Exposure to valproic acid (VPA) reproduces hdac1 loss of function phenotypes in zebrafish.

Histone deacetylases are enzymes that remove acetyl groups from histone tails and are understood to act as repressors of transcriptional activity. Hdac1 has been previously shown to function in eye, pectoral fin, heart, liver, and pharyngeal skeletal development. We show that high doses of Valproic Acid (VPA) reproduce the hdac1 phenotype. We identify tbx5 genes as potential targets of Hdac1 in eye, pectoral fin, and heart development. Using timed exposures, we show that skeletal structures in the pharyngeal arches are impacted by VPA between 24-36 hours post-fertilization, indicating a role for Hdac1 during post-migration patterning, differentiation, or proliferation of cranial neural crest cells.