PUBLICATION
Actomyosin regulation by Eph receptor signaling couples boundary cell formation to border sharpness
- Authors
- Cayuso, J., Xu, Q., Addison, M., Wilkinson, D.G.
- ID
- ZDB-PUB-190911-8
- Date
- 2019
- Source
- eLIFE 8: (Journal)
- Registered Authors
- Wilkinson, David, Xu, Qiling
- Keywords
- Eph receptor, actomyosin, border sharpening, cell specification, developmental biology, hindbrain, tension, zebrafish
- MeSH Terms
-
- Actomyosin/metabolism*
- Animals
- Brain/embryology*
- DNA-Binding Proteins/metabolism
- Gene Expression Regulation, Developmental*
- Nuclear Proteins/metabolism
- Phosphorylation
- Protein Processing, Post-Translational
- Receptor, EphA4/metabolism*
- Signal Transduction*
- Transcription Factors/metabolism
- Zebrafish
- Zebrafish Proteins/metabolism
- PubMed
- 31502954 Full text @ Elife
Citation
Cayuso, J., Xu, Q., Addison, M., Wilkinson, D.G. (2019) Actomyosin regulation by Eph receptor signaling couples boundary cell formation to border sharpness. eLIFE. 8:.
Abstract
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping