa
last_name: Von Baumgarten
- first_name: Jan
full_name: Kranich, Jan
last_name: Kranich
- first_name: Tobias
full_name: Straub, Tobias
last_name: Straub
- first_name: Bastian
full_name: Popper, Bastian
last_name: Popper
- first_name: Vanessa
full_name: Zheden, Vanessa
id: 39C5A68A-F248-11E8-B48F-1D18A9856A87
last_name: Zheden
orcid: 0000-0002-9438-4783
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Chenglong
full_name: Guo, Chenglong
last_name: Guo
- first_name: Guido
full_name: Piontek, Guido
last_name: Piontek
- first_name: Saskia
full_name: Von Stillfried, Saskia
last_name: Von Stillfried
- first_name: Peter
full_name: Boor, Peter
last_name: Boor
- first_name: Marco
full_name: Colonna, Marco
last_name: Colonna
- first_name: Sebastian
full_name: Clauß, Sebastian
last_name: Clauß
- first_name: Christian
full_name: Schulz, Christian
last_name: Schulz
- first_name: Thomas
full_name: Brocker, Thomas
last_name: Brocker
- first_name: Barbara
full_name: Walzog, Barbara
last_name: Walzog
- first_name: Christoph
full_name: Scheiermann, Christoph
last_name: Scheiermann
- first_name: William C.
full_name: Aird, William C.
last_name: Aird
- first_name: Claus
full_name: Nerlov, Claus
last_name: Nerlov
- first_name: Konstantin
full_name: Stark, Konstantin
last_name: Stark
- first_name: Tobias
full_name: Petzold, Tobias
last_name: Petzold
- first_name: Stefan
full_name: Engelhardt, Stefan
last_name: Engelhardt
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Martina
full_name: Rudelius, Martina
last_name: Rudelius
- first_name: Robert A.J.
full_name: Oostendorp, Robert A.J.
last_name: Oostendorp
- first_name: Matteo
full_name: Iannacone, Matteo
last_name: Iannacone
- first_name: Matthias
full_name: Heinig, Matthias
last_name: Heinig
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
citation:
ama: Gärtner FR, Ishikawa-Ankerhold H, Stutte S, et al. Plasmacytoid dendritic cells
control homeostasis of megakaryopoiesis. Nature. 2024;631:645-653. doi:10.1038/s41586-024-07671-y
apa: Gärtner, F. R., Ishikawa-Ankerhold, H., Stutte, S., Fu, W., Weitz, J., Dueck,
A., … Massberg, S. (2024). Plasmacytoid dendritic cells control homeostasis of
megakaryopoiesis. Nature. Springer Nature. https://doi.org/10.1038/s41586-024-07671-y
chicago: Gärtner, Florian R, Hellen Ishikawa-Ankerhold, Susanne Stutte, Wenwen Fu,
Jutta Weitz, Anne Dueck, Bhavishya Nelakuditi, et al. “Plasmacytoid Dendritic
Cells Control Homeostasis of Megakaryopoiesis.” Nature. Springer Nature,
2024. https://doi.org/10.1038/s41586-024-07671-y.
ieee: F. R. Gärtner et al., “Plasmacytoid dendritic cells control homeostasis
of megakaryopoiesis,” Nature, vol. 631. Springer Nature, pp. 645–653, 2024.
ista: Gärtner FR, Ishikawa-Ankerhold H, Stutte S, Fu W, Weitz J, Dueck A, Nelakuditi
B, Fumagalli V, Van Den Heuvel D, Belz L, Sobirova G, Zhang Z, Titova A, Navarro
AM, Pekayvaz K, Lorenz M, Von Baumgarten L, Kranich J, Straub T, Popper B, Zheden
V, Kaufmann W, Guo C, Piontek G, Von Stillfried S, Boor P, Colonna M, Clauß S,
Schulz C, Brocker T, Walzog B, Scheiermann C, Aird WC, Nerlov C, Stark K, Petzold
T, Engelhardt S, Sixt MK, Hauschild R, Rudelius M, Oostendorp RAJ, Iannacone M,
Heinig M, Massberg S. 2024. Plasmacytoid dendritic cells control homeostasis of
megakaryopoiesis. Nature. 631, 645–653.
mla: Gärtner, Florian R., et al. “Plasmacytoid Dendritic Cells Control Homeostasis
of Megakaryopoiesis.” Nature, vol. 631, Springer Nature, 2024, pp. 645–53,
doi:10.1038/s41586-024-07671-y.
short: F.R. Gärtner, H. Ishikawa-Ankerhold, S. Stutte, W. Fu, J. Weitz, A. Dueck,
B. Nelakuditi, V. Fumagalli, D. Van Den Heuvel, L. Belz, G. Sobirova, Z. Zhang,
A. Titova, A.M. Navarro, K. Pekayvaz, M. Lorenz, L. Von Baumgarten, J. Kranich,
T. Straub, B. Popper, V. Zheden, W. Kaufmann, C. Guo, G. Piontek, S. Von Stillfried,
P. Boor, M. Colonna, S. Clauß, C. Schulz, T. Brocker, B. Walzog, C. Scheiermann,
W.C. Aird, C. Nerlov, K. Stark, T. Petzold, S. Engelhardt, M.K. Sixt, R. Hauschild,
M. Rudelius, R.A.J. Oostendorp, M. Iannacone, M. Heinig, S. Massberg, Nature 631
(2024) 645–653.
corr_author: '1'
date_created: 2024-07-21T22:01:02Z
date_published: 2024-07-18T00:00:00Z
date_updated: 2025-09-08T08:14:25Z
day: '18'
ddc:
- '570'
department:
- _id: EM-Fac
- _id: MiSi
- _id: Bio
doi: 10.1038/s41586-024-07671-y
ec_funded: 1
external_id:
isi:
- '001281636500020'
pmid:
- '38987596'
file:
- access_level: open_access
checksum: aa004afc72d2489f0fb0fcbc9919fbbd
content_type: application/pdf
creator: dernst
date_created: 2024-07-22T06:16:11Z
date_updated: 2024-07-22T06:16:11Z
file_id: '17286'
file_name: 2024_Nature_Gaertner.pdf
file_size: 15704819
relation: main_file
success: 1
file_date_updated: 2024-07-22T06:16:11Z
has_accepted_license: '1'
intvolume: ' 631'
isi: 1
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: 645-653
pmid: 1
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: software
url: https://github.com/heiniglab/gaertner_megakaryocytes
scopus_import: '1'
status: public
title: Plasmacytoid dendritic cells control homeostasis of megakaryopoiesis
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 631
year: '2024'
...