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DNA double-strand breaks in telophase lead to coalescence between segregated sister chromatid loci.


ABSTRACT: DNA double strand breaks (DSBs) pose a high risk for genome integrity. Cells repair DSBs through homologous recombination (HR) when a sister chromatid is available. HR is upregulated by the cycling dependent kinase (CDK) despite the paradox of telophase, where CDK is high but a sister chromatid is not nearby. Here we study in the budding yeast the response to DSBs in telophase, and find they activate the DNA damage checkpoint (DDC), leading to a telophase-to-G1 delay. Outstandingly, we observe a partial reversion of sister chromatid segregation, which includes approximation of segregated material, de novo formation of anaphase bridges, and coalescence between sister loci. We finally show that DSBs promote a massive change in the dynamics of telophase microtubules (MTs), together with dephosphorylation and relocalization of kinesin-5 Cin8. We propose that chromosome segregation is not irreversible and that DSB repair using the sister chromatid is possible in telophase.

SUBMITTER: Ayra-Plasencia J 

PROVIDER: S-EPMC6598993 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature

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DNA double-strand breaks in telophase lead to coalescence between segregated sister chromatid loci.

Ayra-Plasencia Jessel J   Machín Félix F  

Nature communications 20190628 1


DNA double strand breaks (DSBs) pose a high risk for genome integrity. Cells repair DSBs through homologous recombination (HR) when a sister chromatid is available. HR is upregulated by the cycling dependent kinase (CDK) despite the paradox of telophase, where CDK is high but a sister chromatid is not nearby. Here we study in the budding yeast the response to DSBs in telophase, and find they activate the DNA damage checkpoint (DDC), leading to a telophase-to-G<sub>1</sub> delay. Outstandingly, w  ...[more]

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