TABLE 2.
Inactivation ofRAD1 and/orRAD10 genes reduces GCR formation in different GCR mutator strains
| Wild type
|
rad1Δ
|
rad10Δ
|
||||
|---|---|---|---|---|---|---|
| Relevant genotype | Strain | Mutation rate | Strain | Mutation rate | Strain | Mutation rate |
| Wild type | RDKY3615 | 3.5 × 10−10 (1) | YKJM1397 | 1.9 × 10−10 (0.5) | YKJM1433 | 1.0 × 10−10 (0.3) |
| pif1-m2 | RDKY4343 | 6.3 × 10−8 (180) | YKJM1399 | 5.2 × 10−8 (149) | YKJM1435 | 5.6 × 10−8 (160) |
| mec1Δ | RDKY3735 | 6.4 × 10−8 (183) | YKJM1684 | 5.4 × 10−9 (15) | YKJM1722 | 2.0 × 10−8 (56) |
| rad5Δ | YKJM1385 | 4.5 × 10−8 (127) | YKJM1709 | 5.3 × 10−9 (15) | YKJM1755 | 2.2 × 10−8 (61) |
| rad18Δ | YKJM1389 | 3.6 × 10−8 (103) | YKJM1897 | 5.2 × 10−9 (15) | YKJM1899 | 6.7 × 10−9 (19) |
| elg1Δ | YKJM1405 | 1.7 × 10−8 (49) | YKJM1724 | <1.1 × 10−9 (3) | YKJM1726 | 1.5 × 10−9 (4) |
| mre11Δ | RDKY3633 | 2.2 × 10−7 (629) | YKJM1686 | 3.9 × 10−8 (111) | YKJM1692 | 6.0 × 10−8 (171) |
| rad52Δ | RDKY4421 | 4.4 × 10−8 (126) | YKJM1713 | 2.4 × 10−9 (7) | NDa | |
| rfa1-t33 | RDKY3617 | 4.7 × 10−7 (1343) | YKJM1698 | 7.4 × 10−9 (21) | YKJM1700 | 5.1 × 10−9 (15) |
| cac1Δ | RDKY4753 | 1.2 × 10−7 (343) | YKJM1688 | <7.7 × 10−10 (2) | YKJM1694 | 4.3 × 10−10 (1) |
| mus81Δ | YKJM219 | 3.8 × 10−8 (109) | YKJM2345 | 4.6 × 10−9 (13) | YKJM2347 | 2.1 × 10−9 (6) |
| mms4Δ | YKJM1525 | 5.9 × 10−8 (169) | YKJM2341 | 1.5 × 10−9 (4) | YKJM2343 | 2.3 × 10−9 (6) |
| rad27Δ | RDKY3630 | 5.0 × 10−7 (1429) | YKJM1707 | 1.7 × 10−7 (471) | YKJM1696 | 2.9 × 10−7 (814) |
All strains are isogenic to the wild-type strain, RDKY3615 [ura3-52 leu2Δ1 trp1Δ63 his3Δ200 lys2ΔBgl hom3-10 ade2Δ1 ade8 YEL069::URA3], with the exception of the indicated mutations. The numbers in parentheses indicate the fold induction of GCR relative to wild type. The GCR rate of the rad1Δ rad10Δ (YKJM1833) strain was <4.1 × 10−10.
Not determined. The pif1-m2 mutation inactivates only the nuclear form of Pif1, since only the second methionine codon for the translation start of the nuclear form of Pif1 is mutated while the first methionine codon for the translation start of the mitochondrial form of Pif1 is intact. Mutation rates are CanR-5-FOAR per generation.