<b>Identification of BAF60b as a chromatin remodeling checkpoint of diet-induced fatty liver disease</b>

• DOI: 10.2337/figshare.26315728
• Publication Date: 2024-07-24T16:18:02Z
• Authors: Jing Zhong; Xiuyu Ji; Yali Zhao; Yihe Jia; Churui Song; Jinghuan Lv; Yuying Chen; Yanping Zhou; Xue Lv; Zhuoyin Yang; Zheyu Zhang; Qiyao Xu; Weihong Wang; Haiyan Chen; Aoyuan Cui; Yu Li; Zhuo-Xian Meng
• Keywords: Steatosis; Lipogenesis

&lt;p dir="ltr"&gt;&lt;b&gt;Abstract&lt;/b&gt;&lt;/p&gt;&lt;p dir="ltr"&gt;&lt;a href="" target="_blank"&gt;Overnutrition has gradually become the primary causative factor of nonalcoholic fatty liver disease (NAFLD)&lt;/a&gt;. &lt;a target="_blank"&gt;However, how nutritional signals are integrated to orchestrate transcriptional programs important for NAFLD progression remains poorly understood.&lt;/a&gt; target="_blank"&gt;Here, we identified hepatic BAF60b as a lipid-sensitive subunit switch/sucrose-nonfermentable (SWI/SNF) chromatin-remodeling complex and is negatively associated with steatosis in mice humans. Hepatic deficiency promotes high-fat diet (HFD)-induced mice, while transgenic expression attenuates HFD-induced obesity NAFLD, both accompanied by marked regulation PPARγ expression. Mechanistically, through motif analysis ATAC-Seq multiple validation experiments, CCAAT/enhancer‐binding protein β (C/EBPβ) transcription that interacts suppress gene expression, thereby controlling lipid accumulation progression.&lt;/a&gt; This work uncovers target="_blank"&gt;hepatic negative regulator C/EBPβ dependent chromatin remodeling.&lt;/a&gt;&lt;/p&gt;&lt;p dir="ltr"&gt;&lt;b&gt;Keyword&lt;/b&gt;&lt;b&gt;：&lt;/b&gt;SWI/SNF complex; BAF60b; NAFLD; Transcriptional regulation&lt;/p&gt;&lt;p dir="ltr"&gt;&lt;b&gt;Article Highlights&lt;/b&gt;&lt;/p&gt;&lt;p dir="ltr"&gt;• We aim understand progression.&lt;/p&gt;&lt;p dietary-lipid sensor steatosis. used liver-specific knockout combining multi-omics techniques, study role Our findings uncover key remodeling checkpoint sensing, accumulation, engaging C/EBPβ/PPARγ axis.&lt;/p&gt;