Outflow tract (OFT) defects make up a significant portion of congenital heart defects (CHDs), the most common birth malformations. The vertebrate OFT is derived from later differentiating second heart field (SHF) progenitors, necessitating a greater understanding of the mechanisms directing proper SHF development. In a screen for effectors of heart development, we identified the cardiac really gone (crg) mutant, which displays a smaller OFT and reduced ventricular cardiomyocytes. Furthermore, we observe a loss of SHF marker gene expression after cardiac differentiation occurs from the earlier differentiating first heart field, suggesting that SHF development is specifically affected in crg mutants. Positional cloning of crg revealed that it is a novel histone deacetylase 1 (hdac1) mutant allele, with a mutation in a nucleotide of the splice donor site for the 7th exon. Consistent with HDAC1 being required to promote SHF addition, embryos treated with the HDAC inhibitor trichostatin A (TSA) or depleted for HDAC1 with morpholinos also display a similar specific loss of ventricular cardiomyocytes and SHF progenitor markers. Interestingly, the specific effects on SHF development are similar to what we have recently found in Cyp26 deficient embryos, which have an increase in retinoic acid (RA) levels. Although HDACs are known to interact with RA receptors (RARs), there are few examples of RARs being required to mediate transcriptional repression during development. Hence, we performed RNA-seq on crg and Cyp26 deficient embryos and identified that the expression of ripply3, a transcriptional co-repressor of TBX transcription factors, is similarly increased in the hearts of both conditions, suggesting that HDAC1-mediated repression of ripply3 may be necessary for SHF development. Consistent with this hypothesis, we find that overexpression of Ripply3 can restrict cardiac development. Altogether, our study reveals a novel mechanism whereby the epigenetic regulator HDAC1 promotes SHF development through repressing the expression of the RA-responsive gene ripply3.