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• W2897716354 abstract "Safeguarding cell function and identity following a genotoxic stress challenge entails a tight coordination of DNA damage signaling and repair with chromatin maintenance. How this coordination is achieved and with what impact on chromatin integrity remains elusive. Here, we address these questions by investigating the mechanisms governing the distribution in mammalian chromatin of the histone variant H2A.X, a central player in damage signaling. We reveal that H2A.X is deposited de novo at sites of DNA damage in a repair-coupled manner, whereas the H2A.Z variant is evicted, thus reshaping the chromatin landscape at repair sites. Our mechanistic studies further identify the histone chaperone FACT (facilitates chromatin transcription) as responsible for the deposition of newly synthesized H2A.X. Functionally, we demonstrate that FACT potentiates H2A.X-dependent signaling of DNA damage. We propose that new H2A.X deposition in chromatin reflects DNA damage experience and may help tailor DNA damage signaling to repair progression." @default.
• W2897716354 created "2018-10-26" @default.
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• W2897716354 date "2018-12-01" @default.
• W2897716354 modified "2023-10-14" @default.
• W2897716354 title "The Histone Chaperone FACT Coordinates H2A.X-Dependent Signaling and Repair of DNA Damage" @default.
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• W2897716354 doi "https://doi.org/10.1016/j.molcel.2018.09.010" @default.
• W2897716354 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6292839" @default.
• W2897716354 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30344095" @default.
• W2897716354 hasPublicationYear "2018" @default.
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