---
_id: '15048'
abstract:
- lang: eng
text: Embryogenesis results from the coordinated activities of different signaling
pathways controlling cell fate specification and morphogenesis. In vertebrate
gastrulation, both Nodal and BMP signaling play key roles in germ layer specification
and morphogenesis, yet their interplay to coordinate embryo patterning with morphogenesis
is still insufficiently understood. Here, we took a reductionist approach using
zebrafish embryonic explants to study the coordination of Nodal and BMP signaling
for embryo patterning and morphogenesis. We show that Nodal signaling triggers
explant elongation by inducing mesendodermal progenitors but also suppressing
BMP signaling activity at the site of mesendoderm induction. Consistent with this,
ectopic BMP signaling in the mesendoderm blocks cell alignment and oriented mesendoderm
intercalations, key processes during explant elongation. Translating these ex
vivo observations to the intact embryo showed that, similar to explants, Nodal
signaling suppresses the effect of BMP signaling on cell intercalations in the
dorsal domain, thus allowing robust embryonic axis elongation. These findings
suggest a dual function of Nodal signaling in embryonic axis elongation by both
inducing mesendoderm and suppressing BMP effects in the dorsal portion of the
mesendoderm.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
acknowledgement: "We thank Patrick Müller for sharing the chordintt250 mutant zebrafish
line as well as the plasmid for chrd-GFP, Katherine Rogers for sharing the bmp2b
plasmid and Andrea Pauli for sharing the draculin plasmid. Diana Pinheiro generated
the MZlefty1,2;Tg(sebox::EGFP) line. We are grateful to Patrick Müller, Diana Pinheiro
and Katherine Rogers and members of the Heisenberg lab for discussions, technical
advice and feedback on the manuscript. We also thank Anna Kicheva and Edouard Hannezo
for discussions. We thank the Imaging and Optics Facility as well as the Life Science
facility at IST Austria for support with microscopy and fish maintenance.\r\nThis
work was supported by a European Research Council Advanced Grant\r\n(MECSPEC 742573
to C.-P.H.). A.S. is a recipient of a DOC Fellowship of the Austrian\r\nAcademy
of Sciences at IST Austria. Open Access funding provided by Institute of\r\nScience
and Technology Austria. "
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Alexandra
full_name: Schauer, Alexandra
id: 30A536BA-F248-11E8-B48F-1D18A9856A87
last_name: Schauer
orcid: 0000-0001-7659-9142
- first_name: Kornelija
full_name: Pranjic-Ferscha, Kornelija
id: 4362B3C2-F248-11E8-B48F-1D18A9856A87
last_name: Pranjic-Ferscha
- 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: Schauer A, Pranjic-Ferscha K, Hauschild R, Heisenberg C-PJ. Robust axis elongation
by Nodal-dependent restriction of BMP signaling. Development. 2024;151(4):1-18.
doi:10.1242/dev.202316
apa: Schauer, A., Pranjic-Ferscha, K., Hauschild, R., & Heisenberg, C.-P. J.
(2024). Robust axis elongation by Nodal-dependent restriction of BMP signaling.
Development. Company of Biologists. https://doi.org/10.1242/dev.202316
chicago: Schauer, Alexandra, Kornelija Pranjic-Ferscha, Robert Hauschild, and Carl-Philipp
J Heisenberg. “Robust Axis Elongation by Nodal-Dependent Restriction of BMP Signaling.”
Development. Company of Biologists, 2024. https://doi.org/10.1242/dev.202316.
ieee: A. Schauer, K. Pranjic-Ferscha, R. Hauschild, and C.-P. J. Heisenberg, “Robust
axis elongation by Nodal-dependent restriction of BMP signaling,” Development,
vol. 151, no. 4. Company of Biologists, pp. 1–18, 2024.
ista: Schauer A, Pranjic-Ferscha K, Hauschild R, Heisenberg C-PJ. 2024. Robust axis
elongation by Nodal-dependent restriction of BMP signaling. Development. 151(4),
1–18.
mla: Schauer, Alexandra, et al. “Robust Axis Elongation by Nodal-Dependent Restriction
of BMP Signaling.” Development, vol. 151, no. 4, Company of Biologists,
2024, pp. 1–18, doi:10.1242/dev.202316.
short: A. Schauer, K. Pranjic-Ferscha, R. Hauschild, C.-P.J. Heisenberg, Development
151 (2024) 1–18.
corr_author: '1'
das_tickbox: '1'
dataavailabilitystatement: A custom MATLAB script for analyzing cell dispersal has
been deposited in the ISTA library (doi:10.15479/AT:ISTA:14926)
date_created: 2024-03-03T23:00:50Z
date_published: 2024-02-01T00:00:00Z
date_updated: 2026-10-01T08:32:34Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
- _id: Bio
doi: 10.1242/dev.202316
ec_funded: 1
external_id:
isi:
- '001170580200001'
pmid:
- '38372390'
file:
- access_level: open_access
checksum: 6961ea10012bf0d266681f9628bb8f13
content_type: application/pdf
creator: dernst
date_created: 2024-03-04T07:24:43Z
date_updated: 2024-03-04T07:24:43Z
file_id: '15050'
file_name: 2024_Development_Schauer.pdf
file_size: 14839986
relation: main_file
success: 1
file_date_updated: 2024-03-04T07:24:43Z
fulldoi: https://doi.org/10.1242/dev.202316
has_accepted_license: '1'
intvolume: ' 151'
isi: 1
issue: '4'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '02'
oa: 1
oa_version: Published Version
page: 1-18
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
- _id: 26B1E39C-B435-11E9-9278-68D0E5697425
grant_number: '25239'
name: 'Mesendoderm specification in zebrafish: The role of extraembryonic tissues'
publication: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
quality_controlled: '1'
related_material:
record:
- id: '14926'
relation: research_data
status: public
researchdata_availability: yes
scopus_import: '1'
status: public
supplementarymaterial: yes
title: Robust axis elongation by Nodal-dependent restriction of BMP signaling
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: 151
year: '2024'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '18940'
abstract:
- lang: eng
text: BMP signaling has a conserved function in patterning the dorsal-ventral body
axis in Bilateria and the directive axis in anthozoan cnidarians. So far, cnidarian
studies have focused on the role of different BMP signaling network components
in regulating pSMAD1/5 gradient formation. Much less is known about the target
genes downstream of BMP signaling. To address this, we generated a genome-wide
list of direct pSMAD1/5 target genes in the anthozoan Nematostella
vectensis, several of which were conserved in Drosophila
and Xenopus. Our ChIP-seq analysis revealed that many
of the regulatory molecules with documented bilaterally symmetric expression in
Nematostella are directly controlled by BMP signaling.
We identified several so far uncharacterized BMP-dependent transcription factors
and signaling molecules, whose bilaterally symmetric expression may be indicative
of their involvement in secondary axis patterning. One of these molecules is zswim4-6,
which encodes a novel nuclear protein that can modulate the pSMAD1/5 gradient
and potentially promote BMP-dependent gene repression.
acknowledgement: This work was funded by the Austrian Science Foundation (FWF) grants
P26962-B21 and P32705-B to GG and by the European Research Council (ERC) under the
European Union’s Horizon 2020 research and innovation program (grant agreement No
637840 [QUANTPATTERN] and 863952 [ACE-OF-SPACE]) to PM. We thank Michaela Schwaiger,
Taras Kreslavsky, Hiromi Tagoh, and Patricio Ferrer Murguia for their help with
the ChIP protocol, Matthias Richter and Christian Hofer for their assistance with
in situ analyses, Emilio Gonzalez Morales for making the measurements for Figure
6—figure supplement 3, Catrin Weiler for the assistance in cloning zebrafish zswim5,
David Mörsdorf for critically reading the manuscript and help with data visualization,
and the Core Facility for Cell Imaging and Ultrastructure Research of the University
of Vienna for access to the confocal microscope.
article_processing_charge: Yes
article_type: original
author:
- first_name: Paul
full_name: Knabl, Paul
last_name: Knabl
- first_name: Alexandra
full_name: Schauer, Alexandra
id: 30A536BA-F248-11E8-B48F-1D18A9856A87
last_name: Schauer
orcid: 0000-0001-7659-9142
- first_name: Autumn P
full_name: Pomreinke, Autumn P
last_name: Pomreinke
- first_name: Bob
full_name: Zimmermann, Bob
last_name: Zimmermann
- first_name: Katherine W
full_name: Rogers, Katherine W
last_name: Rogers
- first_name: Daniel
full_name: Čapek, Daniel
last_name: Čapek
- first_name: Patrick
full_name: Müller, Patrick
last_name: Müller
- first_name: Grigory
full_name: Genikhovich, Grigory
last_name: Genikhovich
citation:
ama: Knabl P, Schauer A, Pomreinke AP, et al. Analysis of SMAD1/5 target genes in
a sea anemone reveals ZSWIM4-6 as a novel BMP signaling modulator. eLife.
2024;13. doi:10.7554/elife.80803
apa: Knabl, P., Schauer, A., Pomreinke, A. P., Zimmermann, B., Rogers, K. W., Čapek,
D., … Genikhovich, G. (2024). Analysis of SMAD1/5 target genes in a sea anemone
reveals ZSWIM4-6 as a novel BMP signaling modulator. ELife. eLife Sciences
Publications. https://doi.org/10.7554/elife.80803
chicago: Knabl, Paul, Alexandra Schauer, Autumn P Pomreinke, Bob Zimmermann, Katherine
W Rogers, Daniel Čapek, Patrick Müller, and Grigory Genikhovich. “Analysis of
SMAD1/5 Target Genes in a Sea Anemone Reveals ZSWIM4-6 as a Novel BMP Signaling
Modulator.” ELife. eLife Sciences Publications, 2024. https://doi.org/10.7554/elife.80803.
ieee: P. Knabl et al., “Analysis of SMAD1/5 target genes in a sea anemone
reveals ZSWIM4-6 as a novel BMP signaling modulator,” eLife, vol. 13. eLife
Sciences Publications, 2024.
ista: Knabl P, Schauer A, Pomreinke AP, Zimmermann B, Rogers KW, Čapek D, Müller
P, Genikhovich G. 2024. Analysis of SMAD1/5 target genes in a sea anemone reveals
ZSWIM4-6 as a novel BMP signaling modulator. eLife. 13.
mla: Knabl, Paul, et al. “Analysis of SMAD1/5 Target Genes in a Sea Anemone Reveals
ZSWIM4-6 as a Novel BMP Signaling Modulator.” ELife, vol. 13, eLife Sciences
Publications, 2024, doi:10.7554/elife.80803.
short: P. Knabl, A. Schauer, A.P. Pomreinke, B. Zimmermann, K.W. Rogers, D. Čapek,
P. Müller, G. Genikhovich, ELife 13 (2024).
das_tickbox: '1'
dataavailabilitystatement: The data generated or analysed during this study are included
in the manuscript and supporting files. Source data files have been provided for
Figure 6D-F', Figure 6Q, Figure 5—figure supplement 1D, Figure 6—figure supplement
2G, Figure 6—figure supplement 3E and F. All the sequencing data are available at
NCBI as an SRA project PRJNA820593.
date_created: 2025-01-29T08:48:34Z
date_published: 2024-02-07T00:00:00Z
date_updated: 2026-10-01T08:31:50Z
day: '07'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.7554/elife.80803
file:
- access_level: open_access
checksum: 24548a184215d3f4547bba535ccfd7b1
content_type: application/pdf
creator: dernst
date_created: 2025-01-29T08:50:18Z
date_updated: 2025-01-29T08:50:18Z
file_id: '18941'
file_name: 2024_eLife_Knabl.pdf
file_size: 11855972
relation: main_file
success: 1
file_date_updated: 2025-01-29T08:50:18Z
fulldoi: https://doi.org/10.7554/elife.80803
has_accepted_license: '1'
intvolume: ' 13'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
researchdata_availability: yes
scopus_import: '1'
status: public
supplementarymaterial: no
title: Analysis of SMAD1/5 target genes in a sea anemone reveals ZSWIM4-6 as a novel
BMP signaling modulator
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: 13
year: '2024'
...
---
_id: '12830'
abstract:
- lang: eng
text: Interstitial fluid (IF) accumulation between embryonic cells is thought to
be important for embryo patterning and morphogenesis. Here, we identify a positive
mechanical feedback loop between cell migration and IF relocalization and find
that it promotes embryonic axis formation during zebrafish gastrulation. We show
that anterior axial mesendoderm (prechordal plate [ppl]) cells, moving in between
the yolk cell and deep cell tissue to extend the embryonic axis, compress the
overlying deep cell layer, thereby causing IF to flow from the deep cell layer
to the boundary between the yolk cell and the deep cell layer, directly ahead
of the advancing ppl. This IF relocalization, in turn, facilitates ppl cell protrusion
formation and migration by opening up the space into which the ppl moves and,
thereby, the ability of the ppl to trigger IF relocalization by pushing against
the overlying deep cell layer. Thus, embryonic axis formation relies on a hydraulic
feedback loop between cell migration and IF relocalization.
acknowledged_ssus:
- _id: PreCl
- _id: Bio
acknowledgement: We thank Andrea Pauli (IMP) and Edouard Hannezo (ISTA) for fruitful
discussions and support with the SPIM experiments; the Heisenberg group, and especially
Feyza Nur Arslan and Alexandra Schauer, for discussions and feedback; Michaela Jović
(ISTA) for help with the quantitative real-time PCR protocol; the bioimaging and
zebrafish facilities of ISTA for continuous support; Stephan Preibisch (Janelia
Research Campus) for support with the SPIM data analysis; and Nobuhiro Nakamura
(Tokyo Institute of Technology) for sharing α1-Na+/K+-ATPase antibody. This work
was supported by funding from the European Union (European Research Council Advanced
grant 742573 to C.-P.H.), postdoctoral fellowships from EMBO (LTF-850-2017) and
HFSP (LT000429/2018-L2) to D.P., and a PhD fellowship from the Studienstiftung des
deutschen Volkes to F.P.
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Karla
full_name: Huljev, Karla
id: 44C6F6A6-F248-11E8-B48F-1D18A9856A87
last_name: Huljev
- first_name: Shayan
full_name: Shamipour, Shayan
id: 40B34FE2-F248-11E8-B48F-1D18A9856A87
last_name: Shamipour
- first_name: Diana C
full_name: Nunes Pinheiro, Diana C
id: 2E839F16-F248-11E8-B48F-1D18A9856A87
last_name: Nunes Pinheiro
orcid: 0000-0003-4333-7503
- first_name: Friedrich
full_name: Preusser, Friedrich
last_name: Preusser
- first_name: Irene
full_name: Steccari, Irene
id: 2705C766-9FE2-11EA-B224-C6773DDC885E
last_name: Steccari
- first_name: Christoph M
full_name: Sommer, Christoph M
id: 4DF26D8C-F248-11E8-B48F-1D18A9856A87
last_name: Sommer
orcid: 0000-0003-1216-9105
- first_name: Suyash
full_name: Naik, Suyash
id: 2C0B105C-F248-11E8-B48F-1D18A9856A87
last_name: Naik
orcid: 0000-0001-8421-5508
- 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: Huljev K, Shamipour S, Nunes Pinheiro DC, et al. A hydraulic feedback loop
between mesendoderm cell migration and interstitial fluid relocalization promotes
embryonic axis formation in zebrafish. Developmental Cell. 2023;58(7):582-596.e7.
doi:10.1016/j.devcel.2023.02.016
apa: Huljev, K., Shamipour, S., Nunes Pinheiro, D. C., Preusser, F., Steccari, I.,
Sommer, C. M., … Heisenberg, C.-P. J. (2023). A hydraulic feedback loop between
mesendoderm cell migration and interstitial fluid relocalization promotes embryonic
axis formation in zebrafish. Developmental Cell. Elsevier. https://doi.org/10.1016/j.devcel.2023.02.016
chicago: Huljev, Karla, Shayan Shamipour, Diana C Nunes Pinheiro, Friedrich Preusser,
Irene Steccari, Christoph M Sommer, Suyash Naik, and Carl-Philipp J Heisenberg.
“A Hydraulic Feedback Loop between Mesendoderm Cell Migration and Interstitial
Fluid Relocalization Promotes Embryonic Axis Formation in Zebrafish.” Developmental
Cell. Elsevier, 2023. https://doi.org/10.1016/j.devcel.2023.02.016.
ieee: K. Huljev et al., “A hydraulic feedback loop between mesendoderm cell
migration and interstitial fluid relocalization promotes embryonic axis formation
in zebrafish,” Developmental Cell, vol. 58, no. 7. Elsevier, p. 582–596.e7,
2023.
ista: Huljev K, Shamipour S, Nunes Pinheiro DC, Preusser F, Steccari I, Sommer CM,
Naik S, Heisenberg C-PJ. 2023. A hydraulic feedback loop between mesendoderm cell
migration and interstitial fluid relocalization promotes embryonic axis formation
in zebrafish. Developmental Cell. 58(7), 582–596.e7.
mla: Huljev, Karla, et al. “A Hydraulic Feedback Loop between Mesendoderm Cell Migration
and Interstitial Fluid Relocalization Promotes Embryonic Axis Formation in Zebrafish.”
Developmental Cell, vol. 58, no. 7, Elsevier, 2023, p. 582–596.e7, doi:10.1016/j.devcel.2023.02.016.
short: K. Huljev, S. Shamipour, D.C. Nunes Pinheiro, F. Preusser, I. Steccari, C.M.
Sommer, S. Naik, C.-P.J. Heisenberg, Developmental Cell 58 (2023) 582–596.e7.
corr_author: '1'
date_created: 2023-04-16T22:01:07Z
date_published: 2023-04-10T00:00:00Z
date_updated: 2025-04-23T08:51:34Z
day: '10'
ddc:
- '570'
department:
- _id: CaHe
- _id: Bio
doi: 10.1016/j.devcel.2023.02.016
ec_funded: 1
external_id:
isi:
- '000982111800001'
pmid:
- '36931269'
file:
- access_level: open_access
checksum: c80ca2ebc241232aacdb5aa4b4c80957
content_type: application/pdf
creator: dernst
date_created: 2023-04-17T07:41:25Z
date_updated: 2023-04-17T07:41:25Z
file_id: '12842'
file_name: 2023_DevelopmentalCell_Huljev.pdf
file_size: 7925886
relation: main_file
success: 1
file_date_updated: 2023-04-17T07:41:25Z
fulldoi: https://doi.org/10.1016/j.devcel.2023.02.016
has_accepted_license: '1'
intvolume: ' 58'
isi: 1
issue: '7'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 582-596.e7
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
- _id: 26520D1E-B435-11E9-9278-68D0E5697425
grant_number: ALTF 850-2017
name: Coordination of mesendoderm cell fate specification and internalization during
zebrafish gastrulation
- _id: 266BC5CE-B435-11E9-9278-68D0E5697425
grant_number: LT000429
name: Coordination of mesendoderm fate specification and internalization during
zebrafish gastrulation
publication: Developmental Cell
publication_identifier:
eissn:
- 1878-1551
issn:
- 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: A hydraulic feedback loop between mesendoderm cell migration and interstitial
fluid relocalization promotes embryonic axis formation in zebrafish
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: 58
year: '2023'
...
---
_id: '13229'
abstract:
- lang: eng
text: Dynamic reorganization of the cytoplasm is key to many core cellular processes,
such as cell division, cell migration, and cell polarization. Cytoskeletal rearrangements
are thought to constitute the main drivers of cytoplasmic flows and reorganization.
In contrast, remarkably little is known about how dynamic changes in size and
shape of cell organelles affect cytoplasmic organization. Here, we show that within
the maturing zebrafish oocyte, the surface localization of exocytosis-competent
cortical granules (Cgs) upon germinal vesicle breakdown (GVBD) is achieved by
the combined activities of yolk granule (Yg) fusion and microtubule aster formation
and translocation. We find that Cgs are moved towards the oocyte surface through
radially outward cytoplasmic flows induced by Ygs fusing and compacting towards
the oocyte center in response to GVBD. We further show that vesicles decorated
with the small Rab GTPase Rab11, a master regulator of vesicular trafficking and
exocytosis, accumulate together with Cgs at the oocyte surface. This accumulation
is achieved by Rab11-positive vesicles being transported by acentrosomal microtubule
asters, the formation of which is induced by the release of CyclinB/Cdk1 upon
GVBD, and which display a net movement towards the oocyte surface by preferentially
binding to the oocyte actin cortex. We finally demonstrate that the decoration
of Cgs by Rab11 at the oocyte surface is needed for Cg exocytosis and subsequent
chorion elevation, a process central in egg activation. Collectively, these findings
unravel a yet unrecognized role of organelle fusion, functioning together with
cytoskeletal rearrangements, in orchestrating cytoplasmic organization during
oocyte maturation.
acknowledgement: This work was supported by funding from the European Union (European
Research Council Advanced grant 742573) to C.-P.H. The funders had no role in study
design, data collection and analysis, decision to publish, or preparation of the
manuscript.
article_processing_charge: No
article_type: original
author:
- first_name: Shayan
full_name: Shamipour, Shayan
id: 40B34FE2-F248-11E8-B48F-1D18A9856A87
last_name: Shamipour
- first_name: Laura
full_name: Hofmann, Laura
id: b88d43f2-dc74-11ea-a0a7-e41b7912e031
last_name: Hofmann
- first_name: Irene
full_name: Steccari, Irene
id: 2705C766-9FE2-11EA-B224-C6773DDC885E
last_name: Steccari
- first_name: Roland
full_name: Kardos, Roland
id: 4039350E-F248-11E8-B48F-1D18A9856A87
last_name: Kardos
- 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: Shamipour S, Hofmann L, Steccari I, Kardos R, Heisenberg C-PJ. Yolk granule
fusion and microtubule aster formation regulate cortical granule translocation
and exocytosis in zebrafish oocytes. PLoS Biology. 2023;21(6):e3002146.
doi:10.1371/journal.pbio.3002146
apa: Shamipour, S., Hofmann, L., Steccari, I., Kardos, R., & Heisenberg, C.-P.
J. (2023). Yolk granule fusion and microtubule aster formation regulate cortical
granule translocation and exocytosis in zebrafish oocytes. PLoS Biology.
Public Library of Science. https://doi.org/10.1371/journal.pbio.3002146
chicago: Shamipour, Shayan, Laura Hofmann, Irene Steccari, Roland Kardos, and Carl-Philipp
J Heisenberg. “Yolk Granule Fusion and Microtubule Aster Formation Regulate Cortical
Granule Translocation and Exocytosis in Zebrafish Oocytes.” PLoS Biology.
Public Library of Science, 2023. https://doi.org/10.1371/journal.pbio.3002146.
ieee: S. Shamipour, L. Hofmann, I. Steccari, R. Kardos, and C.-P. J. Heisenberg,
“Yolk granule fusion and microtubule aster formation regulate cortical granule
translocation and exocytosis in zebrafish oocytes,” PLoS Biology, vol.
21, no. 6. Public Library of Science, p. e3002146, 2023.
ista: Shamipour S, Hofmann L, Steccari I, Kardos R, Heisenberg C-PJ. 2023. Yolk
granule fusion and microtubule aster formation regulate cortical granule translocation
and exocytosis in zebrafish oocytes. PLoS Biology. 21(6), e3002146.
mla: Shamipour, Shayan, et al. “Yolk Granule Fusion and Microtubule Aster Formation
Regulate Cortical Granule Translocation and Exocytosis in Zebrafish Oocytes.”
PLoS Biology, vol. 21, no. 6, Public Library of Science, 2023, p. e3002146,
doi:10.1371/journal.pbio.3002146.
short: S. Shamipour, L. Hofmann, I. Steccari, R. Kardos, C.-P.J. Heisenberg, PLoS
Biology 21 (2023) e3002146.
corr_author: '1'
date_created: 2023-07-16T22:01:09Z
date_published: 2023-06-08T00:00:00Z
date_updated: 2025-04-14T07:46:59Z
day: '08'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1371/journal.pbio.3002146
ec_funded: 1
external_id:
isi:
- '001003199100005'
pmid:
- '37289834'
file:
- access_level: open_access
checksum: 8e88cb0e5a6433a2f1939a9030bed384
content_type: application/pdf
creator: dernst
date_created: 2023-07-18T07:59:58Z
date_updated: 2023-07-18T07:59:58Z
file_id: '13246'
file_name: 2023_PloSBiology_Shamipour.pdf
file_size: 4431723
relation: main_file
success: 1
file_date_updated: 2023-07-18T07:59:58Z
fulldoi: https://doi.org/10.1371/journal.pbio.3002146
has_accepted_license: '1'
intvolume: ' 21'
isi: 1
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: e3002146
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
publication: PLoS Biology
publication_identifier:
eissn:
- 1545-7885
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: Yolk granule fusion and microtubule aster formation regulate cortical granule
translocation and exocytosis in zebrafish oocytes
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 21
year: '2023'
...
---
_id: '14041'
abstract:
- lang: eng
text: Tissue morphogenesis and patterning during development involve the segregation
of cell types. Segregation is driven by differential tissue surface tensions generated
by cell types through controlling cell-cell contact formation by regulating adhesion
and actomyosin contractility-based cellular cortical tensions. We use vertebrate
tissue cell types and zebrafish germ layer progenitors as in vitro models of 3-dimensional
heterotypic segregation and developed a quantitative analysis of their dynamics
based on 3D time-lapse microscopy. We show that general inhibition of actomyosin
contractility by the Rho kinase inhibitor Y27632 delays segregation. Cell type-specific
inhibition of non-muscle myosin2 activity by overexpression of myosin assembly
inhibitor S100A4 reduces tissue surface tension, manifested in decreased compaction
during aggregation and inverted geometry observed during segregation. The same
is observed when we express a constitutively active Rho kinase isoform to ubiquitously
keep actomyosin contractility high at cell-cell and cell-medium interfaces and
thus overriding the interface-specific regulation of cortical tensions. Tissue
surface tension regulation can become an effective tool in tissue engineering.
acknowledgement: "We thank Marton Gulyas (ELTE Eötvös University) for development
of videomicroscopy experiment manager and image analysis software. Authors are grateful
to Gabor Forgacs (University of Missouri) for critical reading of earlier versions
of this manuscript as well as to Zsuzsa Akos and Andras Czirok (ELTE Eötvös University)
for fruitful discussions. This work was supported by EU FP7, ERC COLLMOT Project
No 227878 to TV, the National Research Development and Innovation Fund of Hungary,
K119359 and also Project No 2018-1.2.1-NKP-2018-00005 to LN. This project has received
funding from the European Union’s Horizon 2020 research and innovation programme
under the Marie Sklodowska-Curie grant agreement No 955576. MV was supported by
the Ja´nos Bolyai Fellowship of the Hungarian Academy of Sciences.\r\nOpen access
funding provided by Eötvös Loránd University."
article_number: '817'
article_processing_charge: Yes
article_type: original
author:
- first_name: Elod
full_name: Méhes, Elod
last_name: Méhes
- first_name: Enys
full_name: Mones, Enys
last_name: Mones
- first_name: Máté
full_name: Varga, Máté
last_name: Varga
- first_name: Áron
full_name: Zsigmond, Áron
last_name: Zsigmond
- first_name: Beáta
full_name: Biri-Kovács, Beáta
last_name: Biri-Kovács
- first_name: László
full_name: Nyitray, László
last_name: Nyitray
- first_name: Vanessa
full_name: Barone, Vanessa
id: 419EECCC-F248-11E8-B48F-1D18A9856A87
last_name: Barone
orcid: 0000-0003-2676-3367
- first_name: Gabriel
full_name: Krens, Gabriel
id: 2B819732-F248-11E8-B48F-1D18A9856A87
last_name: Krens
orcid: 0000-0003-4761-5996
- 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
- first_name: Tamás
full_name: Vicsek, Tamás
last_name: Vicsek
citation:
ama: Méhes E, Mones E, Varga M, et al. 3D cell segregation geometry and dynamics
are governed by tissue surface tension regulation. Communications Biology.
2023;6. doi:10.1038/s42003-023-05181-7
apa: Méhes, E., Mones, E., Varga, M., Zsigmond, Á., Biri-Kovács, B., Nyitray, L.,
… Vicsek, T. (2023). 3D cell segregation geometry and dynamics are governed by
tissue surface tension regulation. Communications Biology. Springer Nature.
https://doi.org/10.1038/s42003-023-05181-7
chicago: Méhes, Elod, Enys Mones, Máté Varga, Áron Zsigmond, Beáta Biri-Kovács,
László Nyitray, Vanessa Barone, Gabriel Krens, Carl-Philipp J Heisenberg, and
Tamás Vicsek. “3D Cell Segregation Geometry and Dynamics Are Governed by Tissue
Surface Tension Regulation.” Communications Biology. Springer Nature, 2023.
https://doi.org/10.1038/s42003-023-05181-7.
ieee: E. Méhes et al., “3D cell segregation geometry and dynamics are governed
by tissue surface tension regulation,” Communications Biology, vol. 6.
Springer Nature, 2023.
ista: Méhes E, Mones E, Varga M, Zsigmond Á, Biri-Kovács B, Nyitray L, Barone V,
Krens G, Heisenberg C-PJ, Vicsek T. 2023. 3D cell segregation geometry and dynamics
are governed by tissue surface tension regulation. Communications Biology. 6,
817.
mla: Méhes, Elod, et al. “3D Cell Segregation Geometry and Dynamics Are Governed
by Tissue Surface Tension Regulation.” Communications Biology, vol. 6,
817, Springer Nature, 2023, doi:10.1038/s42003-023-05181-7.
short: E. Méhes, E. Mones, M. Varga, Á. Zsigmond, B. Biri-Kovács, L. Nyitray, V.
Barone, G. Krens, C.-P.J. Heisenberg, T. Vicsek, Communications Biology 6 (2023).
date_created: 2023-08-13T22:01:13Z
date_published: 2023-08-04T00:00:00Z
date_updated: 2023-12-13T12:07:33Z
day: '04'
ddc:
- '570'
department:
- _id: CaHe
- _id: Bio
doi: 10.1038/s42003-023-05181-7
external_id:
isi:
- '001042544100001'
pmid:
- '37542157'
file:
- access_level: open_access
checksum: 1f9324f736bdbb76426b07736651c4cd
content_type: application/pdf
creator: dernst
date_created: 2023-08-14T07:17:36Z
date_updated: 2023-08-14T07:17:36Z
file_id: '14045'
file_name: 2023_CommBiology_Mehes.pdf
file_size: 10181997
relation: main_file
success: 1
file_date_updated: 2023-08-14T07:17:36Z
fulldoi: https://doi.org/10.1038/s42003-023-05181-7
has_accepted_license: '1'
intvolume: ' 6'
isi: 1
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
publication: Communications Biology
publication_identifier:
eissn:
- 2399-3642
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: 3D cell segregation geometry and dynamics are governed by tissue surface tension
regulation
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2023'
...
---
_id: '14080'
abstract:
- lang: eng
text: Extracellular signal-regulated kinase (ERK) has been recognized as a critical
regulator in various physiological and pathological processes. Extensive research
has elucidated the signaling mechanisms governing ERK activation via biochemical
regulations with upstream molecules, particularly receptor tyrosine kinases (RTKs).
However, recent advances have highlighted the role of mechanical forces in activating
the RTK–ERK signaling pathways, thereby opening new avenues of research into mechanochemical
interplay in multicellular tissues. Here, we review the force-induced ERK activation
in cells and propose possible mechanosensing mechanisms underlying the mechanoresponsive
ERK activation. We conclude that mechanical forces are not merely passive factors
shaping cells and tissues but also active regulators of cellular signaling pathways
controlling collective cell behaviors.
acknowledgement: TH was supported by JSPS KAKENHI Grant (no. 21H05290) and the Ministry
of Education under the Research Centres of Excellence programme through the Mechanobiology
Institute at National University of Singapore and by Department of Physiology at
National University of Singapore. NH was supported by JSPS KAKENHI Grant (no. 20K22653).
KA was supported by JSPS KAKENHI Grants (no. 19H05798 and no. 22H02625). MM was
supported by JSPS KAKENHI Grants (no. 19H00993 and no. 20H05898) and JST Moonshot
R&D Grant JPMJPS2022. We appreciate Virgile Viasnoff and the lab members for their
valuable comments on the manuscript. We apologize to authors whose work could not
be highlighted due to space limitations.
article_number: '102217'
article_processing_charge: Yes (in subscription journal)
article_type: review
author:
- first_name: Tsuyoshi
full_name: Hirashima, Tsuyoshi
last_name: Hirashima
- first_name: Naoya
full_name: Hino, Naoya
id: 5299a9ce-7679-11eb-a7bc-d1e62b936307
last_name: Hino
- first_name: Kazuhiro
full_name: Aoki, Kazuhiro
last_name: Aoki
- first_name: Michiyuki
full_name: Matsuda, Michiyuki
last_name: Matsuda
citation:
ama: Hirashima T, Hino N, Aoki K, Matsuda M. Stretching the limits of extracellular
signal-related kinase (ERK) signaling — Cell mechanosensing to ERK activation.
Current Opinion in Cell Biology. 2023;84(10). doi:10.1016/j.ceb.2023.102217
apa: Hirashima, T., Hino, N., Aoki, K., & Matsuda, M. (2023). Stretching the
limits of extracellular signal-related kinase (ERK) signaling — Cell mechanosensing
to ERK activation. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2023.102217
chicago: Hirashima, Tsuyoshi, Naoya Hino, Kazuhiro Aoki, and Michiyuki Matsuda.
“Stretching the Limits of Extracellular Signal-Related Kinase (ERK) Signaling
— Cell Mechanosensing to ERK Activation.” Current Opinion in Cell Biology.
Elsevier, 2023. https://doi.org/10.1016/j.ceb.2023.102217.
ieee: T. Hirashima, N. Hino, K. Aoki, and M. Matsuda, “Stretching the limits of
extracellular signal-related kinase (ERK) signaling — Cell mechanosensing to ERK
activation,” Current Opinion in Cell Biology, vol. 84, no. 10. Elsevier,
2023.
ista: Hirashima T, Hino N, Aoki K, Matsuda M. 2023. Stretching the limits of extracellular
signal-related kinase (ERK) signaling — Cell mechanosensing to ERK activation.
Current Opinion in Cell Biology. 84(10), 102217.
mla: Hirashima, Tsuyoshi, et al. “Stretching the Limits of Extracellular Signal-Related
Kinase (ERK) Signaling — Cell Mechanosensing to ERK Activation.” Current Opinion
in Cell Biology, vol. 84, no. 10, 102217, Elsevier, 2023, doi:10.1016/j.ceb.2023.102217.
short: T. Hirashima, N. Hino, K. Aoki, M. Matsuda, Current Opinion in Cell Biology
84 (2023).
date_created: 2023-08-20T22:01:12Z
date_published: 2023-10-01T00:00:00Z
date_updated: 2024-01-30T12:52:42Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1016/j.ceb.2023.102217
external_id:
isi:
- '001054692200001'
pmid:
- '37574635'
file:
- access_level: open_access
checksum: 25923f8ae71344e8974530dd23c71bdc
content_type: application/pdf
creator: dernst
date_created: 2024-01-30T12:52:12Z
date_updated: 2024-01-30T12:52:12Z
file_id: '14909'
file_name: 2023_CurrentOpinionCellBio_Hirashima.pdf
file_size: 1173762
relation: main_file
success: 1
file_date_updated: 2024-01-30T12:52:12Z
fulldoi: https://doi.org/10.1016/j.ceb.2023.102217
has_accepted_license: '1'
intvolume: ' 84'
isi: 1
issue: '10'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: Current Opinion in Cell Biology
publication_identifier:
eissn:
- 1879-0410
issn:
- 0955-0674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Stretching the limits of extracellular signal-related kinase (ERK) signaling
— Cell mechanosensing to ERK activation
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: 84
year: '2023'
...
---
OA_place: publisher
OA_type: free access
_id: '14082'
abstract:
- lang: eng
text: Epithelial barrier function is commonly analyzed using transepithelial electrical
resistance, which measures ion flux across a monolayer, or by adding traceable
macromolecules and monitoring their passage across the monolayer. Although these
methods measure changes in global barrier function, they lack the sensitivity
needed to detect local or transient barrier breaches, and they do not reveal the
location of barrier leaks. Therefore, we previously developed a method that we
named the zinc-based ultrasensitive microscopic barrier assay (ZnUMBA), which
overcomes these limitations, allowing for detection of local tight junction leaks
with high spatiotemporal resolution. Here, we present expanded applications for
ZnUMBA. ZnUMBA can be used in Xenopus embryos to measure the dynamics of barrier
restoration and actin accumulation following laser injury. ZnUMBA can also be
effectively utilized in developing zebrafish embryos as well as cultured monolayers
of Madin–Darby canine kidney (MDCK) II epithelial cells. ZnUMBA is a powerful
and flexible method that, with minimal optimization, can be applied to multiple
systems to measure dynamic changes in barrier function with spatiotemporal precision.
acknowledged_ssus:
- _id: PreCl
- _id: Bio
acknowledgement: "The authors thank their respective lab members for feedback and
helpful discussions. We thank the bioimaging and zebrafish facilities of IST Austria
for their support.\r\nThis work was supported by the National Institutes of Health
[R01GM112794 to A.L.M.], by Grants-in-Aid for Scientific Research from the Japan
Society for the Promotion of Science [21K06156 to T.H.], by the Grant Program for
Biomedical Engineering Research from the Nakatani Foundation for Advancement of
Measuring Technologies in Biomedical Engineering [to T.H.] and by funding from the
European Research Council [advanced grant 742573 to C.-P.H.]. "
article_number: jcs260668
article_processing_charge: No
article_type: original
author:
- first_name: Tomohito
full_name: Higashi, Tomohito
last_name: Higashi
- first_name: Rachel E.
full_name: Stephenson, Rachel E.
last_name: Stephenson
- first_name: Cornelia
full_name: Schwayer, Cornelia
id: 3436488C-F248-11E8-B48F-1D18A9856A87
last_name: Schwayer
orcid: 0000-0001-5130-2226
- first_name: Karla
full_name: Huljev, Karla
id: 44C6F6A6-F248-11E8-B48F-1D18A9856A87
last_name: Huljev
- first_name: Atsuko Y.
full_name: Higashi, Atsuko Y.
last_name: Higashi
- 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
- first_name: Hideki
full_name: Chiba, Hideki
last_name: Chiba
- first_name: Ann L.
full_name: Miller, Ann L.
last_name: Miller
citation:
ama: Higashi T, Stephenson RE, Schwayer C, et al. ZnUMBA - a live imaging method
to detect local barrier breaches. Journal of Cell Science. 2023;136(15).
doi:10.1242/jcs.260668
apa: Higashi, T., Stephenson, R. E., Schwayer, C., Huljev, K., Higashi, A. Y., Heisenberg,
C.-P. J., … Miller, A. L. (2023). ZnUMBA - a live imaging method to detect local
barrier breaches. Journal of Cell Science. The Company of Biologists. https://doi.org/10.1242/jcs.260668
chicago: Higashi, Tomohito, Rachel E. Stephenson, Cornelia Schwayer, Karla Huljev,
Atsuko Y. Higashi, Carl-Philipp J Heisenberg, Hideki Chiba, and Ann L. Miller.
“ZnUMBA - a Live Imaging Method to Detect Local Barrier Breaches.” Journal
of Cell Science. The Company of Biologists, 2023. https://doi.org/10.1242/jcs.260668.
ieee: T. Higashi et al., “ZnUMBA - a live imaging method to detect local
barrier breaches,” Journal of Cell Science, vol. 136, no. 15. The Company
of Biologists, 2023.
ista: Higashi T, Stephenson RE, Schwayer C, Huljev K, Higashi AY, Heisenberg C-PJ,
Chiba H, Miller AL. 2023. ZnUMBA - a live imaging method to detect local barrier
breaches. Journal of Cell Science. 136(15), jcs260668.
mla: Higashi, Tomohito, et al. “ZnUMBA - a Live Imaging Method to Detect Local Barrier
Breaches.” Journal of Cell Science, vol. 136, no. 15, jcs260668, The Company
of Biologists, 2023, doi:10.1242/jcs.260668.
short: T. Higashi, R.E. Stephenson, C. Schwayer, K. Huljev, A.Y. Higashi, C.-P.J.
Heisenberg, H. Chiba, A.L. Miller, Journal of Cell Science 136 (2023).
date_created: 2023-08-20T22:01:13Z
date_published: 2023-08-01T00:00:00Z
date_updated: 2025-06-25T06:28:45Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
- _id: EvBe
doi: 10.1242/jcs.260668
ec_funded: 1
external_id:
isi:
- '001070149000001'
pmid:
- '37461809'
fulldoi: https://doi.org/10.1242/jcs.260668
has_accepted_license: '1'
intvolume: ' 136'
isi: 1
issue: '15'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1242/jcs.260668
month: '08'
oa: 1
oa_version: None
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
publication: Journal of Cell Science
publication_identifier:
eissn:
- 1477-9137
issn:
- 0021-9533
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: ZnUMBA - a live imaging method to detect local barrier breaches
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 136
year: '2023'
...
---
_id: '14827'
abstract:
- lang: eng
text: Understanding complex living systems, which are fundamentally constrained
by physical phenomena, requires combining experimental data with theoretical physical
and mathematical models. To develop such models, collaborations between experimental
cell biologists and theoreticians are increasingly important but these two groups
often face challenges achieving mutual understanding. To help navigate these challenges,
this Perspective discusses different modelling approaches, including bottom-up
hypothesis-driven and top-down data-driven models, and highlights their strengths
and applications. Using cell mechanics as an example, we explore the integration
of specific physical models with experimental data from the molecular, cellular
and tissue level up to multiscale input. We also emphasize the importance of constraining
model complexity and outline strategies for crosstalk between experimental design
and model development. Furthermore, we highlight how physical models can provide
conceptual insights and produce unifying and generalizable frameworks for biological
phenomena. Overall, this Perspective aims to promote fruitful collaborations that
advance our understanding of complex biological systems.
acknowledgement: "We thank Prisca Liberali and Edouard Hannezo for many inspiring
discussions; Mehmet Can Uçar, Nicoletta I Petridou and Qiutan Yang for a critical
reading of the manuscript, and Claudia Flandoli for the artwork in Figs 2 and 3.
We would also like to thank The Company of Biologists for the opportunity to attend
the 2023 workshop on Collective Cell Migration, and all workshop participants for
discussions.\r\nC.S. was supported by a European Molecular Biology Organization
(EMBO) Postdoctoral Fellowship (ALTF 660-2020) and Human Frontier Science Program
(HFSP) Postdoctoral fellowship (LT000746/2021-L). D.B.B. was supported by the NOMIS
Foundation as a NOMIS Fellow and by an EMBO Postdoctoral Fellowship (ALTF 343-2022)."
article_number: jcs.261515
article_processing_charge: No
article_type: original
author:
- first_name: Cornelia
full_name: Schwayer, Cornelia
id: 3436488C-F248-11E8-B48F-1D18A9856A87
last_name: Schwayer
orcid: 0000-0001-5130-2226
- first_name: David
full_name: Brückner, David
id: e1e86031-6537-11eb-953a-f7ab92be508d
last_name: Brückner
orcid: 0000-0001-7205-2975
citation:
ama: Schwayer C, Brückner D. Connecting theory and experiment in cell and tissue
mechanics. Journal of Cell Science. 2023;136(24). doi:10.1242/jcs.261515
apa: Schwayer, C., & Brückner, D. (2023). Connecting theory and experiment in
cell and tissue mechanics. Journal of Cell Science. The Company of Biologists.
https://doi.org/10.1242/jcs.261515
chicago: Schwayer, Cornelia, and David Brückner. “Connecting Theory and Experiment
in Cell and Tissue Mechanics.” Journal of Cell Science. The Company of
Biologists, 2023. https://doi.org/10.1242/jcs.261515.
ieee: C. Schwayer and D. Brückner, “Connecting theory and experiment in cell and
tissue mechanics,” Journal of Cell Science, vol. 136, no. 24. The Company
of Biologists, 2023.
ista: Schwayer C, Brückner D. 2023. Connecting theory and experiment in cell and
tissue mechanics. Journal of Cell Science. 136(24), jcs. 261515.
mla: Schwayer, Cornelia, and David Brückner. “Connecting Theory and Experiment in
Cell and Tissue Mechanics.” Journal of Cell Science, vol. 136, no. 24,
jcs. 261515, The Company of Biologists, 2023, doi:10.1242/jcs.261515.
short: C. Schwayer, D. Brückner, Journal of Cell Science 136 (2023).
corr_author: '1'
date_created: 2024-01-17T12:46:55Z
date_published: 2023-12-27T00:00:00Z
date_updated: 2025-09-09T14:22:02Z
day: '27'
department:
- _id: EdHa
- _id: CaHe
doi: 10.1242/jcs.261515
external_id:
isi:
- '001165394900011'
pmid:
- '38149871'
fulldoi: https://doi.org/10.1242/jcs.261515
intvolume: ' 136'
isi: 1
issue: '24'
keyword:
- Cell Biology
language:
- iso: eng
month: '12'
oa_version: None
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
publication: Journal of Cell Science
publication_identifier:
eissn:
- 1477-9137
issn:
- 0021-9533
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Connecting theory and experiment in cell and tissue mechanics
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 136
year: '2023'
...
---
_id: '12891'
abstract:
- lang: eng
text: "The tight spatiotemporal coordination of signaling activity determining embryo\r\npatterning
and the physical processes driving embryo morphogenesis renders\r\nembryonic development
robust, such that key developmental processes can unfold\r\nrelatively normally
even outside of the full embryonic context. For instance, embryonic\r\nstem cell
cultures can recapitulate the hallmarks of gastrulation, i.e. break symmetry\r\nleading
to germ layer formation and morphogenesis, in a very reduced environment.\r\nThis
leads to questions on specific contributions of embryo-specific features, such
as\r\nthe presence of extraembryonic tissues, which are inherently involved in
gastrulation\r\nin the full embryonic context. To address this, we established
zebrafish embryonic\r\nexplants without the extraembryonic yolk cell, an important
player as a signaling\r\nsource and for morphogenesis during gastrulation, as
a model of ex vivo development.\r\nWe found that dorsal-marginal determinants
are required and sufficient in these\r\nexplants to form and pattern all three
germ layers. However, formation of tissues,\r\nwhich require the highest Nodal-signaling
levels, is variable, demonstrating a\r\ncontribution of extraembryonic tissues
for reaching peak Nodal signaling levels.\r\nBlastoderm explants also undergo
gastrulation-like axis elongation. We found that this\r\nelongation movement shows
hallmarks of oriented mesendoderm cell intercalations\r\ntypically associated
with dorsal tissues in the intact embryo. These are disrupted by\r\nuniform upregulation
of BMP signaling activity and concomitant explant ventralization,\r\nsuggesting
that tight spatial control of BMP signaling is a prerequisite for explant\r\nmorphogenesis.
This control is achieved by Nodal signaling, which is critical for\r\neffectively
downregulating BMP signaling in the mesendoderm, highlighting that Nodal\r\nsignaling
is not only directly required for mesendoderm cell fate specification and\r\nmorphogenesis,
but also by maintaining low levels of BMP signaling at the dorsal side.\r\nCollectively,
we provide insights into the capacity and organization of signaling and\r\nmorphogenetic
domains to recapitulate features of zebrafish gastrulation outside of\r\nthe full
embryonic context."
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Alexandra
full_name: Schauer, Alexandra
id: 30A536BA-F248-11E8-B48F-1D18A9856A87
last_name: Schauer
orcid: 0000-0001-7659-9142
citation:
ama: 'Schauer A. Mesendoderm formation in zebrafish gastrulation: The role of extraembryonic
tissues. 2023. doi:10.15479/at:ista:12891'
apa: 'Schauer, A. (2023). Mesendoderm formation in zebrafish gastrulation: The
role of extraembryonic tissues. Institute of Science and Technology Austria.
https://doi.org/10.15479/at:ista:12891'
chicago: 'Schauer, Alexandra. “Mesendoderm Formation in Zebrafish Gastrulation:
The Role of Extraembryonic Tissues.” Institute of Science and Technology Austria,
2023. https://doi.org/10.15479/at:ista:12891.'
ieee: 'A. Schauer, “Mesendoderm formation in zebrafish gastrulation: The role of
extraembryonic tissues,” Institute of Science and Technology Austria, 2023.'
ista: 'Schauer A. 2023. Mesendoderm formation in zebrafish gastrulation: The role
of extraembryonic tissues. Institute of Science and Technology Austria.'
mla: 'Schauer, Alexandra. Mesendoderm Formation in Zebrafish Gastrulation: The
Role of Extraembryonic Tissues. Institute of Science and Technology Austria,
2023, doi:10.15479/at:ista:12891.'
short: 'A. Schauer, Mesendoderm Formation in Zebrafish Gastrulation: The Role of
Extraembryonic Tissues, Institute of Science and Technology Austria, 2023.'
corr_author: '1'
date_created: 2023-05-05T08:48:20Z
date_published: 2023-05-05T00:00:00Z
date_updated: 2025-06-12T06:56:58Z
day: '05'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
- _id: CaHe
doi: 10.15479/at:ista:12891
ec_funded: 1
file:
- access_level: open_access
checksum: 59b0303dc483f40a96a610a90aab7ee9
content_type: application/pdf
creator: aschauer
date_created: 2023-05-05T13:01:14Z
date_updated: 2024-05-06T22:30:03Z
embargo: 2024-05-05
file_id: '12907'
file_name: Thesis_Schauer_final.pdf
file_size: 31434230
relation: main_file
- access_level: closed
checksum: 25f54e12479b6adaabd129a20568e6c1
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: aschauer
date_created: 2023-05-05T13:04:15Z
date_updated: 2024-05-06T22:30:03Z
embargo_to: open_access
file_id: '12908'
file_name: Thesis_Schauer_final.docx
file_size: 43809109
relation: source_file
file_date_updated: 2024-05-06T22:30:03Z
fulldoi: https://doi.org/10.15479/at:ista:12891
has_accepted_license: '1'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: '190'
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
- _id: 26B1E39C-B435-11E9-9278-68D0E5697425
grant_number: '25239'
name: 'Mesendoderm specification in zebrafish: The role of extraembryonic tissues'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '7888'
relation: part_of_dissertation
status: public
- id: '8966'
relation: part_of_dissertation
status: public
status: public
supervisor:
- 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
title: 'Mesendoderm formation in zebrafish gastrulation: The role of extraembryonic
tissues'
type: dissertation
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '12209'
abstract:
- lang: eng
text: Embryo development requires biochemical signalling to generate patterns of
cell fates and active mechanical forces to drive tissue shape changes. However,
how these processes are coordinated, and how tissue patterning is preserved despite
the cellular flows occurring during morphogenesis, remains poorly understood.
Gastrulation is a crucial embryonic stage that involves both patterning and internalization
of the mesendoderm germ layer tissue. Here we show that, in zebrafish embryos,
a gradient in Nodal signalling orchestrates pattern-preserving internalization
movements by triggering a motility-driven unjamming transition. In addition to
its role as a morphogen determining embryo patterning, graded Nodal signalling
mechanically subdivides the mesendoderm into a small fraction of highly protrusive
leader cells, able to autonomously internalize via local unjamming, and less protrusive
followers, which need to be pulled inwards by the leaders. The Nodal gradient
further enforces a code of preferential adhesion coupling leaders to their immediate
followers, resulting in a collective and ordered mode of internalization that
preserves mesendoderm patterning. Integrating this dual mechanical role of Nodal
signalling into minimal active particle simulations quantitatively predicts both
physiological and experimentally perturbed internalization movements. This provides
a quantitative framework for how a morphogen-encoded unjamming transition can
bidirectionally couple tissue mechanics with patterning during complex three-dimensional
morphogenesis.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
acknowledgement: "We thank K. Sampath, A. Pauli and Y. Bellaїche for feedback on the
manuscript. We also thank the members of the Heisenberg group, in particular A.
Schauer and F. Nur Arslan, for help, technical advice and discussions, and the Bioimaging
and Life Science facilities at IST\r\nAustria for continuous support. We thank C.
Flandoli for the artwork in the figures. This work was supported by postdoctoral
fellowships from EMBO (LTF-850-2017) and HFSP (LT000429/2018-L2) to D.P. and the
European Union (European Research Council starting grant 851288 to É.H. and European
Research Council advanced grant 742573 to C.-P.H.)."
article_processing_charge: No
article_type: original
author:
- first_name: Diana C
full_name: Nunes Pinheiro, Diana C
id: 2E839F16-F248-11E8-B48F-1D18A9856A87
last_name: Nunes Pinheiro
orcid: 0000-0003-4333-7503
- first_name: Roland
full_name: Kardos, Roland
id: 4039350E-F248-11E8-B48F-1D18A9856A87
last_name: Kardos
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- 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: Nunes Pinheiro DC, Kardos R, Hannezo EB, Heisenberg C-PJ. Morphogen gradient
orchestrates pattern-preserving tissue morphogenesis via motility-driven unjamming.
Nature Physics. 2022;18(12):1482-1493. doi:10.1038/s41567-022-01787-6
apa: Nunes Pinheiro, D. C., Kardos, R., Hannezo, E. B., & Heisenberg, C.-P.
J. (2022). Morphogen gradient orchestrates pattern-preserving tissue morphogenesis
via motility-driven unjamming. Nature Physics. Springer Nature. https://doi.org/10.1038/s41567-022-01787-6
chicago: Nunes Pinheiro, Diana C, Roland Kardos, Edouard B Hannezo, and Carl-Philipp
J Heisenberg. “Morphogen Gradient Orchestrates Pattern-Preserving Tissue Morphogenesis
via Motility-Driven Unjamming.” Nature Physics. Springer Nature, 2022.
https://doi.org/10.1038/s41567-022-01787-6.
ieee: D. C. Nunes Pinheiro, R. Kardos, E. B. Hannezo, and C.-P. J. Heisenberg, “Morphogen
gradient orchestrates pattern-preserving tissue morphogenesis via motility-driven
unjamming,” Nature Physics, vol. 18, no. 12. Springer Nature, pp. 1482–1493,
2022.
ista: Nunes Pinheiro DC, Kardos R, Hannezo EB, Heisenberg C-PJ. 2022. Morphogen
gradient orchestrates pattern-preserving tissue morphogenesis via motility-driven
unjamming. Nature Physics. 18(12), 1482–1493.
mla: Nunes Pinheiro, Diana C., et al. “Morphogen Gradient Orchestrates Pattern-Preserving
Tissue Morphogenesis via Motility-Driven Unjamming.” Nature Physics, vol.
18, no. 12, Springer Nature, 2022, pp. 1482–93, doi:10.1038/s41567-022-01787-6.
short: D.C. Nunes Pinheiro, R. Kardos, E.B. Hannezo, C.-P.J. Heisenberg, Nature
Physics 18 (2022) 1482–1493.
corr_author: '1'
date_created: 2023-01-16T09:45:19Z
date_published: 2022-12-01T00:00:00Z
date_updated: 2025-04-14T07:46:59Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
- _id: EdHa
doi: 10.1038/s41567-022-01787-6
ec_funded: 1
external_id:
isi:
- '000871319900002'
file:
- access_level: open_access
checksum: c86a8e8d80d1bfc46d56a01e88a2526a
content_type: application/pdf
creator: dernst
date_created: 2023-01-27T07:32:01Z
date_updated: 2023-01-27T07:32:01Z
file_id: '12412'
file_name: 2022_NaturePhysics_Pinheiro.pdf
file_size: 36703569
relation: main_file
success: 1
file_date_updated: 2023-01-27T07:32:01Z
fulldoi: https://doi.org/10.1038/s41567-022-01787-6
has_accepted_license: '1'
intvolume: ' 18'
isi: 1
issue: '12'
keyword:
- General Physics and Astronomy
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 1482-1493
project:
- _id: 26520D1E-B435-11E9-9278-68D0E5697425
grant_number: ALTF 850-2017
name: Coordination of mesendoderm cell fate specification and internalization during
zebrafish gastrulation
- _id: 26520D1E-B435-11E9-9278-68D0E5697425
grant_number: ALTF 850-2017
name: Coordination of mesendoderm cell fate specification and internalization during
zebrafish gastrulation
- _id: 05943252-7A3F-11EA-A408-12923DDC885E
call_identifier: H2020
grant_number: '851288'
name: Design Principles of Branching Morphogenesis
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
publication: Nature Physics
publication_identifier:
eissn:
- 1745-2481
issn:
- 1745-2473
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Morphogen gradient orchestrates pattern-preserving tissue morphogenesis via
motility-driven unjamming
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 18
year: '2022'
...
---
OA_place: publisher
OA_type: free access
_id: '12238'
abstract:
- lang: eng
text: Upon the initiation of collective cell migration, the cells at the free edge
are specified as leader cells; however, the mechanism underlying the leader cell
specification remains elusive. Here, we show that lamellipodial extension after
the release from mechanical confinement causes sustained extracellular signal-regulated
kinase (ERK) activation and underlies the leader cell specification. Live-imaging
of Madin-Darby canine kidney (MDCK) cells and mouse epidermis through the use
of Förster resonance energy transfer (FRET)-based biosensors showed that leader
cells exhibit sustained ERK activation in a hepatocyte growth factor (HGF)-dependent
manner. Meanwhile, follower cells exhibit oscillatory ERK activation waves in
an epidermal growth factor (EGF) signaling-dependent manner. Lamellipodial extension
at the free edge increases the cellular sensitivity to HGF. The HGF-dependent
ERK activation, in turn, promotes lamellipodial extension, thereby forming a positive
feedback loop between cell extension and ERK activation and specifying the cells
at the free edge as the leader cells. Our findings show that the integration of
physical and biochemical cues underlies the leader cell specification during collective
cell migration.
acknowledgement: We thank the members of the Matsuda Laboratory for their helpful
discussion and encouragement, and we thank K. Hirano and K. Takakura for their technical
assistance. This work was supported by the Kyoto University Live Imaging Center.
Financial support was provided in the form of JSPS KAKENHI grants (nos. 17J02107
and 20K22653 to N.H., and 20H05898 and 19H00993 to M.M.), a JST CREST grant (no.
JPMJCR1654 to M.M.), a Moonshot R&D grant (no. JPMJPS2022-11 to M.M.), Generalitat
de Catalunya and the CERCA Programme (no. SGR-2017-01602 to X.T.), MICCINN/FEDER
(no. PGC2018-099645-B-I00 to X.T.), and European Research Council (no. Adv-883739
to X.T.). IBEC is a recipient of a Severo Ochoa Award of Excellence from the MINECO.
This work was partly supported by an Extramural Collaborative Research Grant of
Cancer Research Institute, Kanazawa University.
article_processing_charge: No
article_type: original
author:
- first_name: Naoya
full_name: Hino, Naoya
id: 5299a9ce-7679-11eb-a7bc-d1e62b936307
last_name: Hino
- first_name: Kimiya
full_name: Matsuda, Kimiya
last_name: Matsuda
- first_name: Yuya
full_name: Jikko, Yuya
last_name: Jikko
- first_name: Gembu
full_name: Maryu, Gembu
last_name: Maryu
- first_name: Katsuya
full_name: Sakai, Katsuya
last_name: Sakai
- first_name: Ryu
full_name: Imamura, Ryu
last_name: Imamura
- first_name: Shinya
full_name: Tsukiji, Shinya
last_name: Tsukiji
- first_name: Kazuhiro
full_name: Aoki, Kazuhiro
last_name: Aoki
- first_name: Kenta
full_name: Terai, Kenta
last_name: Terai
- first_name: Tsuyoshi
full_name: Hirashima, Tsuyoshi
last_name: Hirashima
- first_name: Xavier
full_name: Trepat, Xavier
last_name: Trepat
- first_name: Michiyuki
full_name: Matsuda, Michiyuki
last_name: Matsuda
citation:
ama: Hino N, Matsuda K, Jikko Y, et al. A feedback loop between lamellipodial extension
and HGF-ERK signaling specifies leader cells during collective cell migration.
Developmental Cell. 2022;57(19):2290-2304.e7. doi:10.1016/j.devcel.2022.09.003
apa: Hino, N., Matsuda, K., Jikko, Y., Maryu, G., Sakai, K., Imamura, R., … Matsuda,
M. (2022). A feedback loop between lamellipodial extension and HGF-ERK signaling
specifies leader cells during collective cell migration. Developmental Cell.
Elsevier. https://doi.org/10.1016/j.devcel.2022.09.003
chicago: Hino, Naoya, Kimiya Matsuda, Yuya Jikko, Gembu Maryu, Katsuya Sakai, Ryu
Imamura, Shinya Tsukiji, et al. “A Feedback Loop between Lamellipodial Extension
and HGF-ERK Signaling Specifies Leader Cells during Collective Cell Migration.”
Developmental Cell. Elsevier, 2022. https://doi.org/10.1016/j.devcel.2022.09.003.
ieee: N. Hino et al., “A feedback loop between lamellipodial extension and
HGF-ERK signaling specifies leader cells during collective cell migration,” Developmental
Cell, vol. 57, no. 19. Elsevier, p. 2290–2304.e7, 2022.
ista: Hino N, Matsuda K, Jikko Y, Maryu G, Sakai K, Imamura R, Tsukiji S, Aoki K,
Terai K, Hirashima T, Trepat X, Matsuda M. 2022. A feedback loop between lamellipodial
extension and HGF-ERK signaling specifies leader cells during collective cell
migration. Developmental Cell. 57(19), 2290–2304.e7.
mla: Hino, Naoya, et al. “A Feedback Loop between Lamellipodial Extension and HGF-ERK
Signaling Specifies Leader Cells during Collective Cell Migration.” Developmental
Cell, vol. 57, no. 19, Elsevier, 2022, p. 2290–2304.e7, doi:10.1016/j.devcel.2022.09.003.
short: N. Hino, K. Matsuda, Y. Jikko, G. Maryu, K. Sakai, R. Imamura, S. Tsukiji,
K. Aoki, K. Terai, T. Hirashima, X. Trepat, M. Matsuda, Developmental Cell 57
(2022) 2290–2304.e7.
corr_author: '1'
date_created: 2023-01-16T09:51:39Z
date_published: 2022-10-01T00:00:00Z
date_updated: 2026-06-18T17:25:21Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1016/j.devcel.2022.09.003
external_id:
isi:
- '000898428700006'
pmid:
- '36174555'
fulldoi: https://doi.org/10.1016/j.devcel.2022.09.003
intvolume: ' 57'
isi: 1
issue: '19'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.devcel.2022.09.003
month: '10'
oa: 1
oa_version: Published Version
page: 2290-2304.e7
pmid: 1
publication: Developmental Cell
publication_identifier:
issn:
- 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: A feedback loop between lamellipodial extension and HGF-ERK signaling specifies
leader cells during collective cell migration
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 57
year: '2022'
...
---
OA_place: publisher
_id: '12368'
abstract:
- lang: eng
text: "Metazoan development relies on the formation and remodeling of cell-cell
contacts. The \r\nbinding of adhesion receptors and remodeling of the actomyosin
cell cortex at cell-cell \r\ninteraction sites have been implicated in cell-cell
contact formation. Yet, how these two \r\nprocesses functionally interact to drive
cell-cell contact expansion and strengthening \r\nremains unclear. Here, we study
how primary germ layer progenitor cells from zebrafish \r\nbind to supported lipid
bilayers (SLB) functionalized with E-cadherin ectodomains as an \r\nassay system
for monitoring cell-cell contact formation at high spatiotemporal resolution.
\r\nWe show that cell-cell contact formation represents a two-tiered process:
E-cadherin\x02mediated downregulation of the small GTPase RhoA at the forming
contact leads to both \r\ndepletion of Myosin-2 and decrease of F-actin. This
is followed by centrifugal actin \r\nnetwork flows at the contact triggered by
a sharp gradient of Myosin-2 at the rim of the \r\ncontact zone, with Myosin-2
displaying higher cortical localization outside than inside of \r\nthe contact.
These centrifugal cortical actin flows, in turn, not only further dilute the actin
\r\nnetwork at the contact disc, but also lead to an accumulation of both F-actin
and E\x02cadherin at the contact rim. Eventually, this combination of actomyosin
downregulation \r\nand flows at the contact contribute to the characteristic molecular
organization implicated \r\nin contact formation and maintenance: depletion of
cortical actomyosin at the contact disc, \r\ndriving contact expansion by lowering
interfacial tension at the contact, and accumulation \r\nof both E-cadherin and
F-actin at the contact rim, mechanically linking the contractile \r\ncortices
of the adhering cells. Thus, using a biomimetic assay, we exemplify how \r\nadhesion
signaling and cell mechanics function together to modulate the spatial \r\norganization
of cell-cell contacts."
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
- _id: NanoFab
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Feyza N
full_name: Arslan, Feyza N
id: 49DA7910-F248-11E8-B48F-1D18A9856A87
last_name: Arslan
orcid: 0000-0001-5809-9566
citation:
ama: Arslan FN. Remodeling of E-cadherin-mediated contacts via cortical flows.
2022. doi:10.15479/at:ista:12153
apa: Arslan, F. N. (2022). Remodeling of E-cadherin-mediated contacts via cortical
flows. Institute of Science and Technology Austria. https://doi.org/10.15479/at:ista:12153
chicago: Arslan, Feyza N. “Remodeling of E-Cadherin-Mediated Contacts via Cortical
Flows.” Institute of Science and Technology Austria, 2022. https://doi.org/10.15479/at:ista:12153.
ieee: F. N. Arslan, “Remodeling of E-cadherin-mediated contacts via cortical flows,”
Institute of Science and Technology Austria, 2022.
ista: Arslan FN. 2022. Remodeling of E-cadherin-mediated contacts via cortical
flows. Institute of Science and Technology Austria.
mla: Arslan, Feyza N. Remodeling of E-Cadherin-Mediated Contacts via Cortical
Flows. Institute of Science and Technology Austria, 2022, doi:10.15479/at:ista:12153.
short: F.N. Arslan, Remodeling of E-Cadherin-Mediated Contacts via Cortical Flows,
Institute of Science and Technology Austria, 2022.
corr_author: '1'
date_created: 2023-01-25T10:43:24Z
date_published: 2022-09-29T00:00:00Z
date_updated: 2026-06-18T19:47:50Z
day: '29'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
- _id: CaHe
doi: 10.15479/at:ista:12153
ec_funded: 1
file:
- access_level: open_access
checksum: e54a3e69b83ebf166544164afd25608e
content_type: application/pdf
creator: cchlebak
date_created: 2023-01-25T10:52:46Z
date_updated: 2023-01-25T10:52:46Z
file_id: '12369'
file_name: THESIS_FINAL_FArslan_pdfa.pdf
file_size: 14581024
relation: main_file
success: 1
file_date_updated: 2023-01-25T10:52:46Z
fulldoi: https://doi.org/10.15479/at:ista:12153
has_accepted_license: '1'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: '113'
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
publication_identifier:
isbn:
- '978-3-99078-025-1 '
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '9350'
relation: part_of_dissertation
status: public
status: public
supervisor:
- 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
title: Remodeling of E-cadherin-mediated contacts via cortical flows
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2022'
...
---
_id: '17066'
abstract:
- lang: eng
text: A cell’s size affects the likelihood that it will die. But how is cell size
controlled in this context and how does cell size impact commitment to the cell
death fate? We present evidence that the caspase CED-3 interacts with the RhoGEF
ECT-2 in Caenorhabditis elegans neuroblasts that generate “unwanted” cells. We
propose that this interaction promotes polar actomyosin contractility, which leads
to unequal neuroblast division and the generation of a daughter cell that is below
the critical “lethal” size threshold. Furthermore, we find that hyperactivation
of ECT-2 RhoGEF reduces the sizes of unwanted cells. Importantly, this suppresses
the “cell death abnormal” phenotype caused by the partial loss of ced-3 caspase
and therefore increases the likelihood that unwanted cells die. A putative null
mutation of ced-3 caspase, however, is not suppressed, which indicates that cell
size affects CED-3 caspase activation and/or activity. Therefore, we have uncovered
novel sequential and reciprocal interactions between the apoptosis pathway and
cell size that impact a cell’s commitment to the cell death fate.
acknowledgement: "We thank members of the Conradt, Lambie, and Hajnal labs for discussions
and comments on the manuscript. We thank M. Bauer, L. Jocham, N. Lebedeva, and L.
McGuinness for excellent technical support; A. Hajnal and T. Kohlbrenner (University
of Zurich, Switzerland) for allele zh135; and H.R. Horvitz (Massachusetts of Technology,
USA) for plasmid pET-CED-3.\r\nSome strains were provided by the Caenorhabditis
Genetics Center (CGC), which is funded by NIH Office of Research Infrastructure
Programs (https://orip.nih.gov/) (P40 OD010440). This work was supported by UCL
(Capital Equipment Fund, CEF2), a predoctoral fellowship from the China Scholarship
Council (https://www.csc.edu.cn/) to HW, a predoctoral fellowship from the Studienstiftung
des Deutschen Volkes (https://www.studienstiftung.de/) to NM, a Wolfson Fellowship
from the Royal Society (https://royalsociety.org/) to BC (RSWF\\R1\\180008), the
Deutsche Forschungsgemeinschaft (https://www.dfg.de/en/index.jsp) (ZA619/3-1 and
ZA619/3-2 to EZ; C0204/10-1 and EXC114 to BC), and the Biotechnology and Biological
Sciences Research Council (https://bbsrc.ukri.org/) (BB/V007572/1 to BC). "
article_number: e3001786
article_processing_charge: Yes
article_type: original
author:
- first_name: Aditya
full_name: Sethi, Aditya
last_name: Sethi
- first_name: Hai
full_name: Wei, Hai
last_name: Wei
- first_name: Nikhil
full_name: Mishra, Nikhil
id: C4D70E82-1081-11EA-B3ED-9A4C3DDC885E
last_name: Mishra
orcid: 0000-0002-6425-5788
- first_name: Ioannis
full_name: Segos, Ioannis
last_name: Segos
- first_name: Eric J.
full_name: Lambie, Eric J.
last_name: Lambie
- first_name: Esther
full_name: Zanin, Esther
last_name: Zanin
- first_name: Barbara
full_name: Conradt, Barbara
last_name: Conradt
citation:
ama: Sethi A, Wei H, Mishra N, et al. A caspase–RhoGEF axis contributes to the cell
size threshold for apoptotic death in developing Caenorhabditis elegans. PLOS
Biology. 2022;20(10). doi:10.1371/journal.pbio.3001786
apa: Sethi, A., Wei, H., Mishra, N., Segos, I., Lambie, E. J., Zanin, E., &
Conradt, B. (2022). A caspase–RhoGEF axis contributes to the cell size threshold
for apoptotic death in developing Caenorhabditis elegans. PLOS Biology.
Public Library of Science. https://doi.org/10.1371/journal.pbio.3001786
chicago: Sethi, Aditya, Hai Wei, Nikhil Mishra, Ioannis Segos, Eric J. Lambie, Esther
Zanin, and Barbara Conradt. “A Caspase–RhoGEF Axis Contributes to the Cell Size
Threshold for Apoptotic Death in Developing Caenorhabditis Elegans.” PLOS Biology.
Public Library of Science, 2022. https://doi.org/10.1371/journal.pbio.3001786.
ieee: A. Sethi et al., “A caspase–RhoGEF axis contributes to the cell size
threshold for apoptotic death in developing Caenorhabditis elegans,” PLOS Biology,
vol. 20, no. 10. Public Library of Science, 2022.
ista: Sethi A, Wei H, Mishra N, Segos I, Lambie EJ, Zanin E, Conradt B. 2022. A
caspase–RhoGEF axis contributes to the cell size threshold for apoptotic death
in developing Caenorhabditis elegans. PLOS Biology. 20(10), e3001786.
mla: Sethi, Aditya, et al. “A Caspase–RhoGEF Axis Contributes to the Cell Size Threshold
for Apoptotic Death in Developing Caenorhabditis Elegans.” PLOS Biology,
vol. 20, no. 10, e3001786, Public Library of Science, 2022, doi:10.1371/journal.pbio.3001786.
short: A. Sethi, H. Wei, N. Mishra, I. Segos, E.J. Lambie, E. Zanin, B. Conradt,
PLOS Biology 20 (2022).
date_created: 2024-05-29T06:09:34Z
date_published: 2022-10-06T00:00:00Z
date_updated: 2024-08-06T07:08:54Z
day: '06'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1371/journal.pbio.3001786
external_id:
pmid:
- '36201522'
file:
- access_level: open_access
checksum: a7b46460b7819c196028481cc18a7c85
content_type: application/pdf
creator: dernst
date_created: 2024-08-06T07:07:52Z
date_updated: 2024-08-06T07:07:52Z
file_id: '17399'
file_name: 2022_PlosBio_Sethi.pdf
file_size: 2515388
relation: main_file
success: 1
file_date_updated: 2024-08-06T07:07:52Z
fulldoi: https://doi.org/10.1371/journal.pbio.3001786
has_accepted_license: '1'
intvolume: ' 20'
issue: '10'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLOS Biology
publication_identifier:
issn:
- 1545-7885
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: A caspase–RhoGEF axis contributes to the cell size threshold for apoptotic
death in developing Caenorhabditis elegans
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: 20
year: '2022'
...
---
_id: '10705'
abstract:
- lang: eng
text: Although rigidity and jamming transitions have been widely studied in physics
and material science, their importance in a number of biological processes, including
embryo development, tissue homeostasis, wound healing, and disease progression,
has only begun to be recognized in the past few years. The hypothesis that biological
systems can undergo rigidity/jamming transitions is attractive, as it would allow
these systems to change their material properties rapidly and strongly. However,
whether such transitions indeed occur in biological systems, how they are being
regulated, and what their physiological relevance might be, is still being debated.
Here, we review theoretical and experimental advances from the past few years,
focusing on the regulation and role of potential tissue rigidity transitions in
different biological processes.
acknowledgement: We thank present and former members of the Heisenberg and Hannezo
groups, in particular Bernat Corominas-Murtra and Nicoletta Petridou, for helpful
discussions, and Claudia Flandoli for the artwork. We apologize for not being able
to cite a number of highly relevant studies, to stay within the maximum allowed
number of citations.
article_processing_charge: No
article_type: original
author:
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- 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: Hannezo EB, Heisenberg C-PJ. Rigidity transitions in development and disease.
Trends in Cell Biology. 2022;32(5):P433-444. doi:10.1016/j.tcb.2021.12.006
apa: Hannezo, E. B., & Heisenberg, C.-P. J. (2022). Rigidity transitions in
development and disease. Trends in Cell Biology. Cell Press. https://doi.org/10.1016/j.tcb.2021.12.006
chicago: Hannezo, Edouard B, and Carl-Philipp J Heisenberg. “Rigidity Transitions
in Development and Disease.” Trends in Cell Biology. Cell Press, 2022.
https://doi.org/10.1016/j.tcb.2021.12.006.
ieee: E. B. Hannezo and C.-P. J. Heisenberg, “Rigidity transitions in development
and disease,” Trends in Cell Biology, vol. 32, no. 5. Cell Press, pp. P433-444,
2022.
ista: Hannezo EB, Heisenberg C-PJ. 2022. Rigidity transitions in development and
disease. Trends in Cell Biology. 32(5), P433-444.
mla: Hannezo, Edouard B., and Carl-Philipp J. Heisenberg. “Rigidity Transitions
in Development and Disease.” Trends in Cell Biology, vol. 32, no. 5, Cell
Press, 2022, pp. P433-444, doi:10.1016/j.tcb.2021.12.006.
short: E.B. Hannezo, C.-P.J. Heisenberg, Trends in Cell Biology 32 (2022) P433-444.
corr_author: '1'
date_created: 2022-01-30T23:01:34Z
date_published: 2022-05-01T00:00:00Z
date_updated: 2024-10-09T21:01:30Z
day: '01'
department:
- _id: EdHa
- _id: CaHe
doi: 10.1016/j.tcb.2021.12.006
external_id:
isi:
- '000795773900009'
pmid:
- '35058104'
fulldoi: https://doi.org/10.1016/j.tcb.2021.12.006
intvolume: ' 32'
isi: 1
issue: '5'
language:
- iso: eng
month: '05'
oa_version: None
page: P433-444
pmid: 1
publication: Trends in Cell Biology
publication_identifier:
eissn:
- 1879-3088
issn:
- 0962-8924
publication_status: published
publisher: Cell Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Rigidity transitions in development and disease
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 32
year: '2022'
...
---
_id: '9336'
abstract:
- lang: eng
text: Mentorship is experience and/or knowledge‐based guidance. Mentors support,
sponsor and advocate for mentees. Having one or more mentors when you seek advice
can significantly influence and improve your research endeavours, well‐being and
career development. Positive mentee–mentor relationships are vital for maintaining
work–life balance and success in careers. Early‐career researchers (ECRs), in
particular, can benefit from mentorship to navigate challenges in academic and
nonacademic life and careers. Yet, strategies for selecting mentors and maintaining
interactions with them are often underdiscussed within research environments.
In this Words of Advice, we provide recommendations for ECRs to seek and manage
mentorship interactions. Our article draws from our experiences as ECRs and published
work, to provide suggestions for mentees to proactively promote beneficial mentorship
interactions. The recommended practices highlight the importance of identifying
mentorship needs, planning and selecting multiple and diverse mentors, setting
goals, and maintaining constructive, and mutually beneficial working relationships
with mentors.
acknowledgement: The authors thank Nicholas Asby of the University of Chicago for
valuable comments on an earlier version of this work. A.P.S. was partially supported
by the NARSAD Young Investigator Grant 27705. S.J.H was supported by the National
Institutes of Health grant R35GM133732.
alternative_title:
- Words of Advice
article_processing_charge: No
article_type: original
author:
- first_name: Sarvenaz
full_name: Sarabipour, Sarvenaz
last_name: Sarabipour
- first_name: Sarah J.
full_name: Hainer, Sarah J.
last_name: Hainer
- first_name: Feyza N
full_name: Arslan, Feyza N
id: 49DA7910-F248-11E8-B48F-1D18A9856A87
last_name: Arslan
orcid: 0000-0001-5809-9566
- first_name: Charlotte M.
full_name: De Winde, Charlotte M.
last_name: De Winde
- first_name: Emily
full_name: Furlong, Emily
last_name: Furlong
- first_name: Natalia
full_name: Bielczyk, Natalia
last_name: Bielczyk
- first_name: Nafisa M.
full_name: Jadavji, Nafisa M.
last_name: Jadavji
- first_name: Aparna P.
full_name: Shah, Aparna P.
last_name: Shah
- first_name: Sejal
full_name: Davla, Sejal
last_name: Davla
citation:
ama: Sarabipour S, Hainer SJ, Arslan FN, et al. Building and sustaining mentor interactions
as a mentee. FEBS Journal. 2022;289(6):1374-1384. doi:10.1111/febs.15823
apa: Sarabipour, S., Hainer, S. J., Arslan, F. N., De Winde, C. M., Furlong, E.,
Bielczyk, N., … Davla, S. (2022). Building and sustaining mentor interactions
as a mentee. FEBS Journal. Wiley. https://doi.org/10.1111/febs.15823
chicago: Sarabipour, Sarvenaz, Sarah J. Hainer, Feyza N Arslan, Charlotte M. De
Winde, Emily Furlong, Natalia Bielczyk, Nafisa M. Jadavji, Aparna P. Shah, and
Sejal Davla. “Building and Sustaining Mentor Interactions as a Mentee.” FEBS
Journal. Wiley, 2022. https://doi.org/10.1111/febs.15823.
ieee: S. Sarabipour et al., “Building and sustaining mentor interactions
as a mentee,” FEBS Journal, vol. 289, no. 6. Wiley, pp. 1374–1384, 2022.
ista: Sarabipour S, Hainer SJ, Arslan FN, De Winde CM, Furlong E, Bielczyk N, Jadavji
NM, Shah AP, Davla S. 2022. Building and sustaining mentor interactions as a mentee.
FEBS Journal. 289(6), 1374–1384.
mla: Sarabipour, Sarvenaz, et al. “Building and Sustaining Mentor Interactions as
a Mentee.” FEBS Journal, vol. 289, no. 6, Wiley, 2022, pp. 1374–84, doi:10.1111/febs.15823.
short: S. Sarabipour, S.J. Hainer, F.N. Arslan, C.M. De Winde, E. Furlong, N. Bielczyk,
N.M. Jadavji, A.P. Shah, S. Davla, FEBS Journal 289 (2022) 1374–1384.
date_created: 2021-04-18T22:01:43Z
date_published: 2022-03-01T00:00:00Z
date_updated: 2026-06-18T19:47:28Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1111/febs.15823
external_id:
isi:
- '000636678800001'
pmid:
- '33818917'
fulldoi: https://doi.org/10.1111/febs.15823
intvolume: ' 289'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1111/febs.15823
month: '03'
oa: 1
oa_version: Published Version
page: 1374-1384
pmid: 1
publication: FEBS Journal
publication_identifier:
eissn:
- 1742-4658
issn:
- 1742-464X
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Building and sustaining mentor interactions as a mentee
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 289
year: '2022'
...
---
_id: '9794'
abstract:
- lang: eng
text: 'Lymph nodes (LNs) comprise two main structural elements: fibroblastic reticular
cells that form dedicated niches for immune cell interaction and capsular fibroblasts
that build a shell around the organ. Immunological challenge causes LNs to increase
more than tenfold in size within a few days. Here, we characterized the biomechanics
of LN swelling on the cellular and organ scale. We identified lymphocyte trapping
by influx and proliferation as drivers of an outward pressure force, causing fibroblastic
reticular cells of the T-zone (TRCs) and their associated conduits to stretch.
After an initial phase of relaxation, TRCs sensed the resulting strain through
cell matrix adhesions, which coordinated local growth and remodeling of the stromal
network. While the expanded TRC network readopted its typical configuration, a
massive fibrotic reaction of the organ capsule set in and countered further organ
expansion. Thus, different fibroblast populations mechanically control LN swelling
in a multitier fashion.'
acknowledged_ssus:
- _id: Bio
- _id: EM-Fac
- _id: PreCl
- _id: LifeSc
acknowledgement: This research was supported by the Scientific Service Units of IST
Austria through resources provided by the Imaging and Optics, Electron Microscopy,
Preclinical and Life Science Facilities. We thank C. Moussion for providing anti-PNAd
antibody and D. Critchley for Talin1-floxed mice, and E. Papusheva for providing
a custom 3D channel alignment script. This work was supported by a European Research
Council grant ERC-CoG-72437 to M.S. M.H. was supported by Czech Sciencundation GACR
20-24603Y and Charles University PRIMUS/20/MED/013.
article_processing_charge: No
article_type: original
author:
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Shayan
full_name: Shamipour, Shayan
id: 40B34FE2-F248-11E8-B48F-1D18A9856A87
last_name: Shamipour
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Tommaso
full_name: Costanzo, Tommaso
id: D93824F4-D9BA-11E9-BB12-F207E6697425
last_name: Costanzo
orcid: 0000-0001-9732-3815
- first_name: Gabriel
full_name: Krens, Gabriel
id: 2B819732-F248-11E8-B48F-1D18A9856A87
last_name: Krens
orcid: 0000-0003-4761-5996
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Burkhard
full_name: Ludewig, Burkhard
last_name: Ludewig
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- 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
- first_name: Wolfgang
full_name: Weninger, Wolfgang
last_name: Weninger
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Sanjiv A.
full_name: Luther, Sanjiv A.
last_name: Luther
- first_name: Jens V.
full_name: Stein, Jens V.
last_name: Stein
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-4561-241X
citation:
ama: Assen FP, Abe J, Hons M, et al. Multitier mechanics control stromal adaptations
in swelling lymph nodes. Nature Immunology. 2022;23:1246-1255. doi:10.1038/s41590-022-01257-4
apa: Assen, F. P., Abe, J., Hons, M., Hauschild, R., Shamipour, S., Kaufmann, W.,
… Sixt, M. K. (2022). Multitier mechanics control stromal adaptations in swelling
lymph nodes. Nature Immunology. Springer Nature. https://doi.org/10.1038/s41590-022-01257-4
chicago: Assen, Frank P, Jun Abe, Miroslav Hons, Robert Hauschild, Shayan Shamipour,
Walter Kaufmann, Tommaso Costanzo, et al. “Multitier Mechanics Control Stromal
Adaptations in Swelling Lymph Nodes.” Nature Immunology. Springer Nature,
2022. https://doi.org/10.1038/s41590-022-01257-4.
ieee: F. P. Assen et al., “Multitier mechanics control stromal adaptations
in swelling lymph nodes,” Nature Immunology, vol. 23. Springer Nature,
pp. 1246–1255, 2022.
ista: Assen FP, Abe J, Hons M, Hauschild R, Shamipour S, Kaufmann W, Costanzo T,
Krens G, Brown M, Ludewig B, Hippenmeyer S, Heisenberg C-PJ, Weninger W, Hannezo
EB, Luther SA, Stein JV, Sixt MK. 2022. Multitier mechanics control stromal adaptations
in swelling lymph nodes. Nature Immunology. 23, 1246–1255.
mla: Assen, Frank P., et al. “Multitier Mechanics Control Stromal Adaptations in
Swelling Lymph Nodes.” Nature Immunology, vol. 23, Springer Nature, 2022,
pp. 1246–55, doi:10.1038/s41590-022-01257-4.
short: F.P. Assen, J. Abe, M. Hons, R. Hauschild, S. Shamipour, W. Kaufmann, T.
Costanzo, G. Krens, M. Brown, B. Ludewig, S. Hippenmeyer, C.-P.J. Heisenberg,
W. Weninger, E.B. Hannezo, S.A. Luther, J.V. Stein, M.K. Sixt, Nature Immunology
23 (2022) 1246–1255.
corr_author: '1'
date_created: 2021-08-06T09:09:11Z
date_published: 2022-07-11T00:00:00Z
date_updated: 2025-06-11T13:52:43Z
day: '11'
ddc:
- '570'
department:
- _id: SiHi
- _id: CaHe
- _id: EdHa
- _id: EM-Fac
- _id: Bio
- _id: MiSi
doi: 10.1038/s41590-022-01257-4
ec_funded: 1
external_id:
isi:
- '000822975900002'
pmid:
- '35817845'
file:
- access_level: open_access
checksum: 628e7b49809f22c75b428842efe70c68
content_type: application/pdf
creator: dernst
date_created: 2022-07-25T07:11:32Z
date_updated: 2022-07-25T07:11:32Z
file_id: '11642'
file_name: 2022_NatureImmunology_Assen.pdf
file_size: 11475325
relation: main_file
success: 1
file_date_updated: 2022-07-25T07:11:32Z
fulldoi: https://doi.org/10.1038/s41590-022-01257-4
has_accepted_license: '1'
intvolume: ' 23'
isi: 1
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: 1246-1255
pmid: 1
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular Navigation Along Spatial Gradients
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: Multitier mechanics control stromal adaptations in swelling lymph nodes
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: 23
year: '2022'
...
---
_id: '10766'
abstract:
- lang: eng
text: Tension of the actomyosin cell cortex plays a key role in determining cell–cell
contact growth and size. The level of cortical tension outside of the cell–cell
contact, when pulling at the contact edge, scales with the total size to which
a cell–cell contact can grow [J.-L. Maître et al., Science 338, 253–256 (2012)].
Here, we show in zebrafish primary germ-layer progenitor cells that this monotonic
relationship only applies to a narrow range of cortical tension increase and that
above a critical threshold, contact size inversely scales with cortical tension.
This switch from cortical tension increasing to decreasing progenitor cell–cell
contact size is caused by cortical tension promoting E-cadherin anchoring to the
actomyosin cytoskeleton, thereby increasing clustering and stability of E-cadherin
at the contact. After tension-mediated E-cadherin stabilization at the contact
exceeds a critical threshold level, the rate by which the contact expands in response
to pulling forces from the cortex sharply drops, leading to smaller contacts at
physiologically relevant timescales of contact formation. Thus, the activity of
cortical tension in expanding cell–cell contact size is limited by tension-stabilizing
E-cadherin–actin complexes at the contact.
acknowledged_ssus:
- _id: Bio
- _id: EM-Fac
- _id: PreCl
acknowledgement: 'We thank Guillaume Salbreaux, Silvia Grigolon, Edouard Hannezo,
and Vanessa Barone for discussions and comments on the manuscript and Shayan Shamipour
and Daniel Capek for help with data analysis. We also thank the Imaging & Optics,
Electron Microscopy, and Zebrafish Facility Scientific Service Units at the Institute
of Science and Technology Austria (ISTA)Nasser Darwish-Miranda for continuous support.
We acknowledge Hitoshi Morita for the gift of VinculinB-GFP plasmid. This research
was supported by an ISTA Fellow Marie-Curie Co-funding of regional, national, and
international programmes Grant P_IST_EU01 (to J.S.), European Molecular Biology
Organization Long-Term Fellowship Grant, ALTF reference number: 187-2013 (to M.S.),
Schroedinger Fellowship J4332-B28 (to M.S.), and European Research Council Advanced
Grant (MECSPEC; to C.-P.H.).'
article_number: e2122030119
article_processing_charge: No
article_type: original
author:
- first_name: Jana
full_name: Slovakova, Jana
id: 30F3F2F0-F248-11E8-B48F-1D18A9856A87
last_name: Slovakova
- first_name: Mateusz K
full_name: Sikora, Mateusz K
id: 2F74BCDE-F248-11E8-B48F-1D18A9856A87
last_name: Sikora
- first_name: Feyza N
full_name: Arslan, Feyza N
id: 49DA7910-F248-11E8-B48F-1D18A9856A87
last_name: Arslan
orcid: 0000-0001-5809-9566
- 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: Gabriel
full_name: Krens, Gabriel
id: 2B819732-F248-11E8-B48F-1D18A9856A87
last_name: Krens
orcid: 0000-0003-4761-5996
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- 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: Slovakova J, Sikora MK, Arslan FN, et al. Tension-dependent stabilization of
E-cadherin limits cell-cell contact expansion in zebrafish germ-layer progenitor
cells. Proceedings of the National Academy of Sciences of the United States
of America. 2022;119(8). doi:10.1073/pnas.2122030119
apa: Slovakova, J., Sikora, M. K., Arslan, F. N., Caballero Mancebo, S., Krens,
G., Kaufmann, W., … Heisenberg, C.-P. J. (2022). Tension-dependent stabilization
of E-cadherin limits cell-cell contact expansion in zebrafish germ-layer progenitor
cells. Proceedings of the National Academy of Sciences of the United States
of America. National Academy of Sciences. https://doi.org/10.1073/pnas.2122030119
chicago: Slovakova, Jana, Mateusz K Sikora, Feyza N Arslan, Silvia Caballero Mancebo,
Gabriel Krens, Walter Kaufmann, Jack Merrin, and Carl-Philipp J Heisenberg. “Tension-Dependent
Stabilization of E-Cadherin Limits Cell-Cell Contact Expansion in Zebrafish Germ-Layer
Progenitor Cells.” Proceedings of the National Academy of Sciences of the United
States of America. National Academy of Sciences, 2022. https://doi.org/10.1073/pnas.2122030119.
ieee: J. Slovakova et al., “Tension-dependent stabilization of E-cadherin
limits cell-cell contact expansion in zebrafish germ-layer progenitor cells,”
Proceedings of the National Academy of Sciences of the United States of America,
vol. 119, no. 8. National Academy of Sciences, 2022.
ista: Slovakova J, Sikora MK, Arslan FN, Caballero Mancebo S, Krens G, Kaufmann
W, Merrin J, Heisenberg C-PJ. 2022. Tension-dependent stabilization of E-cadherin
limits cell-cell contact expansion in zebrafish germ-layer progenitor cells. Proceedings
of the National Academy of Sciences of the United States of America. 119(8), e2122030119.
mla: Slovakova, Jana, et al. “Tension-Dependent Stabilization of E-Cadherin Limits
Cell-Cell Contact Expansion in Zebrafish Germ-Layer Progenitor Cells.” Proceedings
of the National Academy of Sciences of the United States of America, vol.
119, no. 8, e2122030119, National Academy of Sciences, 2022, doi:10.1073/pnas.2122030119.
short: J. Slovakova, M.K. Sikora, F.N. Arslan, S. Caballero Mancebo, G. Krens, W.
Kaufmann, J. Merrin, C.-P.J. Heisenberg, Proceedings of the National Academy of
Sciences of the United States of America 119 (2022).
corr_author: '1'
date_created: 2022-02-20T23:01:31Z
date_published: 2022-02-14T00:00:00Z
date_updated: 2026-07-06T12:45:39Z
day: '14'
ddc:
- '570'
department:
- _id: CaHe
- _id: EM-Fac
- _id: Bio
doi: 10.1073/pnas.2122030119
ec_funded: 1
external_id:
isi:
- '000766926900009'
pmid:
- '35165179'
file:
- access_level: open_access
checksum: d49f83c3580613966f71768ddb9a55a5
content_type: application/pdf
creator: dernst
date_created: 2022-02-21T08:45:11Z
date_updated: 2022-02-21T08:45:11Z
file_id: '10780'
file_name: 2022_PNAS_Slovakova.pdf
file_size: 1609678
relation: main_file
success: 1
file_date_updated: 2022-02-21T08:45:11Z
fulldoi: https://doi.org/10.1073/pnas.2122030119
has_accepted_license: '1'
intvolume: ' 119'
isi: 1
issue: '8'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
- _id: 2521E28E-B435-11E9-9278-68D0E5697425
grant_number: 187-2013
name: Modulation of adhesion function in cell-cell contact formation by cortical
tension
publication: Proceedings of the National Academy of Sciences of the United States
of America
publication_identifier:
eissn:
- 1091-6490
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
related_material:
record:
- id: '9750'
relation: earlier_version
status: public
scopus_import: '1'
status: public
title: Tension-dependent stabilization of E-cadherin limits cell-cell contact expansion
in zebrafish germ-layer progenitor cells
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 119
year: '2022'
...
---
_id: '12231'
abstract:
- lang: eng
text: Ventral tail bending, which is transient but pronounced, is found in many
chordate embryos and constitutes an interesting model of how tissue interactions
control embryo shape. Here, we identify one key upstream regulator of ventral
tail bending in embryos of the ascidian Ciona. We show that during the early tailbud
stages, ventral epidermal cells exhibit a boat-shaped morphology (boat cell) with
a narrow apical surface where phosphorylated myosin light chain (pMLC) accumulates.
We further show that interfering with the function of the BMP ligand Admp led
to pMLC localizing to the basal instead of the apical side of ventral epidermal
cells and a reduced number of boat cells. Finally, we show that cutting ventral
epidermal midline cells at their apex using an ultraviolet laser relaxed ventral
tail bending. Based on these results, we propose a previously unreported function
for Admp in localizing pMLC to the apical side of ventral epidermal cells, which
causes the tail to bend ventrally by resisting antero-posterior notochord extension
at the ventral side of the tail.
acknowledgement: "iona intestinalis adults were provided by Dr Yutaka Satou (Kyoto
University) and Dr Manabu Yoshida (the University of Tokyo) with support from the
National Bio-Resource Project of AMED, Japan. We thank Dr Hidehiko Hashimoto and
Dr Yuji Mizotani for technical information about 1P-myosin antibody staining. We
thank Dr Kaoru Imai and Dr Yutaka Satou for valuable discussion about Admp and for
the DNA construct of Bmp2/4 under the Dlx.b upstream sequence. We thank Ms Maki
Kogure for constructing the FUSION360 of the intercalating epidermal cell.\r\nThis
work was supported by funding from the Japan Society for the Promotion of Science
(JP16H01451, JP21H00440). Open Access funding provided by Keio University: Keio
Gijuku Daigaku."
article_number: dev200215
article_processing_charge: No
article_type: original
author:
- first_name: Yuki S.
full_name: Kogure, Yuki S.
last_name: Kogure
- first_name: Hiromochi
full_name: Muraoka, Hiromochi
last_name: Muraoka
- first_name: Wataru C.
full_name: Koizumi, Wataru C.
last_name: Koizumi
- first_name: Raphaël
full_name: Gelin-alessi, Raphaël
last_name: Gelin-alessi
- first_name: Benoit G
full_name: Godard, Benoit G
id: 33280250-F248-11E8-B48F-1D18A9856A87
last_name: Godard
- first_name: Kotaro
full_name: Oka, Kotaro
last_name: Oka
- 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
- first_name: Kohji
full_name: Hotta, Kohji
last_name: Hotta
citation:
ama: Kogure YS, Muraoka H, Koizumi WC, et al. Admp regulates tail bending by controlling
ventral epidermal cell polarity via phosphorylated myosin localization in Ciona.
Development. 2022;149(21). doi:10.1242/dev.200215
apa: Kogure, Y. S., Muraoka, H., Koizumi, W. C., Gelin-alessi, R., Godard, B. G.,
Oka, K., … Hotta, K. (2022). Admp regulates tail bending by controlling ventral
epidermal cell polarity via phosphorylated myosin localization in Ciona. Development.
Company of Biologists. https://doi.org/10.1242/dev.200215
chicago: Kogure, Yuki S., Hiromochi Muraoka, Wataru C. Koizumi, Raphaël Gelin-alessi,
Benoit G Godard, Kotaro Oka, Carl-Philipp J Heisenberg, and Kohji Hotta. “Admp
Regulates Tail Bending by Controlling Ventral Epidermal Cell Polarity via Phosphorylated
Myosin Localization in Ciona.” Development. Company of Biologists, 2022.
https://doi.org/10.1242/dev.200215.
ieee: Y. S. Kogure et al., “Admp regulates tail bending by controlling ventral
epidermal cell polarity via phosphorylated myosin localization in Ciona,” Development,
vol. 149, no. 21. Company of Biologists, 2022.
ista: Kogure YS, Muraoka H, Koizumi WC, Gelin-alessi R, Godard BG, Oka K, Heisenberg
C-PJ, Hotta K. 2022. Admp regulates tail bending by controlling ventral epidermal
cell polarity via phosphorylated myosin localization in Ciona. Development. 149(21),
dev200215.
mla: Kogure, Yuki S., et al. “Admp Regulates Tail Bending by Controlling Ventral
Epidermal Cell Polarity via Phosphorylated Myosin Localization in Ciona.” Development,
vol. 149, no. 21, dev200215, Company of Biologists, 2022, doi:10.1242/dev.200215.
short: Y.S. Kogure, H. Muraoka, W.C. Koizumi, R. Gelin-alessi, B.G. Godard, K. Oka,
C.-P.J. Heisenberg, K. Hotta, Development 149 (2022).
corr_author: '1'
date_created: 2023-01-16T09:50:12Z
date_published: 2022-11-01T00:00:00Z
date_updated: 2026-08-12T09:59:24Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1242/dev.200215
external_id:
isi:
- '000903991700002'
pmid:
- '36227591'
file:
- access_level: open_access
checksum: 871b9c58eb79b9e60752de25a46938d6
content_type: application/pdf
creator: dernst
date_created: 2023-01-27T10:36:50Z
date_updated: 2023-01-27T10:36:50Z
file_id: '12423'
file_name: 2022_Development_Kogure.pdf
file_size: 9160451
relation: main_file
success: 1
file_date_updated: 2023-01-27T10:36:50Z
fulldoi: https://doi.org/10.1242/dev.200215
has_accepted_license: '1'
intvolume: ' 149'
isi: 1
issue: '21'
keyword:
- Developmental Biology
- Molecular Biology
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Admp regulates tail bending by controlling ventral epidermal cell polarity
via phosphorylated myosin localization in Ciona
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: 149
year: '2022'
...
---
_id: '15264'
abstract:
- lang: eng
text: Signaling by the B cell antigen receptor (BCR) initiates actin remodeling.
The assembly of branched actin networks that are nucleated by the Arp2/3 complex
exert outward force on the plasma membrane, allowing B cells to form membrane
protrusions that can scan the surface of antigen-presenting cells (APCs). The
resulting Arp2/3 complex-dependent actin retrograde flow promotes the centripetal
movement and progressive coalescence of BCR microclusters, which amplifies BCR
signaling. Glia maturation factor γ (GMFγ) is an actin disassembly-protein that
releases Arp2/3 complex-nucleated actin filaments from actin networks. By doing
so, GMFγ could either oppose the actions of the Arp2/3 complex or support Arp2/3
complex-nucleated actin polymerization by contributing to the recycling of actin
monomers and Arp2/3 complexes. We now show that reducing the levels of GMFγ in
human B cell lines via transfection with a specific siRNA impairs the ability
of B cells to spread on antigen-coated surfaces, decreases the velocity of actin
retrograde flow, diminishes the coalescence of BCR microclusters into a central
cluster at the B cell-APC contact site, and decreases APC-induced BCR signaling.
These effects of depleting GMFγ are similar to what occurs when the Arp2/3 complex
is inhibited. This suggests that GMFγ cooperates with the Arp2/3 complex to support
BCR-induced actin remodeling and amplify BCR signaling at the immune synapse.
article_number: '647063'
article_processing_charge: No
article_type: original
author:
- first_name: Nikola
full_name: Deretic, Nikola
last_name: Deretic
- 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: Kate
full_name: Choi, Kate
last_name: Choi
- first_name: Libin
full_name: Abraham, Libin
last_name: Abraham
- first_name: Michael R.
full_name: Gold, Michael R.
last_name: Gold
citation:
ama: Deretic N, Bolger-Munro M, Choi K, Abraham L, Gold MR. The actin-disassembly
protein glia maturation factor γ enhances actin remodeling and B cell antigen
receptor signaling at the immune synapse. Frontiers in Cell and Developmental
Biology. 2021;9. doi:10.3389/fcell.2021.647063
apa: Deretic, N., Bolger-Munro, M., Choi, K., Abraham, L., & Gold, M. R. (2021).
The actin-disassembly protein glia maturation factor γ enhances actin remodeling
and B cell antigen receptor signaling at the immune synapse. Frontiers in Cell
and Developmental Biology. Frontiers Media. https://doi.org/10.3389/fcell.2021.647063
chicago: Deretic, Nikola, Madison Bolger-Munro, Kate Choi, Libin Abraham, and Michael
R. Gold. “The Actin-Disassembly Protein Glia Maturation Factor γ Enhances Actin
Remodeling and B Cell Antigen Receptor Signaling at the Immune Synapse.” Frontiers
in Cell and Developmental Biology. Frontiers Media, 2021. https://doi.org/10.3389/fcell.2021.647063.
ieee: N. Deretic, M. Bolger-Munro, K. Choi, L. Abraham, and M. R. Gold, “The actin-disassembly
protein glia maturation factor γ enhances actin remodeling and B cell antigen
receptor signaling at the immune synapse,” Frontiers in Cell and Developmental
Biology, vol. 9. Frontiers Media, 2021.
ista: Deretic N, Bolger-Munro M, Choi K, Abraham L, Gold MR. 2021. The actin-disassembly
protein glia maturation factor γ enhances actin remodeling and B cell antigen
receptor signaling at the immune synapse. Frontiers in Cell and Developmental
Biology. 9, 647063.
mla: Deretic, Nikola, et al. “The Actin-Disassembly Protein Glia Maturation Factor
γ Enhances Actin Remodeling and B Cell Antigen Receptor Signaling at the Immune
Synapse.” Frontiers in Cell and Developmental Biology, vol. 9, 647063,
Frontiers Media, 2021, doi:10.3389/fcell.2021.647063.
short: N. Deretic, M. Bolger-Munro, K. Choi, L. Abraham, M.R. Gold, Frontiers in
Cell and Developmental Biology 9 (2021).
date_created: 2024-04-03T07:34:08Z
date_published: 2021-07-01T00:00:00Z
date_updated: 2024-04-03T14:10:25Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.3389/fcell.2021.647063
external_id:
pmid:
- '34336818'
file:
- access_level: open_access
checksum: f6330b5c6718d6780383c0300fd4ef12
content_type: application/pdf
creator: dernst
date_created: 2024-04-03T14:08:05Z
date_updated: 2024-04-03T14:08:05Z
file_id: '15291'
file_name: 2021_Frontiers_Deretic.pdf
file_size: 7430029
relation: main_file
success: 1
file_date_updated: 2024-04-03T14:08:05Z
fulldoi: https://doi.org/10.3389/fcell.2021.647063
has_accepted_license: '1'
intvolume: ' 9'
keyword:
- Cell Biology
- Developmental Biology
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: Frontiers in Cell and Developmental Biology
publication_identifier:
issn:
- 2296-634X
publication_status: published
publisher: Frontiers Media
quality_controlled: '1'
scopus_import: '1'
status: public
title: The actin-disassembly protein glia maturation factor γ enhances actin remodeling
and B cell antigen receptor signaling at the immune synapse
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2021'
...
---
_id: '10202'
abstract:
- lang: eng
text: Zygotic genome activation (ZGA) initiates regionalized transcription underlying
distinct cellular identities. ZGA is dependent upon dynamic chromatin architecture
sculpted by conserved DNA-binding proteins. However, the direct mechanistic link
between the onset of ZGA and the tissue-specific transcription remains unclear.
Here, we have addressed the involvement of chromatin organizer Satb2 in orchestrating
both processes during zebrafish embryogenesis. Integrative analysis of transcriptome,
genome-wide occupancy and chromatin accessibility reveals contrasting molecular
activities of maternally deposited and zygotically synthesized Satb2. Maternal
Satb2 prevents premature transcription of zygotic genes by influencing the interplay
between the pluripotency factors. By contrast, zygotic Satb2 activates transcription
of the same group of genes during neural crest development and organogenesis.
Thus, our comparative analysis of maternal versus zygotic function of Satb2 underscores
how these antithetical activities are temporally coordinated and functionally
implemented highlighting the evolutionary implications of the biphasic and bimodal
regulation of landmark developmental transitions by a single determinant.
acknowledgement: 'We are grateful to the members of C.-P.H. and SG lab for discussions.
Authors thank Shubha Tole for providing embryonic mouse tissues. Authors are grateful
to Alessandro Mongera and Chetana Sachidanandan for generous help with Tg: Sox10:
GFP line. Authors would like to thank Satyajeet Khare, Vanessa Barone, Jyothish
S., Shalini Mishra, Yoshita Bhide, and Keshav Jha for assistance in experiments.
We would also like to thank Chaitanya Dingare for valuable suggestions. We thank
Diana Pinhiero and Alexandra Schauer for critical reading of early versions of the
manuscript. This work was supported by the Centre of Excellence in Epigenetics program
of the Department of Biotechnology, Government of India Phase I (BT/01/COE/09/07)
to S.G. and R.K.M., and Phase II (BT/COE/34/SP17426/2016) to S.G. and JC Bose Fellowship
(JCB/2019/000013) from Science and Engineering Research Board, Government of India
to S.G., DST-BMWF Indo-Austrian bilateral program grant to S.G. and C.-P.H. The
work using animal models was partly supported by the infrastructure support grants
from the Department of Biotechnology (National Facility for Laboratory Model Organisms:
BT/INF/22/SP17358/2016 and Establishment of a Pune Biotech Cluster, Model Organism
to Human Disease: B-2 Whole Animal Imaging & Tissue Processing FacilityBT/Pune-Biocluster/01/2015).
S.J.P. was supported by Fellowship from the Council of Scientific and Industrial
Research, India and travel fellowship from the Company of Biologists, UK. P.C.R.
was supported by the Early Career Fellowship of the Wellcome Trust-DBT India Alliance
(IA/E/16/1/503057). A.S. was supported by UGC and R.S. was supported by CSIR India.
M.S. was supported by core funding from the Tata Institute of Fundamental Research
(TIFR 12P-121).'
article_number: '6094'
article_processing_charge: Yes
article_type: original
author:
- first_name: Saurabh J.
full_name: Pradhan, Saurabh J.
last_name: Pradhan
- first_name: Puli Chandramouli
full_name: Reddy, Puli Chandramouli
last_name: Reddy
- first_name: Michael
full_name: Smutny, Michael
id: 3FE6E4E8-F248-11E8-B48F-1D18A9856A87
last_name: Smutny
orcid: 0000-0002-5920-9090
- first_name: Ankita
full_name: Sharma, Ankita
last_name: Sharma
- first_name: Keisuke
full_name: Sako, Keisuke
id: 3BED66BE-F248-11E8-B48F-1D18A9856A87
last_name: Sako
orcid: 0000-0002-6453-8075
- first_name: Meghana S.
full_name: Oak, Meghana S.
last_name: Oak
- first_name: Rini
full_name: Shah, Rini
last_name: Shah
- first_name: Mrinmoy
full_name: Pal, Mrinmoy
last_name: Pal
- first_name: Ojas
full_name: Deshpande, Ojas
last_name: Deshpande
- first_name: Greg
full_name: Dsilva, Greg
last_name: Dsilva
- first_name: Yin
full_name: Tang, Yin
last_name: Tang
- first_name: Rakesh
full_name: Mishra, Rakesh
last_name: Mishra
- first_name: Girish
full_name: Deshpande, Girish
last_name: Deshpande
- first_name: Antonio J.
full_name: Giraldez, Antonio J.
last_name: Giraldez
- first_name: Mahendra
full_name: Sonawane, Mahendra
last_name: Sonawane
- 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
- first_name: Sanjeev
full_name: Galande, Sanjeev
last_name: Galande
citation:
ama: Pradhan SJ, Reddy PC, Smutny M, et al. Satb2 acts as a gatekeeper for major
developmental transitions during early vertebrate embryogenesis. Nature Communications.
2021;12(1). doi:10.1038/s41467-021-26234-7
apa: Pradhan, S. J., Reddy, P. C., Smutny, M., Sharma, A., Sako, K., Oak, M. S.,
… Galande, S. (2021). Satb2 acts as a gatekeeper for major developmental transitions
during early vertebrate embryogenesis. Nature Communications. Springer
Nature. https://doi.org/10.1038/s41467-021-26234-7
chicago: Pradhan, Saurabh J., Puli Chandramouli Reddy, Michael Smutny, Ankita Sharma,
Keisuke Sako, Meghana S. Oak, Rini Shah, et al. “Satb2 Acts as a Gatekeeper for
Major Developmental Transitions during Early Vertebrate Embryogenesis.” Nature
Communications. Springer Nature, 2021. https://doi.org/10.1038/s41467-021-26234-7.
ieee: S. J. Pradhan et al., “Satb2 acts as a gatekeeper for major developmental
transitions during early vertebrate embryogenesis,” Nature Communications,
vol. 12, no. 1. Springer Nature, 2021.
ista: Pradhan SJ, Reddy PC, Smutny M, Sharma A, Sako K, Oak MS, Shah R, Pal M, Deshpande
O, Dsilva G, Tang Y, Mishra R, Deshpande G, Giraldez AJ, Sonawane M, Heisenberg
C-PJ, Galande S. 2021. Satb2 acts as a gatekeeper for major developmental transitions
during early vertebrate embryogenesis. Nature Communications. 12(1), 6094.
mla: Pradhan, Saurabh J., et al. “Satb2 Acts as a Gatekeeper for Major Developmental
Transitions during Early Vertebrate Embryogenesis.” Nature Communications,
vol. 12, no. 1, 6094, Springer Nature, 2021, doi:10.1038/s41467-021-26234-7.
short: S.J. Pradhan, P.C. Reddy, M. Smutny, A. Sharma, K. Sako, M.S. Oak, R. Shah,
M. Pal, O. Deshpande, G. Dsilva, Y. Tang, R. Mishra, G. Deshpande, A.J. Giraldez,
M. Sonawane, C.-P.J. Heisenberg, S. Galande, Nature Communications 12 (2021).
corr_author: '1'
date_created: 2021-10-31T23:01:29Z
date_published: 2021-10-19T00:00:00Z
date_updated: 2026-04-02T11:57:41Z
day: '19'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1038/s41467-021-26234-7
external_id:
isi:
- '000709050300016'
pmid:
- '34667153'
file:
- access_level: open_access
checksum: c40a69ae94435ecd3a30c9874a11ef2b
content_type: application/pdf
creator: cziletti
date_created: 2021-11-09T13:59:26Z
date_updated: 2021-11-09T13:59:26Z
file_id: '10262'
file_name: 2021_NatureComm_Pradhan.pdf
file_size: 7144437
relation: main_file
success: 1
file_date_updated: 2021-11-09T13:59:26Z
fulldoi: https://doi.org/10.1038/s41467-021-26234-7
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
issue: '1'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: Preprint
relation: earlier_version
url: 'https://doi.org/10.1101/2020.11.23.394171 '
scopus_import: '1'
status: public
title: Satb2 acts as a gatekeeper for major developmental transitions during early
vertebrate embryogenesis
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: 12
year: '2021'
...