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 gene in zebrafish and analyzed cardiac phenotypes in single, double and triple mutants. The analysis confirmed that loss of causes and validated functional redundancies for in cardiac precursor specification. Surprisingly, we discovered that is dispensable for early zebrafish development, while loss of one allele can suppress the phenotype of the mutant. The 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 alleles rather than a specific gene. We also identify a specific role for in controlling ventricle morphogenesis through regulation of both the first and second heart field, while loss of both eliminates the ventricle. Thus, different developmental programs are dependent on total dosage, certain pairs, or specific genes during embryonic cardiogenesis.This article has an associated First Person interview with the first author of the paper.