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However, the cellular origins of these effects and the extent to which axonal changes causally contribute to behavioral impairments remain unclear. We hypothesized that\n                    <jats:italic>Tbx1<\/jats:italic>\n                    deficiency specifically within the oligodendrocyte lineage contributes to myelin and behavioral phenotypes. To test this hypothesis, we first demonstrated through in vitro siRNA knockdown that\n                    <jats:italic>Tbx1<\/jats:italic>\n                    regulates both OPCs and mature oligodendrocytes. Subsequently, we assessed the impact of\n                    <jats:italic>Tbx1<\/jats:italic>\n                    heterozygosity initiated in OPCs on behavioral and myelin phenotypes in male conditional Pdgfr\u03b1Cre;\n                    <jats:italic>Tbx1<\/jats:italic>\n                    <jats:sup>+\/flox<\/jats:sup>\n                    mice. These mice exhibited Cre-mediated recombination in Pdgfr\u03b1-expressing brain regions and in the OPC progeny within the fimbria. At one month of age, the mutants displayed a higher rate of spontaneous alternation at the longest inter-trial interval in the T-maze compared to their wild-type littermates\u2014an effect that was dissipated at two months. No significant phenotypic abnormalities were observed in conditional Pdgfr\u03b1Cre;\n                    <jats:italic>Tbx1<\/jats:italic>\n                    <jats:sup>+\/flox<\/jats:sup>\n                    mice regarding neonatal ultrasonic vocalizations, social interaction, novel object approach, anxiety-like behavior (elevated plus maze), or open-field locomotion and thigmotaxis. Electron microscopic analysis revealed a compositional shift in myelinated axons within the fimbria of adult male mutants, characterized by an increased number of myelinated axons in the 300\u2013800\u00a0nm diameter range and a decreased number in the\u2009~\u20091,200\u00a0nm and\u2009~\u20091,400\u00a0nm ranges, with myelin thickness remaining unchanged across diameters. These findings indicate that\n                    <jats:italic>Tbx1<\/jats:italic>\n                    heterozygosity in the oligodendrocyte lineage leads to a selective shift towards smaller myelinated axons in the fimbria and a transiently higher level of capacity for working memory and cognitive flexibility. However, it does not replicate the full spectrum of myelination abnormalities or the broader cognitive and social deficits observed in constitutive\n                    <jats:italic>Tbx1<\/jats:italic>\n                    heterozygotes, suggesting that\n                    <jats:italic>Tbx1<\/jats:italic>\n                    deficiency in non-oligodendrocyte lineage cells may lead to altered myelination and neurodevelopmental behavioral impairments.\n                  <\/jats:p>","DOI":"10.1186\/s13041-026-01311-4","type":"journal-article","created":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T11:08:25Z","timestamp":1779275305000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Tbx1 heterozygosity in the oligodendrocyte lineage shifts myelinated axon composition in the mouse fimbria without behavioral impairments"],"prefix":"10.1186","volume":"19","author":[{"given":"Anne Marie","family":"Wells","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takaki","family":"Tanifuji","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takeshi","family":"Takano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arumu","family":"Endo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gina","family":"Kang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marisa","family":"Esparza","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qian","family":"Shi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manzoor A.","family":"Bhat","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noboru","family":"Hiroi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,5,20]]},"reference":[{"issue":"8","key":"1311_CR1","doi-asserted-by":"publisher","first-page":"488","DOI":"10.1093\/ijnp\/pyz026","volume":"22","author":"N Hiroi","year":"2019","unstructured":"Hiroi N, Yamauchi T. 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