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Cohesin still drives homologous recombination repair of DNA double-strand breaks in late mitosis

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Abstract The cohesin complex maintains sister chromatid cohesion from S phase to anaphase onset. Cohesin also plays roles in chromosome structure and DNA repair. At anaphase onset, the cohesin subunit Scc1 is cleaved to allow segregation in an orderly manner, although some residual cohesin subunits remain to maintain chromosome structure. Efficient DNA double-strand break (DSB) repair by homologous recombination (HR) with the sister chromatid also depends on cohesin. Here, we have tested whether residual cohesin is important during DSB repair in anaphase/telophase (late mitosis). Using the well-established MAT switching system, we first show that HR is molecularly functional in late mitosis, and then show that cohesin is required for its efficiency. During DSBs in late mitosis, the segregated sister loci get closer and have episodes of coalescence, which may favour repair by HR. Here, we also show that these cytological phenotypes also depend on cohesin. Finally, full-length Scc1 returns after DSBs in late mitosis, suggesting that de novo widespread cohesin complexes can support these retrograde behaviours.
Title: Cohesin still drives homologous recombination repair of DNA double-strand breaks in late mitosis
Description:
Abstract The cohesin complex maintains sister chromatid cohesion from S phase to anaphase onset.
Cohesin also plays roles in chromosome structure and DNA repair.
At anaphase onset, the cohesin subunit Scc1 is cleaved to allow segregation in an orderly manner, although some residual cohesin subunits remain to maintain chromosome structure.
Efficient DNA double-strand break (DSB) repair by homologous recombination (HR) with the sister chromatid also depends on cohesin.
Here, we have tested whether residual cohesin is important during DSB repair in anaphase/telophase (late mitosis).
Using the well-established MAT switching system, we first show that HR is molecularly functional in late mitosis, and then show that cohesin is required for its efficiency.
During DSBs in late mitosis, the segregated sister loci get closer and have episodes of coalescence, which may favour repair by HR.
Here, we also show that these cytological phenotypes also depend on cohesin.
Finally, full-length Scc1 returns after DSBs in late mitosis, suggesting that de novo widespread cohesin complexes can support these retrograde behaviours.

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