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 strande d DNA generated from a DSB. We show that cells lacking the recombination pr otein Tid1p are unable to adapt, but that this defect is distinct from any role in recombination. As with the adaptation-detective mutations yku70 Del ta 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 suppre ssed 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 tid 1 Delta defect cannot be complemented by overexpressing the homolog Rad54p, nor is it affected in rad51 Delta tid1 Delta, rad54 Delta tid1 Delta, or r ad52 Delta tid1 Delta double mutants that prevent essentially all homologou s recombination. We suggest that Tid1p participates in monitoring the exten t of single-stranded DNA produced by resection of DNA ends in a fashion tha t is distinct from its role in recombination.