Figure 6 — WRN helicase defective in the premature aging disorder Werner syndrome genetically interacts with topoisomerase 3 and restores the top3 slow growth phenotype of sgs1 top3

Research Paper|Volume 1, Issue 2|pp. 219–233

WRN helicase defective in the premature aging disorder Werner syndrome genetically interacts with topoisomerase 3 and restores the top3 slow growth phenotype of sgs1 top3

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Figure 6.Effect of WRN expression on the MMS and HU sensitivity of sgs1 top3 strain. Logarithmically growing cultures of sgs1 top3 strain transformed with YEp112SpGAL, YEp112SpGAL-WRN, exonuclease-dead (YEp195SpGAL-WRN E84A), ATPase/helicase-dead (YEp195SpGAL-WRN K577M), RQC mutant (YEp195SpGAL-WRN K1016A), polymorphic mutant (YEp195SpGAL-WRN R834C), YEp112SpGAL-SGS1 and vector transformed wild type parental strains were spotted in a ten-fold serial dilutions onto SC-Trp plates containing glu or gal and either MMS or HU at the indicated concentrations. Plates were incubated at 30°C for 2 days (control plates) and 4 days (MMS and HU plates) and then photographed.