Mitosis is usually shorter than other phases of the cell cycle and maintains a consistent duration despite variations in cell size and spindle size. This suggests the existence of a compensatory mechanism that ensures a short duration, possibly as a protective measure against irreversible damage, such as DNA damage. To explore the link between prolonged mitosis and DNA damage, we develop a microscopy-based assay utilizing Rad52-GFP as a marker for mitotic DNA damage. Through this assay, we provide evidence that mutants with prolonged mitosis exhibit increased Rad52 puncta, indicating an elevation in endogenous DNA damage.
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