The Saccharomyces recombination protein Tid1p is required for adaptation from G2/M arrest induced by a double-strand break

Saccharomyces cells with a single unrepaired double strand break (DSB) will adapt to checkpoint-mediated G2/M arrest and resume cell cycle progression. The decision to adapt is finely regulated by the extent of single stranded DNA generated from a DSB. We show that cells lacking the recombination protein Tid1p are unable to adapt, but that this defect is distinct from any role in recombination. As with the adaptation-detective mutations yku70 Delta and cdc5-ad, permanent arrest in tid1 Delta is bypassed by the deletion of the checkpoint gene RADS. Permanent arrest of tid1 Delta cells is suppressed by the rfa1-t11 mutation in the ssDNA binding complex RPA, similar to yku70 Delta, whereas the defect in cdc5-ad is not suppressed. Unlike yku70 Delta, tid1 Delta does not affect 5'-to-3' degradation of Use ends. The tid1 Delta defect cannot be complemented by overexpressing the homolog Rad54p, nor is it affected in rad51 Delta tid1 Delta, rad54 Delta tid1 Delta, or rad52 Delta tid1 Delta double mutants that prevent essentially all homologous recombination. We suggest that Tid1p participates in monitoring the extent of single-stranded DNA produced by resection of DNA ends in a fashion that is distinct from its role in recombination.