PUBLICATION

Grhl3 promotes retention of epidermal cells under endocytic stress to maintain epidermal architecture in zebrafish

Authors
Phatak, M., Kulkarni, S., Miles, L.B., Anjum, N., Dworkin, S., Sonawane, M.
ID
ZDB-PUB-210928-19
Date
2021
Source
PLoS Genetics   17: e1009823 (Journal)
Registered Authors
Dworkin, Seb, Miles, Lee, Sonawane, Mahendra
Keywords
none
Datasets
GEO:GSE173649
MeSH Terms
  • Animals
  • Endocytosis*
  • Epidermal Cells/cytology
  • Epidermal Cells/metabolism*
  • Mutation
  • Stress, Physiological*
  • Transcriptome
  • Up-Regulation
  • Zebrafish/embryology
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/physiology*
PubMed
34570762 Full text @ PLoS Genet.
Abstract
Epithelia such as epidermis cover large surfaces and are crucial for survival. Maintenance of tissue homeostasis by balancing cell proliferation, cell size, and cell extrusion ensures epidermal integrity. Although the mechanisms of cell extrusion are better understood, how epithelial cells that round up under developmental or perturbed genetic conditions are reintegrated in the epithelium to maintain homeostasis remains unclear. Here, we performed live imaging in zebrafish embryos to show that epidermal cells that round up due to membrane homeostasis defects in the absence of goosepimples/myosinVb (myoVb) function, are reintegrated into the epithelium. Transcriptome analysis and genetic interaction studies suggest that the transcription factor Grainyhead-like 3 (Grhl3) induces the retention of rounded cells by regulating E-cadherin levels. Moreover, Grhl3 facilitates the survival of MyoVb deficient embryos by regulating cell adhesion, cell retention and epidermal architecture. Our analyses have unraveled a mechanism of retention of rounded cells and its importance in epithelial homeostasis.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping