---
OA_place: publisher
OA_type: hybrid
PlanS_conform: '1'
_id: '21015'
abstract:
- lang: eng
text: Early embryo geometry is one of the most invariant species-specific traits,
yet its role in ensuring developmental reproducibility and robustness remains
underexplored. Here we show that in zebrafish, the geometry of the fertilized
egg—specifically its curvature and volume—serves as a critical initial condition
triggering a cascade of events that influence development. The embryo geometry
guides patterned asymmetric cell divisions in the blastoderm, generating radial
gradients of cell volume and nucleocytoplasmic ratio. These gradients generate
mitotic phase waves, with the nucleocytoplasmic ratio determining individual cell
cycle periods independently of other cells. We demonstrate that reducing cell
autonomy reshapes these waves, emphasizing the instructive role of geometry-derived
volume patterns in setting the intrinsic period of the cell cycle oscillator.
In addition to organizing cell cycles, early embryo geometry spatially patterns
zygotic genome activation at the midblastula transition, a key step in establishing
embryonic autonomy. Disrupting the embryo shape alters the zygotic genome activation
pattern and causes ectopic germ layer specification, underscoring the developmental
significance of geometry. Together, our findings reveal a symmetry-breaking function
of early embryo geometry in coordinating cell cycle and transcriptional patterning.
acknowledged_ssus:
- _id: PreCl
- _id: Bio
- _id: ScienComp
- _id: LifeSc
acknowledgement: We thank N. Petridou (EMBL) for sharing results before publication.
N.M. was supported by funding from the European Union’s Horizon 2020 programme under
the Marie Skłodowska-Curie COFUND Actions ISTplus grant agreement number 754411.
Y.I.L. acknowledges funding from the European Union’s Horizon 2020 research and
innovation programme under the Marie Skłodowska-Curie grant agreement number 101034413.
The research was supported by funding to C.-P.H. from the NOMIS Foundation, Project
ID 1.844. We would like to thank past and present members of the Heisenberg and
Hannezo groups for discussions, particularly S. Shamipour, V. Doddihal, M. Jovic,
N. Hino, F. N. Arslan, R. Kobylinska and C. Camelo for feedback on the draft manuscript.
This research was supported by the Scientific Service Units (SSU) of Institute of
Science and Technology Austria through resources provided by the Aquatics Facility,
Imaging & Optics Facility (IOF), Scientific Computing (SciComp) facility and Lab
Support Facility (LSF). Open access funding provided by Institute of Science and
Technology (IST Austria).
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Nikhil
full_name: Mishra, Nikhil
id: C4D70E82-1081-11EA-B3ED-9A4C3DDC885E
last_name: Mishra
orcid: 0000-0002-6425-5788
- first_name: Yuting I
full_name: Li, Yuting I
id: ee7a5ca8-8b71-11ed-b662-b3341c05b7eb
last_name: Li
- 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: Mishra N, Li YI, Hannezo EB, Heisenberg C-PJ. Geometry-driven asymmetric cell
divisions pattern cell cycles and zygotic genome activation in the zebrafish embryo.
Nature Physics. 2026;22:139-150. doi:10.1038/s41567-025-03122-1
apa: Mishra, N., Li, Y. I., Hannezo, E. B., & Heisenberg, C.-P. J. (2026). Geometry-driven
asymmetric cell divisions pattern cell cycles and zygotic genome activation in
the zebrafish embryo. Nature Physics. Springer Nature. https://doi.org/10.1038/s41567-025-03122-1
chicago: Mishra, Nikhil, Yuting I Li, Edouard B Hannezo, and Carl-Philipp J Heisenberg.
“Geometry-Driven Asymmetric Cell Divisions Pattern Cell Cycles and Zygotic Genome
Activation in the Zebrafish Embryo.” Nature Physics. Springer Nature, 2026.
https://doi.org/10.1038/s41567-025-03122-1.
ieee: N. Mishra, Y. I. Li, E. B. Hannezo, and C.-P. J. Heisenberg, “Geometry-driven
asymmetric cell divisions pattern cell cycles and zygotic genome activation in
the zebrafish embryo,” Nature Physics, vol. 22. Springer Nature, pp. 139–150,
2026.
ista: Mishra N, Li YI, Hannezo EB, Heisenberg C-PJ. 2026. Geometry-driven asymmetric
cell divisions pattern cell cycles and zygotic genome activation in the zebrafish
embryo. Nature Physics. 22, 139–150.
mla: Mishra, Nikhil, et al. “Geometry-Driven Asymmetric Cell Divisions Pattern Cell
Cycles and Zygotic Genome Activation in the Zebrafish Embryo.” Nature Physics,
vol. 22, Springer Nature, 2026, pp. 139–50, doi:10.1038/s41567-025-03122-1.
short: N. Mishra, Y.I. Li, E.B. Hannezo, C.-P.J. Heisenberg, Nature Physics 22 (2026)
139–150.
corr_author: '1'
date_created: 2026-01-20T10:12:19Z
date_published: 2026-01-05T00:00:00Z
date_updated: 2026-04-28T12:55:30Z
day: '05'
ddc:
- '570'
department:
- _id: EdHa
- _id: CaHe
doi: 10.1038/s41567-025-03122-1
ec_funded: 1
external_id:
oaworkid:
- W7118187193
file:
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checksum: 0ab7ac2fbcb61a364dba57152db64ed7
content_type: application/pdf
creator: dernst
date_created: 2026-01-21T08:21:11Z
date_updated: 2026-01-21T08:21:11Z
file_id: '21026'
file_name: 2026_NaturePhysics_Mishra.pdf
file_size: 7335694
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success: 1
file_date_updated: 2026-01-21T08:21:11Z
has_accepted_license: '1'
intvolume: ' 22'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '01'
oa: 1
oa_version: Published Version
oaworkid: 1
page: 139-150
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: fc2ed2f7-9c52-11eb-aca3-c01059dda49c
call_identifier: H2020
grant_number: '101034413'
name: 'IST-BRIDGE: International postdoctoral program'
- _id: 917c023a-16d5-11f0-9cad-eb5cafc52090
name: Cytoplasmic self-organization into cell-like compartments as a common guiding
principle in early animal development
publication: Nature Physics
publication_identifier:
eissn:
- 1745-2481
issn:
- 1745-2473
issnl:
- ' 1745-2473'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on ISTA website
relation: research_data
url: https://ista.ac.at/en/news/geometry-shapes-life/
scopus_import: '1'
status: public
title: Geometry-driven asymmetric cell divisions pattern cell cycles and zygotic genome
activation in the zebrafish embryo
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: 22
year: '2026'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
PlanS_conform: '1'
_id: '20183'
abstract:
- lang: eng
text: The unequal segregation of organelles has been proposed to be an intrinsic
mechanism that contributes to cell fate divergence during asymmetric cell division;
however, in vivo evidence is sparse. Using super-resolution microscopy, we analysed
the segregation of organelles during the division of the neuroblast QL.p in C.
elegans larvae. QL.p divides to generate a daughter that survives, QL.pa, and
a daughter that dies, QL.pp. We found that mitochondria segregate unequally by
density and morphology and that this is dependent on mitochondrial dynamics. Furthermore,
we found that mitochondrial density in QL.pp correlates with the time it takes
QL.pp to die. We propose that low mitochondrial density in QL.pp promotes the
cell death fate and ensures that QL.pp dies in a highly reproducible and timely
manner. Our results provide in vivo evidence that the unequal segregation of mitochondria
can contribute to cell fate divergence during asymmetric cell division in a developing
animal.
acknowledgement: We thank members of the Conradt lab, the Center for Cell and Molecular
Dynamics (https://www.uclccmd.co.uk/) and T. Schedl for discussions and comments
on the manuscript. We thank L. McGuinness for excellent technical support. Some
strains were provided by the Caenorhabditis Genetics Center (CGC), which is funded
by NIH Office of Research Infrastructure Programs (P40 OD010440). We thank Alex
Hajnal (University of Zurich, Switzerland) and Andrew deMello (ETH Zurich, Switzerland)
for their support of S.B. This work was supported by a predoctoral fellowship from
the Studienstiftung des deutschen Volkes to NM, funds from UCL (Division of Biosciences,
UCL LSM Capital Equipment Fund) to B.C., and a Wolfson Fellowship from the Royal
Society (https://royalsociety.org/) to B.C. (RSWF\R1\180008), and the Biotechnology
and Biological Sciences Research Council (https://bbsrc.ukri.org/) (BB/V007572/1
and BB/V015648/1to B.C.).
article_number: '7174'
article_processing_charge: Yes
article_type: original
author:
- first_name: Ioannis
full_name: Segos, Ioannis
last_name: Segos
- first_name: Jens
full_name: Van Eeckhoven, Jens
last_name: Van Eeckhoven
- first_name: Simon
full_name: Berger, Simon
last_name: Berger
- first_name: Nikhil
full_name: Mishra, Nikhil
id: C4D70E82-1081-11EA-B3ED-9A4C3DDC885E
last_name: Mishra
orcid: 0000-0002-6425-5788
- first_name: Eric J.
full_name: Lambie, Eric J.
last_name: Lambie
- first_name: Barbara
full_name: Conradt, Barbara
last_name: Conradt
citation:
ama: Segos I, Van Eeckhoven J, Berger S, Mishra N, Lambie EJ, Conradt B. Unequal
segregation of mitochondria during asymmetric cell division contributes to cell
fate divergence in sister cells in vivo. Nature Communications. 2025;16.
doi:10.1038/s41467-025-62484-5
apa: Segos, I., Van Eeckhoven, J., Berger, S., Mishra, N., Lambie, E. J., &
Conradt, B. (2025). Unequal segregation of mitochondria during asymmetric cell
division contributes to cell fate divergence in sister cells in vivo. Nature
Communications. Springer Nature. https://doi.org/10.1038/s41467-025-62484-5
chicago: Segos, Ioannis, Jens Van Eeckhoven, Simon Berger, Nikhil Mishra, Eric J.
Lambie, and Barbara Conradt. “Unequal Segregation of Mitochondria during Asymmetric
Cell Division Contributes to Cell Fate Divergence in Sister Cells in Vivo.” Nature
Communications. Springer Nature, 2025. https://doi.org/10.1038/s41467-025-62484-5.
ieee: I. Segos, J. Van Eeckhoven, S. Berger, N. Mishra, E. J. Lambie, and B. Conradt,
“Unequal segregation of mitochondria during asymmetric cell division contributes
to cell fate divergence in sister cells in vivo,” Nature Communications,
vol. 16. Springer Nature, 2025.
ista: Segos I, Van Eeckhoven J, Berger S, Mishra N, Lambie EJ, Conradt B. 2025.
Unequal segregation of mitochondria during asymmetric cell division contributes
to cell fate divergence in sister cells in vivo. Nature Communications. 16, 7174.
mla: Segos, Ioannis, et al. “Unequal Segregation of Mitochondria during Asymmetric
Cell Division Contributes to Cell Fate Divergence in Sister Cells in Vivo.” Nature
Communications, vol. 16, 7174, Springer Nature, 2025, doi:10.1038/s41467-025-62484-5.
short: I. Segos, J. Van Eeckhoven, S. Berger, N. Mishra, E.J. Lambie, B. Conradt,
Nature Communications 16 (2025).
date_created: 2025-08-17T22:01:35Z
date_published: 2025-08-04T00:00:00Z
date_updated: 2025-09-01T09:47:29Z
day: '04'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1038/s41467-025-62484-5
external_id:
pmid:
- '40759648'
file:
- access_level: open_access
checksum: f28e73963ea1f55876d0d1afca0f706a
content_type: application/pdf
creator: dernst
date_created: 2025-09-01T09:46:44Z
date_updated: 2025-09-01T09:46:44Z
file_id: '20261'
file_name: 2025_NatureComm_Segos.pdf
file_size: 3775190
relation: main_file
success: 1
file_date_updated: 2025-09-01T09:46:44Z
has_accepted_license: '1'
intvolume: ' 16'
language:
- iso: eng
month: '08'
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'
scopus_import: '1'
status: public
title: Unequal segregation of mitochondria during asymmetric cell division contributes
to cell fate divergence in sister cells in vivo
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: 16
year: '2025'
...
---
_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
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'
...
---
OA_place: publisher
OA_type: free access
_id: '10406'
abstract:
- lang: eng
text: Multicellular organisms develop complex shapes from much simpler, single-celled
zygotes through a process commonly called morphogenesis. Morphogenesis involves
an interplay between several factors, ranging from the gene regulatory networks
determining cell fate and differentiation to the mechanical processes underlying
cell and tissue shape changes. Thus, the study of morphogenesis has historically
been based on multidisciplinary approaches at the interface of biology with physics
and mathematics. Recent technological advances have further improved our ability
to study morphogenesis by bridging the gap between the genetic and biophysical
factors through the development of new tools for visualizing, analyzing, and perturbing
these factors and their biochemical intermediaries. Here, we review how a combination
of genetic, microscopic, biophysical, and biochemical approaches has aided our
attempts to understand morphogenesis and discuss potential approaches that may
be beneficial to such an inquiry in the future.
acknowledgement: The authors would like to thank Feyza Nur Arslan, Suyash Naik, Diana
Pinheiro, Alexandra Schauer, and Shayan Shamipour for their comments on the draft.
N.M. is supported by an ISTplus postdoctoral fellowship (H2020 Marie-Sklodowska-Curie
COFUND Action).
article_processing_charge: No
article_type: original
author:
- first_name: Nikhil
full_name: Mishra, Nikhil
id: C4D70E82-1081-11EA-B3ED-9A4C3DDC885E
last_name: Mishra
orcid: 0000-0002-6425-5788
- 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: Mishra N, Heisenberg C-PJ. Dissecting organismal morphogenesis by bridging
genetics and biophysics. Annual Review of Genetics. 2021;55:209-233. doi:10.1146/annurev-genet-071819-103748
apa: Mishra, N., & Heisenberg, C.-P. J. (2021). Dissecting organismal morphogenesis
by bridging genetics and biophysics. Annual Review of Genetics. Annual
Reviews. https://doi.org/10.1146/annurev-genet-071819-103748
chicago: Mishra, Nikhil, and Carl-Philipp J Heisenberg. “Dissecting Organismal Morphogenesis
by Bridging Genetics and Biophysics.” Annual Review of Genetics. Annual
Reviews, 2021. https://doi.org/10.1146/annurev-genet-071819-103748.
ieee: N. Mishra and C.-P. J. Heisenberg, “Dissecting organismal morphogenesis by
bridging genetics and biophysics,” Annual Review of Genetics, vol. 55.
Annual Reviews, pp. 209–233, 2021.
ista: Mishra N, Heisenberg C-PJ. 2021. Dissecting organismal morphogenesis by bridging
genetics and biophysics. Annual Review of Genetics. 55, 209–233.
mla: Mishra, Nikhil, and Carl-Philipp J. Heisenberg. “Dissecting Organismal Morphogenesis
by Bridging Genetics and Biophysics.” Annual Review of Genetics, vol. 55,
Annual Reviews, 2021, pp. 209–33, doi:10.1146/annurev-genet-071819-103748.
short: N. Mishra, C.-P.J. Heisenberg, Annual Review of Genetics 55 (2021) 209–233.
corr_author: '1'
date_created: 2021-12-05T23:01:41Z
date_published: 2021-08-30T00:00:00Z
date_updated: 2026-06-18T08:39:48Z
day: '30'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1146/annurev-genet-071819-103748
ec_funded: 1
external_id:
isi:
- '000747220900010'
pmid:
- '34460295'
intvolume: ' 55'
isi: 1
keyword:
- morphogenesis
- forward genetics
- high-resolution microscopy
- biophysics
- biochemistry
- patterning
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1146/annurev-genet-071819-103748
month: '08'
oa: 1
oa_version: Published Version
page: 209-233
pmid: 1
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
publication: Annual Review of Genetics
publication_identifier:
eissn:
- 1545-2948
issn:
- 0066-4197
publication_status: published
publisher: Annual Reviews
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dissecting organismal morphogenesis by bridging genetics and biophysics
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 55
year: '2021'
...