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
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.