PUBLICATION
Gata6 functions in zebrafish endoderm to regulate late differentiating arterial pole cardiogenesis
- Authors
- Sam, J., Torregroza, I., Evans, T.
- ID
- ZDB-PUB-240813-4
- Date
- 2024
- Source
- Development (Cambridge, England) 151(17): (Journal)
- Registered Authors
- Evans, Todd
- Keywords
- Congenital heart disease, FGF signaling, Heart development, Morphogenesis, Second heart field
- MeSH Terms
-
- Endoderm*/cytology
- Endoderm*/embryology
- Endoderm*/metabolism
- Myocytes, Cardiac/cytology
- Myocytes, Cardiac/metabolism
- Cell Differentiation*/genetics
- Zebrafish*/embryology
- Zebrafish*/genetics
- Heart*/embryology
- Dual Specificity Phosphatase 6/genetics
- Dual Specificity Phosphatase 6/metabolism
- Signal Transduction
- GATA6 Transcription Factor*/genetics
- GATA6 Transcription Factor*/metabolism
- Fibroblast Growth Factors/genetics
- Fibroblast Growth Factors/metabolism
- Animals
- Zebrafish Proteins*/genetics
- Zebrafish Proteins*/metabolism
- Organogenesis/genetics
- Gene Expression Regulation, Developmental
- GATA Transcription Factors
- PubMed
- 39133135 Full text @ Development
Citation
Sam, J., Torregroza, I., Evans, T. (2024) Gata6 functions in zebrafish endoderm to regulate late differentiating arterial pole cardiogenesis. Development (Cambridge, England). 151(17):.
Abstract
Mutations in GATA6 are associated with congenital heart disease, most notably conotruncal structural defects. However, how GATA6 regulates cardiac morphology during embryogenesis is undefined. We used knockout and conditional mutant zebrafish alleles to investigate the spatiotemporal role of gata6 during cardiogenesis. Loss of gata6 specifically impacts atrioventricular valve formation and recruitment of epicardium, with a prominent loss of arterial pole cardiac cells including for the ventricle and outflow tract. However, there are no obvious defects in cardiac progenitor cell specification, proliferation, or death. Conditional loss of gata6 starting at 24 hr is sufficient to disrupt the addition of late differentiating cardiomyocytes at the arterial pole with decreased expression levels of anterior second heart field (aSHF) markers spry4 and mef2cb. Conditional loss of gata6 in the endoderm is sufficient to phenocopy the straight knockout resulting in a significant loss of ventricular and outflow tract tissue. Exposure to a Dusp6 inhibitor largely rescues the loss of ventricular cells in gata6-/- larvae. Thus, gata6 functions in endoderm mediated by FGF signaling to regulate the addition of anterior SHF progenitor derivatives during heart formation.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping