ArticlebioRxiv : the preprint server for biology2025
ATR promotes genome instability via CENP-A eviction from centromeres under replication stress.
Article in bioRxiv : the preprint server for biology, 2025. 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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Authors and funding
8 authors.
Funding
Abstract
Replication stress leads to genome instability in part by promoting missegregation of chromosomes lacking centromeres. Yet the molecular mechanism linking replication stress to centromere dysfunction has remained elusive. Here, we show that sustained replication stress induces eviction of the histone H3 variant CENP-A. Displaced CENP-A relocalizes to nucleoli. This process is dependent on the DNA damage response kinase, ATR, and occurs in both human and mouse cells. We show that ATR promotes CENP-A eviction by recruiting the AAA+ ATPase VCP to centromeres, destabilizing CENP-A-containing nucleosomes. The canonical CENP-A chaperone, HJURP, but not H3 histone chaperones DAXX or ATRX, is necessary for nucleolar CENP-A localization. Importantly, ATR-dependent CENP-A eviction endures after cell-cycle re-entry and correlates with the emergence of acentric chromosomes, linking replication stress directly to segregation defects. Our findings reveal an undiscovered role for ATR in regulating centromere identity under stress and uncover a mechanistic pathway that drives genome instability.
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