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While it is well\u2010established that global YY1 knockout (KO) leads to embryonic death in mice and that YY1 deletion in neurons or oligodendrocytes induces impaired brain function, the role of astrocytic YY1 in the brain remains unknown. We investigated the role of astrocytic YY1 in the brain using a glial fibrillary acidic protein (GFAP)\u2010specific YY1 conditional KO (YY1 cKO) mouse model to delete astrocytic YY1. Astrocytic YY1 cKO mice were tested for behavioral phenotypes, such as locomotor activity, coordination, and cognition, followed by an assessment of relevant biological pathways using RNA\u2010sequencing analysis, immunoblotting, and immunohistochemistry in the cortex, midbrain, and cerebellum. YY1 cKO mice showed abnormal phenotypes, movement deficits, and cognitive dysfunction. At the molecular level, astrocytic YY1 deletion altered the expression of genes associated with proliferation and differentiation, p53\/caspase apoptotic pathways, oxidative stress response, and inflammatory signaling including NF\u2010\u03baB, STAT, and IRF in all regions. Astrocytic YY1 deletion significantly increased the expression of GFAP as astrocytic activation and Iba1 as microglial activation, indicating astrocytic YY1 deletion activated microglia as well. Accordingly, multiple inflammatory cytokines and chemokines including TNF\u2010\u03b1 and CXCL10 were elevated. Combined, these novel findings suggest that astrocytic YY1 is a critical transcription factor for normal brain development and locomotor activity, motor coordination, and cognition. Astrocytic YY1 is also essential in preventing pathological oxidative stress, apoptosis, and inflammation.<\/jats:p>","DOI":"10.1002\/glia.24286","type":"journal-article","created":{"date-parts":[[2022,10,27]],"date-time":"2022-10-27T06:32:32Z","timestamp":1666852352000},"page":"450-466","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Astrocytic Yin Yang 1 is critical for murine brain development and protection against apoptosis, oxidative stress, and inflammation"],"prefix":"10.1002","volume":"71","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5044-7607","authenticated-orcid":false,"given":"Edward","family":"Pajarillo","sequence":"first","affiliation":[{"name":"Department of Pharmaceutical Sciences Florida A&amp;M University  Tallahassee Florida USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivan","family":"Nyarko\u2010Danquah","sequence":"additional","affiliation":[{"name":"Department 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