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• W2954700532 abstract "Following injury, differentiated epithelial cells can serve as a stem cell-independent source for tissue regeneration by undergoing reprogramming into other cell types. The intrinsic molecular basis underlying plasticity of differentiated cells remains largely unaddressed. Here we show that Arid1a, a key component of the SWI/SNF chromatin remodeling complex, controls liver regeneration and gene expression associated with emergence of injury-induced liver-progenitor-like cells (LPLCs). Hepatocyte-specific Arid1a ablation reduces LPLC gene expression in several models of periportal liver injury and impairs liver regeneration, leading to organ dysfunction. Arid1a establishes a permissive chromatin state at LPLC-enriched genes during homeostasis, suggesting it endows hepatocytes with competence to respond to injury-induced signals. Consistently, Arid1a facilitates binding of YAP, a critical regeneration signaling pathway, to LPLC-enriched genes, and Arid1a deletion prevents their YAP-associated induction following injury. Together, these findings provide a framework for studying the contributions of injury-induced LPLCs to periportal liver regeneration." @default.
• W2954700532 created "2019-07-12" @default.
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• W2954700532 date "2019-07-01" @default.
• W2954700532 modified "2023-10-18" @default.
• W2954700532 title "A Homeostatic Arid1a-Dependent Permissive Chromatin State Licenses Hepatocyte Responsiveness to Liver-Injury-Associated YAP Signaling" @default.
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• W2954700532 doi "https://doi.org/10.1016/j.stem.2019.06.008" @default.
• W2954700532 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31271748" @default.
• W2954700532 hasPublicationYear "2019" @default.
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