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The cellular mechanisms underlying the emergence of abnormal sensory sensitivity in ASD are not fully understood. Recent studies in rodent models of ASD identified differences in dorsal root ganglia (DRG) neurons that convey somatosensory information to the central nervous system. However, it is unknown how ASD\u2010associated alterations in DRG neurons emerge during development and if these phenotypes are conserved across ASD models. We examined\n                    <jats:italic>Pten<\/jats:italic>\n                    (phosphatase and tensin homolog) heterozygous mice (\n                    <jats:italic>Pten<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>Het<\/jats:italic>\n                    <\/jats:sup>\n                    ) as a model for syndromic ASD and identified altered responses to sensory stimuli. Transcriptomic and in\u00a0vivo analysis identified alterations in subtype\u2010specific markers of DRG neurons in\n                    <jats:italic>Pten<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>Het<\/jats:italic>\n                    <\/jats:sup>\n                    mice, emerging during early DRG development and involving dysregulation of signaling pathways downstream of PTEN. Finally, we show that mice harboring an ASD\u2010associated mutation (\n                    <jats:italic>Pten<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>Y69H<\/jats:italic>\n                    <\/jats:sup>\n                    ) show nearly identical alterations in the expression of somatosensory neuron subtype\u2010specific markers. These results show that precise levels of PTEN are required for proper somatosensory development and provide insight into the molecular and cellular basis of sensory abnormalities in a model for syndromic ASD.\n                  <\/jats:p>","DOI":"10.1002\/aur.70119","type":"journal-article","created":{"date-parts":[[2025,9,13]],"date-time":"2025-09-13T03:13:42Z","timestamp":1757733222000},"page":"2192-2209","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Altered Primary Somatosensory Neuron Development in a\n                    <i>Pten<\/i>\n                    Heterozygous Model for Autism Spectrum Disorder"],"prefix":"10.1002","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5489-5300","authenticated-orcid":false,"given":"Alejandra","family":"Fernandez","sequence":"first","affiliation":[{"name":"Vollum Institute Oregon Health &amp; Science University  Portland Oregon USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nick","family":"Sarn","sequence":"additional","affiliation":[{"name":"Genomic Medicine Institute Lerner Research Institute, Cleveland Clinic  Cleveland Ohio USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Charis","family":"Eng","sequence":"additional","affiliation":[{"name":"Genomic Medicine Institute Lerner Research Institute, Cleveland Clinic  Cleveland Ohio USA"},{"name":"Center for Personalized Genetic Healthcare, Medical Specialties Institute Cleveland Clinic  Cleveland Ohio USA"},{"name":"Department of Genetics and Genome Sciences Case Western Reserve University School of Medicine  Cleveland Ohio USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5094-5270","authenticated-orcid":false,"given":"Kevin M.","family":"Wright","sequence":"additional","affiliation":[{"name":"Vollum Institute Oregon Health &amp; 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