Table 2.
Gross-chromosomal rearrangement rates and analysis of events in independent clones grown in the absence or presence of mitomycin C.
| Genotype | GCR rate*‡ | 95% confidence interval |
Telomere addition (clones analyzed) |
|---|---|---|---|
| WT | 1.0 ± 0.5† | 0.18–2.27 | 0% (10) † |
| WT + MMC | 5 ± 4 | 2.52–11.5 | N.D. |
| sgs1Δ | 16 ± 5† | 5.15–37.4 | 0% (15) † |
| sgs1-KA | 14 ± 3 | 13.1–40.1 | 46±14% (24) |
| hrq1Δ | 4 ± 2 | 3.19–12.6 | 77 ± 2.9% (26) |
| hrq1Δ + MMC | 115 ± 30 | 89.6–188 | N.D. |
| hrq1-KA | 5 ± 3 | 3.48–16.7 | 4.5 ± 3.9% (22) |
| hrq1-KA + MMC | 132 ± 42 | 46.5–246 | N.D. |
| pif1-m2 | 76 ± 8† | 36.4–125 | 93 ± 7.6% (56) † |
Gross-chromosomal rearrangement (GCR) rates are the average of ≥3 independent experiments and are normalized to the WT rate (1.5±0.7×10−10 events/generation). ± denotes standard deviation. + MMC denotes growth in media containing mitomycin C.
p-values were calculated for the GCR rates for all pairwise combinations of strains. All mutant rates are significantly different from WT (p=0.025, sgs1Δ; p=0.020, sgs1-KA; p=0.043, hrq1Δ; p=0.048, hrq1-KA; and p<0.00005, pif1-m2). All rates are significantly different from pif1-m2 (all p≤0.008). The hrq1Δ and hrq1-KA GCR rates are not significantly different from either the sgs1Δ or sgs1-KA rates (all p≥0.078). For telomere additions, the frequency in pif1-m2 cells was significantly different from all other strains (all p<0.030), and the frequencies between hrq1Δ and hrq1-KA were also significantly different (p=0.0002).
Data from (Paeschke et al., 2013), though it was collected at the same time as the other data.