FIG. 6.

Model of checkpoint regulation of pathway competition in DNA repair. In wild-type cells, several pathways compete for the repair of DNA damage like a DSB (36, 61). In S. cerevisiae, the damage is preferentially repaired by recombinational repair, resulting primarily in gene conversions which are rarely (0 to 20%) associated with a crossing over (for a detailed discussion see reference 61 and references therein). This avoidance of crossing over may be related to the frequent nondisjunction observed for mitotic crossing-over products (11). Under genotoxic stress, Rad55p is essential for the recombinational repair pathway (36, 61). A defect in the checkpoint (mec1) fails to phosphorylate Rad55p in response to DNA damage, which we hypothesize will lead to decreased efficiency in Rad51p filament formation (see reference 79) and a less efficient recombinational repair pathway. Under these conditions, other pathways will contribute more noticeably. BIR results in a genetic outcome that resembles a crossing-over (7, 48, 55, 61). NHEJ will not lead to recombinants (36, 53, 61). Depicted is a diploid cell in G₁ with two homologues carrying three heterozygous markers (aA/bB/cC).