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

Author

Listed:
  • Jessel Ayra-Plasencia

    (Hospital Universitario Nuestra Señora de Candelaria
    Universidad de La Laguna)

  • Félix Machín

    (Hospital Universitario Nuestra Señora de Candelaria
    Universidad de La Laguna)

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.

Suggested Citation

  • Jessel Ayra-Plasencia & Félix Machín, 2019. "DNA double-strand breaks in telophase lead to coalescence between segregated sister chromatid loci," Nature Communications, Nature, vol. 10(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-10742-8
    DOI: 10.1038/s41467-019-10742-8
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    Cited by:

    1. Adrián Campos & Facundo Ramos & Lydia Iglesias & Celia Delgado & Eva Merino & Antonio Esperilla-Muñoz & Jaime Correa-Bordes & Andrés Clemente-Blanco, 2023. "Cdc14 phosphatase counteracts Cdk-dependent Dna2 phosphorylation to inhibit resection during recombinational DNA repair," Nature Communications, Nature, vol. 14(1), pages 1-20, December.

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