---
_id: '14356'
abstract:
- lang: eng
text: Aminoacyl-tRNA synthetases (ARSs) are essential enzymes for faithful assignment
of amino acids to their cognate tRNA. Variants in ARS genes are frequently associated
with clinically heterogeneous phenotypes in humans and follow both autosomal dominant
or recessive inheritance patterns in many instances. Variants in tryptophanyl-tRNA
synthetase 1 (WARS1) cause autosomal dominantly inherited distal hereditary motor
neuropathy and Charcot-Marie-Tooth disease. Presently, only one family with biallelic
WARS1 variants has been described. We present three affected individuals from
two families with biallelic variants (p.Met1? and p.(Asp419Asn)) in WARS1, showing
varying severities of developmental delay and intellectual disability. Hearing
impairment and microcephaly, as well as abnormalities of the brain, skeletal system,
movement/gait, and behavior were variable features. Phenotyping of knocked down
wars-1 in a Caenorhabditis elegans model showed depletion is associated with defects
in germ cell development. A wars1 knockout vertebrate model recapitulates the
human clinical phenotypes, confirms variant pathogenicity, and uncovers evidence
implicating the p.Met1? variant as potentially impacting an exon critical for
normal hearing. Together, our findings provide consolidating evidence for biallelic
disruption of WARS1 as causal for an autosomal recessive neurodevelopmental syndrome
and present a vertebrate model that recapitulates key phenotypes observed in patients.
article_processing_charge: No
article_type: original
author:
- first_name: Sheng-Jia
full_name: Lin, Sheng-Jia
last_name: Lin
- first_name: Barbara
full_name: Vona, Barbara
last_name: Vona
- first_name: Hillary M.
full_name: Porter, Hillary M.
last_name: Porter
- first_name: Mahmoud
full_name: Izadi, Mahmoud
last_name: Izadi
- first_name: Kevin
full_name: Huang, Kevin
id: 3b3d2888-1ff6-11ee-9fa6-8f209ca91fe3
last_name: Huang
orcid: 0000-0002-2512-7812
- first_name: Yves
full_name: Lacassie, Yves
last_name: Lacassie
- first_name: Jill A.
full_name: Rosenfeld, Jill A.
last_name: Rosenfeld
- first_name: Saadullah
full_name: Khan, Saadullah
last_name: Khan
- first_name: Cassidy
full_name: Petree, Cassidy
last_name: Petree
- first_name: Tayyiba A.
full_name: Ali, Tayyiba A.
last_name: Ali
- first_name: Nazif
full_name: Muhammad, Nazif
last_name: Muhammad
- first_name: Sher A.
full_name: Khan, Sher A.
last_name: Khan
- first_name: Noor
full_name: Muhammad, Noor
last_name: Muhammad
- first_name: Pengfei
full_name: Liu, Pengfei
last_name: Liu
- first_name: Marie-Louise
full_name: Haymon, Marie-Louise
last_name: Haymon
- first_name: Franz
full_name: Rueschendorf, Franz
last_name: Rueschendorf
- first_name: Il-Keun
full_name: Kong, Il-Keun
last_name: Kong
- first_name: Linda
full_name: Schnapp, Linda
last_name: Schnapp
- first_name: Natasha
full_name: Shur, Natasha
last_name: Shur
- first_name: Lynn
full_name: Chorich, Lynn
last_name: Chorich
- first_name: Lawrence
full_name: Layman, Lawrence
last_name: Layman
- first_name: Thomas
full_name: Haaf, Thomas
last_name: Haaf
- first_name: Ehsan
full_name: Pourkarimi, Ehsan
last_name: Pourkarimi
- first_name: Hyung-Goo
full_name: Kim, Hyung-Goo
last_name: Kim
- first_name: Gaurav K.
full_name: Varshney, Gaurav K.
last_name: Varshney
citation:
ama: Lin S-J, Vona B, Porter HM, et al. Biallelic variants in WARS1 cause a highly
variable neurodevelopmental syndrome and implicate a critical exon for normal
auditory function. Human Mutation. 2022;43(10):1472-1489. doi:10.1002/humu.24435
apa: Lin, S.-J., Vona, B., Porter, H. M., Izadi, M., Huang, K., Lacassie, Y., …
Varshney, G. K. (2022). Biallelic variants in WARS1 cause a highly variable neurodevelopmental
syndrome and implicate a critical exon for normal auditory function. Human
Mutation. Wiley. https://doi.org/10.1002/humu.24435
chicago: Lin, Sheng-Jia, Barbara Vona, Hillary M. Porter, Mahmoud Izadi, Kevin Huang,
Yves Lacassie, Jill A. Rosenfeld, et al. “Biallelic Variants in WARS1 Cause a
Highly Variable Neurodevelopmental Syndrome and Implicate a Critical Exon for
Normal Auditory Function.” Human Mutation. Wiley, 2022. https://doi.org/10.1002/humu.24435.
ieee: S.-J. Lin et al., “Biallelic variants in WARS1 cause a highly variable
neurodevelopmental syndrome and implicate a critical exon for normal auditory
function,” Human Mutation, vol. 43, no. 10. Wiley, pp. 1472–1489, 2022.
ista: Lin S-J, Vona B, Porter HM, Izadi M, Huang K, Lacassie Y, Rosenfeld JA, Khan
S, Petree C, Ali TA, Muhammad N, Khan SA, Muhammad N, Liu P, Haymon M-L, Rueschendorf
F, Kong I-K, Schnapp L, Shur N, Chorich L, Layman L, Haaf T, Pourkarimi E, Kim
H-G, Varshney GK. 2022. Biallelic variants in WARS1 cause a highly variable neurodevelopmental
syndrome and implicate a critical exon for normal auditory function. Human Mutation.
43(10), 1472–1489.
mla: Lin, Sheng-Jia, et al. “Biallelic Variants in WARS1 Cause a Highly Variable
Neurodevelopmental Syndrome and Implicate a Critical Exon for Normal Auditory
Function.” Human Mutation, vol. 43, no. 10, Wiley, 2022, pp. 1472–89, doi:10.1002/humu.24435.
short: S.-J. Lin, B. Vona, H.M. Porter, M. Izadi, K. Huang, Y. Lacassie, J.A. Rosenfeld,
S. Khan, C. Petree, T.A. Ali, N. Muhammad, S.A. Khan, N. Muhammad, P. Liu, M.-L.
Haymon, F. Rueschendorf, I.-K. Kong, L. Schnapp, N. Shur, L. Chorich, L. Layman,
T. Haaf, E. Pourkarimi, H.-G. Kim, G.K. Varshney, Human Mutation 43 (2022) 1472–1489.
date_created: 2023-09-20T20:58:24Z
date_published: 2022-10-01T00:00:00Z
date_updated: 2023-09-25T08:54:14Z
day: '01'
ddc:
- '570'
doi: 10.1002/humu.24435
extern: '1'
file:
- access_level: open_access
checksum: 74b01d4e4084b2f64c30ed32b18ee928
content_type: application/pdf
creator: dernst
date_created: 2023-09-25T08:52:54Z
date_updated: 2023-09-25T08:52:54Z
file_id: '14370'
file_name: 2022_HumanMutation_Lin.pdf
file_size: 12131312
relation: main_file
success: 1
file_date_updated: 2023-09-25T08:52:54Z
has_accepted_license: '1'
intvolume: ' 43'
issue: '10'
keyword:
- autosomal recessive
- biallelic variants
- C
- elegans
- translation initiation sites
- tryptophanyl-tRNA synthetase 1 (WARS1)
- WHEP domain
- zebrafish
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: 1472-1489
publication: Human Mutation
publication_identifier:
issn:
- 1059-7794
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Biallelic variants in WARS1 cause a highly variable neurodevelopmental syndrome
and implicate a critical exon for normal auditory function
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: 43
year: '2022'
...
---
_id: '14357'
abstract:
- lang: eng
text: 'Aminoacylation of transfer RNA (tRNA) is a key step in protein biosynthesis,
carried out by highly specific aminoacyl-tRNA synthetases (ARSs). ARSs have been
implicated in autosomal dominant and autosomal recessive human disorders. Autosomal
dominant variants in tryptophanyl-tRNA synthetase 1 (WARS1) are known to cause
distal hereditary motor neuropathy and Charcot-Marie-Tooth disease, but a recessively
inherited phenotype is yet to be clearly defined. Seryl-tRNA synthetase 1 (SARS1)
has rarely been implicated in an autosomal recessive developmental disorder. Here,
we report five individuals with biallelic missense variants in WARS1 or SARS1,
who presented with an overlapping phenotype of microcephaly, developmental delay,
intellectual disability, and brain anomalies. Structural mapping showed that the
SARS1 variant is located directly within the enzyme’s active site, most likely
diminishing activity, while the WARS1 variant is located in the N-terminal domain.
We further characterize the identified WARS1 variant by showing that it negatively
impacts protein abundance and is unable to rescue the phenotype of a CRISPR/Cas9
wars1 knockout zebrafish model. In summary, we describe two overlapping autosomal
recessive syndromes caused by variants in WARS1 and SARS1, present functional
insights into the pathogenesis of the WARS1-related syndrome and define an emerging
disease spectrum: ARS-related developmental disorders with or without microcephaly.'
article_processing_charge: No
article_type: original
author:
- first_name: Nina
full_name: Boegershausen, Nina
last_name: Boegershausen
- first_name: Hannah E.
full_name: Krawczyk, Hannah E.
last_name: Krawczyk
- first_name: Rami A.
full_name: Jamra, Rami A.
last_name: Jamra
- first_name: Sheng-Jia
full_name: Lin, Sheng-Jia
last_name: Lin
- first_name: Goekhan
full_name: Yigit, Goekhan
last_name: Yigit
- first_name: Irina
full_name: Huening, Irina
last_name: Huening
- first_name: Anna M.
full_name: Polo, Anna M.
last_name: Polo
- first_name: Barbara
full_name: Vona, Barbara
last_name: Vona
- first_name: Kevin
full_name: Huang, Kevin
id: 3b3d2888-1ff6-11ee-9fa6-8f209ca91fe3
last_name: Huang
orcid: 0000-0002-2512-7812
- first_name: Julia
full_name: Schmidt, Julia
last_name: Schmidt
- first_name: Janine
full_name: Altmueller, Janine
last_name: Altmueller
- first_name: Johannes
full_name: Luppe, Johannes
last_name: Luppe
- first_name: Konrad
full_name: Platzer, Konrad
last_name: Platzer
- first_name: Beate B.
full_name: Doergeloh, Beate B.
last_name: Doergeloh
- first_name: Andreas
full_name: Busche, Andreas
last_name: Busche
- first_name: Saskia
full_name: Biskup, Saskia
last_name: Biskup
- first_name: Marisa
full_name: Mendes, I, Marisa
last_name: Mendes, I
- first_name: Desiree E. C.
full_name: Smith, Desiree E. C.
last_name: Smith
- first_name: Gajja S.
full_name: Salomons, Gajja S.
last_name: Salomons
- first_name: Arne
full_name: Zibat, Arne
last_name: Zibat
- first_name: Eva
full_name: Bueltmann, Eva
last_name: Bueltmann
- first_name: Peter
full_name: Nuernberg, Peter
last_name: Nuernberg
- first_name: Malte
full_name: Spielmann, Malte
last_name: Spielmann
- first_name: Johannes R.
full_name: Lemke, Johannes R.
last_name: Lemke
- first_name: Yun
full_name: Li, Yun
last_name: Li
- first_name: Martin
full_name: Zenker, Martin
last_name: Zenker
- first_name: Gaurav K.
full_name: Varshney, Gaurav K.
last_name: Varshney
- first_name: Hauke S.
full_name: Hillen, Hauke S.
last_name: Hillen
- first_name: Christian P.
full_name: Kratz, Christian P.
last_name: Kratz
- first_name: Bernd
full_name: Wollnik, Bernd
last_name: Wollnik
citation:
ama: 'Boegershausen N, Krawczyk HE, Jamra RA, et al. WARS1 and SARS1: Two tRNA synthetases
implicated in autosomal recessive microcephaly. Human Mutation. 2022;43(10):1454-1471.
doi:10.1002/humu.24430'
apa: 'Boegershausen, N., Krawczyk, H. E., Jamra, R. A., Lin, S.-J., Yigit, G., Huening,
I., … Wollnik, B. (2022). WARS1 and SARS1: Two tRNA synthetases implicated in
autosomal recessive microcephaly. Human Mutation. Wiley. https://doi.org/10.1002/humu.24430'
chicago: 'Boegershausen, Nina, Hannah E. Krawczyk, Rami A. Jamra, Sheng-Jia Lin,
Goekhan Yigit, Irina Huening, Anna M. Polo, et al. “WARS1 and SARS1: Two TRNA
Synthetases Implicated in Autosomal Recessive Microcephaly.” Human Mutation.
Wiley, 2022. https://doi.org/10.1002/humu.24430.'
ieee: 'N. Boegershausen et al., “WARS1 and SARS1: Two tRNA synthetases implicated
in autosomal recessive microcephaly,” Human Mutation, vol. 43, no. 10.
Wiley, pp. 1454–1471, 2022.'
ista: 'Boegershausen N, Krawczyk HE, Jamra RA, Lin S-J, Yigit G, Huening I, Polo
AM, Vona B, Huang K, Schmidt J, Altmueller J, Luppe J, Platzer K, Doergeloh BB,
Busche A, Biskup S, Mendes, I M, Smith DEC, Salomons GS, Zibat A, Bueltmann E,
Nuernberg P, Spielmann M, Lemke JR, Li Y, Zenker M, Varshney GK, Hillen HS, Kratz
CP, Wollnik B. 2022. WARS1 and SARS1: Two tRNA synthetases implicated in autosomal
recessive microcephaly. Human Mutation. 43(10), 1454–1471.'
mla: 'Boegershausen, Nina, et al. “WARS1 and SARS1: Two TRNA Synthetases Implicated
in Autosomal Recessive Microcephaly.” Human Mutation, vol. 43, no. 10,
Wiley, 2022, pp. 1454–71, doi:10.1002/humu.24430.'
short: N. Boegershausen, H.E. Krawczyk, R.A. Jamra, S.-J. Lin, G. Yigit, I. Huening,
A.M. Polo, B. Vona, K. Huang, J. Schmidt, J. Altmueller, J. Luppe, K. Platzer,
B.B. Doergeloh, A. Busche, S. Biskup, M. Mendes, I, D.E.C. Smith, G.S. Salomons,
A. Zibat, E. Bueltmann, P. Nuernberg, M. Spielmann, J.R. Lemke, Y. Li, M. Zenker,
G.K. Varshney, H.S. Hillen, C.P. Kratz, B. Wollnik, Human Mutation 43 (2022) 1454–1471.
date_created: 2023-09-20T20:59:33Z
date_published: 2022-10-01T00:00:00Z
date_updated: 2023-09-25T08:43:06Z
day: '01'
ddc:
- '570'
doi: 10.1002/humu.24430
extern: '1'
external_id:
pmid:
- '35790048'
file:
- access_level: open_access
checksum: c31fc91e0445c35b9da83eb911a9b552
content_type: application/pdf
creator: dernst
date_created: 2023-09-25T08:41:23Z
date_updated: 2023-09-25T08:41:23Z
file_id: '14367'
file_name: 2022_HumanMutation_Boegershausen.pdf
file_size: 4863605
relation: main_file
success: 1
file_date_updated: 2023-09-25T08:41:23Z
has_accepted_license: '1'
intvolume: ' 43'
issue: '10'
keyword:
- aminoacylation
- aminoacyl-tRNA synthetase
- ARS
- CRISPR
- Cas9
- intellectual disability
- microcephaly
- SARS1
- tRNA
- WARS1
- zebrafish
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: 1454-1471
pmid: 1
publication: Human Mutation
publication_identifier:
issn:
- 1059-7794
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'WARS1 and SARS1: Two tRNA synthetases implicated in autosomal recessive microcephaly'
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 43
year: '2022'
...
---
_id: '9245'
abstract:
- lang: eng
text: Tissue morphogenesis is driven by mechanical forces triggering cell movements
and shape changes. Quantitatively measuring tension within tissues is of great
importance for understanding the role of mechanical signals acting on the cell
and tissue level during morphogenesis. Here we introduce laser ablation as a useful
tool to probe tissue tension within the granulosa layer, an epithelial monolayer
of somatic cells that surround the zebrafish female gamete during folliculogenesis.
We describe in detail how to isolate follicles, mount samples, perform laser surgery,
and analyze the data.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: We thank Prof. Masazumi Tada and Roland Dosch for providing transgenic
zebrafish lines, the Heisenberg lab for technical assistance and feedback on the
manuscript, and the Bioimaging and Fish facilities of IST Austria for continuous
support. This work was funded by an ERC advanced grant (MECSPEC to C.-P.H.).
alternative_title:
- Methods in Molecular Biology
article_processing_charge: No
author:
- first_name: Peng
full_name: Xia, Peng
id: 4AB6C7D0-F248-11E8-B48F-1D18A9856A87
last_name: Xia
orcid: 0000-0002-5419-7756
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: 'Xia P, Heisenberg C-PJ. Quantifying tissue tension in the granulosa layer
after laser surgery. In: Dosch R, ed. Germline Development in the Zebrafish.
Vol 2218. Humana; 2021:117-128. doi:10.1007/978-1-0716-0970-5_10'
apa: Xia, P., & Heisenberg, C.-P. J. (2021). Quantifying tissue tension in the
granulosa layer after laser surgery. In R. Dosch (Ed.), Germline Development
in the Zebrafish (Vol. 2218, pp. 117–128). Humana. https://doi.org/10.1007/978-1-0716-0970-5_10
chicago: Xia, Peng, and Carl-Philipp J Heisenberg. “Quantifying Tissue Tension in
the Granulosa Layer after Laser Surgery.” In Germline Development in the Zebrafish,
edited by Roland Dosch, 2218:117–28. Humana, 2021. https://doi.org/10.1007/978-1-0716-0970-5_10.
ieee: P. Xia and C.-P. J. Heisenberg, “Quantifying tissue tension in the granulosa
layer after laser surgery,” in Germline Development in the Zebrafish, vol.
2218, R. Dosch, Ed. Humana, 2021, pp. 117–128.
ista: 'Xia P, Heisenberg C-PJ. 2021.Quantifying tissue tension in the granulosa
layer after laser surgery. In: Germline Development in the Zebrafish. Methods
in Molecular Biology, vol. 2218, 117–128.'
mla: Xia, Peng, and Carl-Philipp J. Heisenberg. “Quantifying Tissue Tension in the
Granulosa Layer after Laser Surgery.” Germline Development in the Zebrafish,
edited by Roland Dosch, vol. 2218, Humana, 2021, pp. 117–28, doi:10.1007/978-1-0716-0970-5_10.
short: P. Xia, C.-P.J. Heisenberg, in:, R. Dosch (Ed.), Germline Development in
the Zebrafish, Humana, 2021, pp. 117–128.
date_created: 2021-03-14T23:01:34Z
date_published: 2021-02-20T00:00:00Z
date_updated: 2022-06-03T10:57:55Z
day: '20'
department:
- _id: CaHe
doi: 10.1007/978-1-0716-0970-5_10
ec_funded: 1
editor:
- first_name: Roland
full_name: Dosch, Roland
last_name: Dosch
external_id:
pmid:
- '33606227'
intvolume: ' 2218'
keyword:
- Tissue tension
- Morphogenesis
- Laser ablation
- Zebrafish folliculogenesis
- Granulosa cells
language:
- iso: eng
month: '02'
oa_version: None
page: 117-128
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: Germline Development in the Zebrafish
publication_identifier:
eisbn:
- 978-1-0716-0970-5
eissn:
- 1940-6029
isbn:
- 978-1-0716-0969-9
issn:
- 1064-3745
publication_status: published
publisher: Humana
quality_controlled: '1'
scopus_import: '1'
status: public
title: Quantifying tissue tension in the granulosa layer after laser surgery
type: book_chapter
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 2218
year: '2021'
...
---
_id: '9999'
abstract:
- lang: eng
text: 'The developmental strategies used by progenitor cells to endure a safe journey
from their induction place towards the site of terminal differentiation are still
poorly understood. Here we uncovered a progenitor cell allocation mechanism that
stems from an incomplete process of epithelial delamination that allows progenitors
to coordinate their movement with adjacent extra-embryonic tissues. Progenitors
of the zebrafish laterality organ originate from the surface epithelial enveloping
layer by an apical constriction process of cell delamination. During this process,
progenitors retain long-term apical contacts that enable the epithelial layer
to pull a subset of progenitors along their way towards the vegetal pole. The
remaining delaminated progenitors follow apically-attached progenitors’ movement
by a co-attraction mechanism, avoiding sequestration by the adjacent endoderm,
ensuring their fate and collective allocation at the differentiation site. Thus,
we reveal that incomplete delamination serves as a cellular platform for coordinated
tissue movements during development. Impact Statement: Incomplete delamination
serves as a cellular platform for coordinated tissue movements during development,
guiding newly formed progenitor cell groups to the differentiation site.'
article_number: e66483
article_processing_charge: Yes
article_type: original
author:
- first_name: Eduardo
full_name: Pulgar, Eduardo
last_name: Pulgar
- first_name: Cornelia
full_name: Schwayer, Cornelia
id: 3436488C-F248-11E8-B48F-1D18A9856A87
last_name: Schwayer
orcid: 0000-0001-5130-2226
- first_name: Néstor
full_name: Guerrero, Néstor
last_name: Guerrero
- first_name: Loreto
full_name: López, Loreto
last_name: López
- first_name: Susana
full_name: Márquez, Susana
last_name: Márquez
- first_name: Steffen
full_name: Härtel, Steffen
last_name: Härtel
- first_name: Rodrigo
full_name: Soto, Rodrigo
last_name: Soto
- first_name: Carl Philipp
full_name: Heisenberg, Carl Philipp
last_name: Heisenberg
- first_name: Miguel L.
full_name: Concha, Miguel L.
last_name: Concha
citation:
ama: Pulgar E, Schwayer C, Guerrero N, et al. Apical contacts stemming from incomplete
delamination guide progenitor cell allocation through a dragging mechanism. eLife.
2021;10. doi:10.7554/eLife.66483
apa: Pulgar, E., Schwayer, C., Guerrero, N., López, L., Márquez, S., Härtel, S.,
… Concha, M. L. (2021). Apical contacts stemming from incomplete delamination
guide progenitor cell allocation through a dragging mechanism. ELife. eLife
Sciences Publications. https://doi.org/10.7554/eLife.66483
chicago: Pulgar, Eduardo, Cornelia Schwayer, Néstor Guerrero, Loreto López, Susana
Márquez, Steffen Härtel, Rodrigo Soto, Carl Philipp Heisenberg, and Miguel L.
Concha. “Apical Contacts Stemming from Incomplete Delamination Guide Progenitor
Cell Allocation through a Dragging Mechanism.” ELife. eLife Sciences Publications,
2021. https://doi.org/10.7554/eLife.66483.
ieee: E. Pulgar et al., “Apical contacts stemming from incomplete delamination
guide progenitor cell allocation through a dragging mechanism,” eLife,
vol. 10. eLife Sciences Publications, 2021.
ista: Pulgar E, Schwayer C, Guerrero N, López L, Márquez S, Härtel S, Soto R, Heisenberg
CP, Concha ML. 2021. Apical contacts stemming from incomplete delamination guide
progenitor cell allocation through a dragging mechanism. eLife. 10, e66483.
mla: Pulgar, Eduardo, et al. “Apical Contacts Stemming from Incomplete Delamination
Guide Progenitor Cell Allocation through a Dragging Mechanism.” ELife,
vol. 10, e66483, eLife Sciences Publications, 2021, doi:10.7554/eLife.66483.
short: E. Pulgar, C. Schwayer, N. Guerrero, L. López, S. Márquez, S. Härtel, R.
Soto, C.P. Heisenberg, M.L. Concha, ELife 10 (2021).
date_created: 2021-09-12T22:01:23Z
date_published: 2021-08-27T00:00:00Z
date_updated: 2023-08-14T06:53:33Z
day: '27'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.7554/eLife.66483
ec_funded: 1
external_id:
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keyword:
- cell delamination
- apical constriction
- dragging
- mechanical forces
- collective 18 locomotion
- dorsal forerunner cells
- zebrafish
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
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call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
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title: Apical contacts stemming from incomplete delamination guide progenitor cell
allocation through a dragging mechanism
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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: 10
year: '2021'
...