Actomyosin regulation by Eph receptor signaling couples boundary cell formation to border sharpness.
Actomyosin
/ metabolism
Acyltransferases
Animals
Brain
/ embryology
DNA-Binding Proteins
/ metabolism
Gene Expression Regulation, Developmental
Nuclear Proteins
/ metabolism
Phosphorylation
Protein Processing, Post-Translational
Receptor, EphA4
/ metabolism
Signal Transduction
TEA Domain Transcription Factors
Transcription Factors
/ metabolism
Zebrafish
Zebrafish Proteins
/ metabolism
Eph receptor
actomyosin
border sharpening
cell specification
developmental biology
hindbrain
tension
zebrafish
Journal
eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614
Informations de publication
Date de publication:
10 09 2019
10 09 2019
Historique:
received:
26
06
2019
accepted:
23
08
2019
entrez:
11
9
2019
pubmed:
11
9
2019
medline:
20
2
2020
Statut:
epublish
Résumé
The segregation of cells with distinct regional identity underlies formation of a sharp border, which in some tissues serves to organise a boundary signaling centre. It is unclear whether or how border sharpness is coordinated with induction of boundary-specific gene expression. We show that forward signaling of EphA4 is required for border sharpening and induction of boundary cells in the zebrafish hindbrain, which we find both require kinase-dependent signaling, with a lesser input of PDZ domain-dependent signaling. We find that boundary-specific gene expression is regulated by myosin II phosphorylation, which increases actomyosin contraction downstream of EphA4 signaling. Myosin phosphorylation leads to nuclear translocation of Taz, which together with Tead1a is required for boundary marker expression. Since actomyosin contraction maintains sharp borders, there is direct coupling of border sharpness to boundary cell induction that ensures correct organisation of signaling centres.
Identifiants
pubmed: 31502954
doi: 10.7554/eLife.49696
pii: 49696
pmc: PMC6739871
doi:
pii:
Substances chimiques
DNA-Binding Proteins
0
Nuclear Proteins
0
TEA Domain Transcription Factors
0
Transcription Factors
0
Zebrafish Proteins
0
tead1a protein, zebrafish
0
Actomyosin
9013-26-7
Acyltransferases
EC 2.3.-
tafazzin protein, zebrafish
EC 2.3.1.-
Receptor, EphA4
EC 2.7.10.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Cancer Research UK
ID : FC001217
Pays : United Kingdom
Organisme : Medical Research Council
ID : FC001217
Pays : United Kingdom
Organisme : Wellcome Trust
ID : FC001217
Pays : United Kingdom
Informations de copyright
© 2019, Cayuso et al.
Déclaration de conflit d'intérêts
JC, QX, MA, DW No competing interests declared
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