Figure 2.

Factors affecting the suppression and promotion of chromosomal translocations between short segments of homology in CAN1, LYP1 and ALP1 in cells lacking Sgs1. In the absence of Sgs1, translocations between CAN1, LYP1 and ALP1 (referred to as C/L/A) are independently suppressed by the checkpoint components Mec3 and Tel1 (shown in red font), as suggested by the synergistic increases in the GCR rate and the C/L/A translocation rate of the sgs1Δ mutant upon deletion of MEC3 (sgs1Δ mec3Δ) and subsequently TEL1 (sgs1Δ mec3Δ tel1Δ). If Mec3 is absent (sgs1Δ mec3Δ), C/L/A translocations form through a pathway that requires Mec1, Dun1 and homologous recombination (HR) factors (shown in green font), especially Rad52 and Rad59. Mec1 most likely promotes translocations by inhibiting de novo telomere additions by regulating Pif1 and Cdc13. In addition to mutagenic repair that leads to C/L/A translocations, other types of mutagenic repair (e.g., translocations between other genes, de novo telomere additions, deletions, insertions, inversions) and most likely also nonmutagenic repair products are formed. If, in addition to Mec3, Tel1 is also absent (e.g., sgs1Δ mec3Δ tel1Δ), an even greater number of DNA lesions are channeled through the Mec1-dependent, C/L/A-promoting pathway. In contrast to dun1Δ, the chk1Δ mutation does not lead to a significant GCR rate increase in the sgs1Δ mec3Δ mutant and does not inhibit C/L/A translocation formation. Possibly, the inability to regulate cell cycle progression in the absence of Chk1 leads to increased formation of inviable GCRs. Dotted lines indicate events that occur in the absence of the protein from which the arrow originates; full lines indicate events that occur in the presence of the protein.