The recruitment of ACF1 and SMARCA5 to DNA lesions relies on ADP-ribosylation dependent chromatin unfolding

ADP-ribosylation
DOI: 10.1091/mbc.e23-07-0281 Publication Date: 2024-01-03T16:51:15Z
ABSTRACT
ADP-ribosylation signaling orchestrates the recruitment of various repair actors and chromatin remodeling processes promoting access to lesions during early stages DNA damage response. The remodeler complex ACF, composed ATPase subunit SMARCA5/SNF2H cofactor ACF1/BAZ1A, is among factors that accumulate at in an dependent manner. In this work, we show each ACF accumulates breaks independently from its partner. Furthermore, demonstrate SMARCA5 ACF1 sites not due direct binding ADP-ribose moieties but facilitated relaxed ADP-ribosylated chromatin. Therefore, our work provides new insights regarding mechanisms underlying timely accumulation lesions, where they contribute efficient resolution.
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