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. 2008 Nov 13;3(11):e3717. doi: 10.1371/journal.pone.0003717

Figure 3. Epistasis analysis of ANC1 with PRR pathway members.

Figure 3

A. Genetic relationships within the PRR pathway in yeast. Epistasis was determined by sensitivity of mutants to damaging agents. srs2Δ only suppresses the damage sensitivity of rad5Δ, ubc13Δ and mms2Δ mutants (modified from Ulrich, 2006). Survival after chronic MMS treatment for: B. WT (▪), anc1Δ (▴), srs2Δ (▾), srs2anc1Δ (♦), C. WT (▪), anc1Δ (▴), mms2Δ (▾), mms2anc1Δ (♦) D. WT (▪), anc1Δ (▴), ubc13Δ (▾), ubc13anc1Δ (♦), E. WT (▪), anc1Δ (▴), rev3Δ (▾), rev3anc1Δ (♦) F. WT (▪), anc1Δ (▴), rad30Δ (▾), rad30anc1Δ (♦). We made several attempts to create a rad18anc1Δ strain for epistasis analysis, but were unable to produce the double mutant by either mating or recombination, even in the presence of a covering plasmid bearing an intact RAD18. Log-phase cells were diluted and plated on freshly poured MMS-containing YPD-agar plates or onto control plates with no MMS. Colonies were allowed to grow at 30°C for 2–5 days before counting. Results are average of at least 2 replicates, error bars = SD, except in F.; gradient plate replica for F. in Figure S2. We were unable to create a rad18anc1Δ double mutant by either mating or transformation, even with Rad18 expressed from a covering plasmid during transformation.