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Whole-genome duplications (WGDs) have played a central role in the evolution of genomes and constitute an important source of genome instability in cancer. Here, we show in  Saccharomyces cerevisiae  that abnormal accumulations of histones are sufficient to induce WGDs. Our results link these WGDs to a reduced incorporation of the histone variant H2A.Z to chromatin. Moreover, we show that high levels of histones promote Swe1 WEE1  stabilisation thereby triggering the phosphorylation and inhibition of Cdc28 CDK1  through a mechanism different of the canonical DNA damage response. Our results link high levels of histones to a specific type of genome instability that is quite frequently observed in cancer and uncovers a new mechanism that might be able to respond to high levels of histones.

High levels of histones promote whole-genome-duplications and trigger a Swe1 WEE1 -dependent phosphorylation of Cdc28 CDK1