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The Gata4/5/6 sub-family of zinc finger transcription factors regulate many aspects of cardiogenesis. However, critical roles in extra-embryonic endoderm also challenge comprehensive analysis during early mouse cardiogenesis, while zebrafish models have previously relied on knockdown assays. We generated targeted deletions to disrupt each  gata4/5/6  gene in zebrafish and analyzed cardiac phenotypes in single, double and triple mutants. The analysis confirmed that loss of  gata5  causes  cardia bifida  and validated functional redundancies for  gata5/6  in cardiac precursor specification. Surprisingly, we discovered that  gata4  is dispensable for early zebrafish development, while loss of one  gata4  allele can suppress the  bifid  phenotype of the  gata5  mutant. The  gata4  mutants eventually develop an age-dependent cardiomyopathy. By combining combinations of mutant alleles, we show that cardiac specification depends primarily on an overall dosage of  gata4/5/6  alleles rather than a specific gene. We also identify a specific role for  gata6  in controlling ventricle morphogenesis through regulation of both the first and second heart field, while loss of both  gata4/6  eliminates the ventricle. Thus, different developmental programs are dependent on total dosage, certain pairs, or specific  gata4/5/6  genes during embryonic cardiogenesis.   This article has an associated First Person interview with the first author of the paper.

Specificity, redundancy and dosage thresholds among gata4/5/6 genes during zebrafish cardiogenesis