TABLE 2.

rad55Δ has an intact cell cycle arrest in response to DNA damage^a

Strain	% Lethality	% Arrest	Arrest/lethality
Wild type	21	18	0.86
rad9	40	5	0.13
rad51	54	44	0.81
rad55	58	46	0.79
rad57	48	34	0.71

^aThe following strains (Table 1) used were: FF18984 (wild-type), WDHY1020 (rad9Δ), WDHY994 (rad51Δ), WDHY837 (rad55Δ), and WDHY839 (rad57Δ). The presence of the G₂ DNA damage checkpoint-induced cell cycle arrest was monitored as described in Materials and Methods using an established assay (89, 90). The ratio of percent arrested cells (microcolonies with either a large-budded cell or with two adjacent large-budded cells) to the percent of inviable cells provides a metric of the efficiency of cell cycle arrest. For wild-type cells this metric approaches 1.0 because essentially all cells with unrepairable DNA breaks die in the G₂ phase; haploid cells in the G₁ or postanaphase stages when irradiated cannot repair the DNA DSBs, arrest in the next G₂ phase, and die as large-budded and two adjacent large-budded cells, respectively. Wild-type cells that can repair DSBs (S and G₂ phase cells) form large microcolonies that are not counted. In contrast, checkpoint mutants cells that die after irradiation do not usually arrest immediately; rather, they continue to divide for a few generations. Therefore, in checkpoint mutants, the ratio of arrested cells to inviable cells is <<1.0 and typically is <0.3 (see reference 90).