Extended DNA damage-induced G2/M arrests lead to aberrant mitoses through accumulation of securin.

In yeast with double-stranded DNA breaks and nonfunctional telomeres, extended Chk1-dependent G2/M arrest durations correlate with aberrant mitoses, including miscoordination of nuclear division and cytokinesis.

• Why it matters: DNA damage can yield different stress-survival outcomes, but how arrest timing at single-cell resolution shapes mitosis failure and genomic instability risk is unclear.
• What they did: Using time-lapse microscopy, the study quantified single-cell G2/M arrest durations in yeast and linked longer arrests to securin (Pds1) phosphorylation and progressive securin accumulation during arrest.
• The result: Longer arrests led to grossly delayed or missed nuclear divisions and cell death, and the phenotype was suppressed by LTE1 deletion or by lowering securin levels.

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