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The high mobility group transcription factor  SOX9  is expressed in stem cells, progenitor cells, and differentiated cell-types in developing and mature organs. Exposure to a variety of toxicants including dioxin, di(2-ethylhexyl) phthalate, 6:2 chlorinated polyfluorinated ether sulfonate, and chlorpyrifos results in the downregulation of tetrapod  Sox9  and/or zebrafish  sox9b . Disruption of  Sox9/sox9b  function through environmental exposures or genetic mutations produce a wide range of phenotypes and adversely affect organ development and health. We generated a dominant-negative  sox9b  ( dnsox9b ) to inhibit  sox9b  target gene expression and used the Gal4/UAS system to drive  dnsox9b  specifically in cardiomyocytes. Cardiomyocyte-specific inhibition of  sox9b  function resulted in a decrease in ventricular cardiomyocytes, an increase in atrial cardiomyocytes, hypoplastic endothelial cushions, and impaired epicardial development, ultimately culminating in heart failure. Cardiomyocyte-specific  dnsox9b  expression significantly reduced end diastolic volume, which corresponded with a decrease in stroke volume, ejection fraction, and cardiac output. Further analysis of isolated cardiac tissue by RT-qPCR revealed cardiomyocyte-specific inhibition of  sox9b  function significantly decreased the expression of the critical cardiac development genes  nkx2.5 ,  nkx2.7 , and  myl7 , as well as  c-fos , an immediate early gene necessary for cardiomyocyte progenitor differentiation. Together our studies indicate  sox9b  transcriptional regulation is necessary for cardiomyocyte development and function.

sox9b is required in cardiomyocytes for cardiac morphogenesis and function