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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2022,11,15]]},"abstract":"<jats:p>\n                    The in\u00a0vivo mechanisms underlying dominant syndromes caused by mutations in SRY-Box Transcription Factor 9 (\n                    <jats:italic>SOX9<\/jats:italic>\n                    ) and\n                    <jats:italic>SOX10<\/jats:italic>\n                    (\n                    <jats:italic>SOXE<\/jats:italic>\n                    ) transcription factors, when they either are expressed alone or are coexpressed, are ill-defined. We created a mouse model for the campomelic dysplasia\n                    <jats:italic>\n                      SOX9\n                      <jats:sup>Y440X<\/jats:sup>\n                    <\/jats:italic>\n                    mutation, which truncates the transactivation domain but leaves DNA binding and dimerization intact. Here, we find that\n                    <jats:italic>\n                      SOX9\n                      <jats:sup>Y440X<\/jats:sup>\n                    <\/jats:italic>\n                    causes deafness via distinct mechanisms in the endolymphatic sac (ES)\/duct and cochlea. By contrast, conditional heterozygous\n                    <jats:italic>Sox9<\/jats:italic>\n                    -null mice are normal. During the ES development of\n                    <jats:italic>\n                      Sox9\n                      <jats:sup>Y440X\/+<\/jats:sup>\n                    <\/jats:italic>\n                    heterozygotes,\n                    <jats:italic>Sox10<\/jats:italic>\n                    and genes important for ionic homeostasis are down-regulated, and there is developmental persistence of progenitors, resulting in fewer mature cells.\n                    <jats:italic>Sox10<\/jats:italic>\n                    heterozygous null mutants also display persistence of ES\/duct progenitors. By contrast, SOX10 retains its expression in the early\n                    <jats:italic>\n                      Sox9\n                      <jats:sup>Y440X\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mutant cochlea. Later, in the postnatal stria vascularis, dominant interference by SOX9\n                    <jats:sup>Y440X<\/jats:sup>\n                    is implicated in impairing the normal cooperation of SOX9 and SOX10 in repressing the expression of the water channel Aquaporin 3, thereby contributing to endolymphatic hydrops. Our study shows that for a functioning endolymphatic system in the inner ear, SOX9 regulates\n                    <jats:italic>Sox10<\/jats:italic>\n                    , and depending on the cell type and target gene, it works either independently of or cooperatively with SOX10. SOX9\n                    <jats:sup>Y440X<\/jats:sup>\n                    can interfere with the activity of both SOXE factors, exerting effects that can be classified as haploinsufficient\/hypomorphic or dominant negative depending on the cell\/gene context. This model of disruption of transcription factor partnerships may be applicable to congenital deafness, which affects \u223c0.3% of newborns, and other syndromic disorders.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2122121119","type":"journal-article","created":{"date-parts":[[2022,11,7]],"date-time":"2022-11-07T15:17:01Z","timestamp":1667834221000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":35,"title":["SOX9 and SOX10 control fluid homeostasis in the inner ear for hearing through independent and cooperative mechanisms"],"prefix":"10.1073","volume":"119","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3925-1136","authenticated-orcid":false,"given":"Irene Y. 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