{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T07:04:08Z","timestamp":1791270248547,"version":"4.1.0"},"reference-count":83,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2020,2,7]],"date-time":"2020-02-07T00:00:00Z","timestamp":1581033600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Comparative Neurology"],"published-print":{"date-parts":[[2020,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    During inner ear development, primary auditory neurons named spiral ganglion neurons (SGNs) are surrounded by otic mesenchyme cells, which express the transcription factor Pou3f4. Mutations in\n                    <jats:italic>Pou3f4<\/jats:italic>\n                    are associated with DFNX2, the most common form of X\u2010linked deafness and typically include developmental malformations of the middle ear and inner ear. It is known that interactions between Pou3f4\u2010expressing mesenchyme cells and SGNs are important for proper axon bundling during development. However, Pou3f4 continues to be expressed through later phases of development, and potential interactions between Pou3f4 and SGNs during this period had not been explored. To address this, we documented Pou3f4 protein expression in the early postnatal mouse cochlea and compared SGNs in\n                    <jats:italic>Pou3f4<\/jats:italic>\n                    knockout mice and littermate controls. In\n                    <jats:italic>Pou3f4<\/jats:italic>\n                    <jats:sup>y\/\u2212<\/jats:sup>\n                    mice, SGN density begins to decline by the end of the first postnatal week, with approximately 25% of SGNs ultimately lost. This period of SGN loss in\n                    <jats:italic>Pou3f4<\/jats:italic>\n                    <jats:sup>y\/\u2212<\/jats:sup>\n                    cochleae coincides with significant elevations in SGN apoptosis. Interestingly, this period also coincides with the presence of a transient population of Pou3f4\u2010expressing cells around and within the spiral ganglion. To determine if Pou3f4 is normally required for SGN peripheral axon extension into the sensory domain, we used a genetic sparse labeling approach to track SGNs and found no differences compared with controls. We also found that\n                    <jats:italic>Pou3f4<\/jats:italic>\n                    loss did not lead to changes in the proportions of Type I SGN subtypes. Overall, these data suggest that otic mesenchyme cells may play a role in maintaining SGN populations during the early postnatal period.\n                  <\/jats:p>","DOI":"10.1002\/cne.24867","type":"journal-article","created":{"date-parts":[[2020,1,29]],"date-time":"2020-01-29T06:10:46Z","timestamp":1580278246000},"page":"1967-1985","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Pou3f4\u2010expressing otic mesenchyme cells promote spiral ganglion neuron survival in the postnatal mouse cochlea"],"prefix":"10.1002","volume":"528","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8886-6850","authenticated-orcid":false,"given":"Paige M.","family":"Brooks","sequence":"first","affiliation":[{"name":"Department of Biology Georgetown University  Washington District of Columbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin P.","family":"Rose","sequence":"additional","affiliation":[{"name":"Department of Otorhinolaryngology Head and Neck Surgery University of Maryland School of Medicine, University of Maryland  Baltimore Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meaghan L.","family":"MacRae","sequence":"additional","affiliation":[{"name":"Department of Biology Georgetown University  Washington District of Columbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katherine M.","family":"Rangoussis","sequence":"additional","affiliation":[{"name":"Department of Biology Georgetown University  Washington District of Columbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1613-5191","authenticated-orcid":false,"given":"Mansa","family":"Gurjar","sequence":"additional","affiliation":[{"name":"Department of Biology Georgetown University  Washington District of Columbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronna","family":"Hertzano","sequence":"additional","affiliation":[{"name":"Department of Otorhinolaryngology Head and Neck Surgery University of Maryland School of Medicine, University of Maryland  Baltimore Maryland"},{"name":"Department of Anatomy and Neurobiology University of Maryland School of Medicine, University of Maryland  Baltimore Maryland"},{"name":"Institute for Genome Sciences University of Maryland School of Medicine, University of Maryland  Baltimore Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2301-1151","authenticated-orcid":false,"given":"Thomas M.","family":"Coate","sequence":"additional","affiliation":[{"name":"Department of Biology Georgetown University  Washington District of Columbia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2020,2,7]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/cne.10244"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1002\/dvg.20454"},{"key":"e_1_2_8_4_1","unstructured":"Allen Institute for Brain Science. 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