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High levels of histones promote whole-genome-duplications and trigger a Swe1(WEE1)-dependent phosphorylation of Cdc213(CDK1)

Abstract : 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.
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https://hal-amu.archives-ouvertes.fr/hal-02143673
Contributor : Ghislain Bidaut <>
Submitted on : Wednesday, May 29, 2019 - 2:53:00 PM
Last modification on : Thursday, December 12, 2019 - 8:54:02 AM

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Douglas Maya Miles, Xenia Penate, Trinidad Sanmartin Olmo, Frederic Jourquin, Maria Cruz Munoz Centeno, et al.. High levels of histones promote whole-genome-duplications and trigger a Swe1(WEE1)-dependent phosphorylation of Cdc213(CDK1). Elife, 2018, 7, ⟨10.7554/eLife.35337.001⟩. ⟨hal-02143673⟩

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