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Its etiology involves a combination of genetic and environmental factors, and it is more prevalent in males. Bisphenol A (BPA), an endocrine-disrupting chemical commonly found in plastics, has been linked to an increased risk of ASD. However, the molecular mechanisms by which BPA affects gene regulation remain poorly understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In this study, hippocampal tissues were collected from rat offspring prenatally exposed to BPA at a dose of 5,000\u00a0\u00b5g\/kg of maternal body weight, equivalent to the NOAEL. RNA sequencing was performed to identify genes exhibiting differential alternative splicing. ASD-related alternatively spliced genes were selected for validation using high-resolution melting (HRM) analysis. Ingenuity Pathway Analysis (IPA) was used to predict associated biological functions, diseases, and molecular interaction networks. Additionally, BPA-responsive transcription factors, RNA-binding proteins, splicing regulators, and differentially expressed genes were analyzed to identify upstream regulatory mechanisms. Gene expression was validated by qRT-PCR, and transcription factor binding was confirmed via chromatin immunoprecipitation-qPCR (ChIP-qPCR).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      RNA-seq analysis revealed that prenatal BPA exposure altered the alternative splicing of ASD-related genes in the hippocampus, including\n                      <jats:italic>Agap1<\/jats:italic>\n                      ,\n                      <jats:italic>Ap2b1<\/jats:italic>\n                      , and\n                      <jats:italic>Kifap3<\/jats:italic>\n                      . Gene ontology and pathway analyses indicated that differentially spliced genes were involved in mRNA splicing processes in males and neuronal functions in females, patterns that align with ASD-related phenotypes. ChIP-qPCR revealed sex-specific differences in YY1 transcription factor binding at the\n                      <jats:italic>Matr3<\/jats:italic>\n                      promoter, with males showing reduced binding, leading to downregulation of\n                      <jats:italic>Matr3<\/jats:italic>\n                      expression. Notably,\n                      <jats:italic>Agap1<\/jats:italic>\n                      , a target of MATR3, exhibited increased alternative splicing specifically in the hippocampus of male offspring.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      This study provides the first evidence that prenatal BPA exposure disrupts the alternative splicing and transcriptional regulation of ASD-related genes in offspring\u2019s hippocampus in a sex-specific manner. These disruptions, particularly the YY1-mediated regulation of\n                      <jats:italic>Matr3<\/jats:italic>\n                      and downstream effects on\n                      <jats:italic>Agap1<\/jats:italic>\n                      splicing in males, offer new insights into the molecular mechanisms by which BPA may contribute to ASD pathogenesis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s13293-025-00744-1","type":"journal-article","created":{"date-parts":[[2025,8,11]],"date-time":"2025-08-11T09:17:22Z","timestamp":1754903842000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Sex-dependent epigenetic disruption of YY1 binding by prenatal BPA exposure downregulates Matr3 and alters Agap1 splicing in the offspring hippocampus"],"prefix":"10.1186","volume":"16","author":[{"given":"Pattanachat","family":"Lertpeerapan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Songphon","family":"Kanlayaprasit","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Surangrat","family":"Thongkorn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kasidit","family":"Kasitipradit","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pawinee","family":"Panjabud","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kwanjira","family":"Songsritaya","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thanawin","family":"Jantheang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masanobu","family":"Morita","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takaaki","family":"Akaike","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valerie W.","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Depicha","family":"Jindatip","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thanit","family":"Saeliw","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tewarit","family":"Sarachana","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,8,11]]},"reference":[{"issue":"3","key":"744_CR1","doi-asserted-by":"publisher","first-page":"302","DOI":"10.1007\/s10567-011-0097-0","volume":"14","author":"FJ van Steensel","year":"2011","unstructured":"van Steensel FJ, B\u00f6gels SM, Perrin S. 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