{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T12:55:01Z","timestamp":1789131301892,"version":"build-2803163510"},"reference-count":77,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,3,19]],"date-time":"2024-03-19T00:00:00Z","timestamp":1710806400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Neurosci."],"abstract":"<jats:sec><jats:title>Introduction<\/jats:title><jats:p>Hair cells (HCs) of the cochlea are responsible for sound transduction and hearing perception in mammals. Genetic mutations in the transcription factor <jats:italic>Pou4f3<\/jats:italic> cause non-syndromic autosomal dominant hearing loss in humans (DFNA15) which varies in the age of onset depending on the individual mutation. Mouse models with germline deletion or mutations in <jats:italic>Pou4f3<\/jats:italic> have previously demonstrated its critical role in the maturation and survival of cochlear HCs during embryonic development. However, the role of <jats:italic>Pou4f3<\/jats:italic> in auditory function and in the survival or maintenance of cochlear HCs after birth and during adulthood has not been studied.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Therefore, using the inducible CreER-loxP system, we deleted <jats:italic>Pou4f3<\/jats:italic> from mouse cochlear HCs at different postnatal ages, relevant to specific stages of HC maturation and hearing function.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results and discussion<\/jats:title><jats:p>Elevated auditory brainstem response thresholds and significant HC loss were detected in mice with <jats:italic>Pou4f3<\/jats:italic> deletion compared to their control littermates, regardless of the age when <jats:italic>Pou4f3<\/jats:italic> was deleted. However, HC loss occurred more rapidly when <jats:italic>Pou4f3<\/jats:italic> was deleted from immature HCs. Additionally, HC loss caused by <jats:italic>Pou4f3<\/jats:italic> deletion did not affect the number of cochlear supporting cells, but caused a delayed loss of spiral ganglion neurons at 4 months after the deletion. In conclusion, <jats:italic>Pou4f3<\/jats:italic> is necessary for the survival of cochlear HCs and normal hearing at all postnatal ages regardless of their maturation state. Our data also suggest that <jats:italic>Pou4f3<\/jats:italic> indirectly regulates the survival of spiral ganglion neurons.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fncel.2024.1369282","type":"journal-article","created":{"date-parts":[[2024,3,19]],"date-time":"2024-03-19T04:28:17Z","timestamp":1710822497000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":13,"title":["The transcription factor Pou4f3 is essential for the survival of postnatal and adult mouse cochlear hair cells and normal hearing"],"prefix":"10.3389","volume":"18","author":[{"given":"Jarnail","family":"Singh","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle R.","family":"Randle","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bradley J.","family":"Walters","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brandon C.","family":"Cox","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2024,3,19]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"270","DOI":"10.1006\/mcne.2001.1018","article-title":"Role of STAT3 and PI 3-kinase\/Akt in mediating the survival actions of cytokines on sensory neurons","volume":"18","author":"Alonzi","year":"2001","journal-title":"Mol. 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