ArticleCommunications biology2026
ISWI/CHRAC orchestrates sequential chromatin-remodeling activities by mobilizing DNA polymerase ε for homologous recombination.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
ATP-dependent chromatin remodeling is essential for replication, transcription, and DNA repair, especially DNA double-strand break (DSB) repair. However, the mechanisms underlying chromatin remodeling remain elusive. Here, we investigated the role of CHRAC17, a component of the chromatin assembly complex (CHRAC), in maintaining genome stability. In response to DSBs, the ISWI-family ATPase complex SNF2H-ACF1 is immediately recruited to DSBs through the H2B-type histone-fold protein CHRAC17, forming CHRAC, which promotes nucleosome assembly and recruits BRCA1 and RAD51 to the DSB site. CHRAC promotes later RAD51-mediated HR steps through additional nucleosome-remodeling activity, including nucleosome sliding activity. CHRAC17, also known as POLE3, is a subunit of DNA polymerase ε (Polε). Polε is recruited to DSBs via CHRAC17, facilitating RAD51-mediated homologous recombination (HR) and conferring resistance to PARP inhibitors. These findings define a mechanism of homologous recombination driven by coordinated regulation of nucleosome dynamics by CHRAC and Polε, thereby ensuring genome stability.
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