However, in agreement with studies in human WS cells [45], wrn DT40 do not exhibit elevated spontaneous SCE or an exaggerated SCE response following exposure to NQO and the wrn/rad18 double mutant behaves the same as the rad18 single mutant within the sensitivity limit of this assay (Fig. 2B).
Likewise, the BCL9 mutants behaved the same as in the TOPFLASH assays (Fig. 2E), with L366K and L366K ΔHD1 displaying clear DN effects (Fig. 3B).
Eventually, 38 mutant strains recorded higher antibiotic MIC values than that of the wild-type (Additional file 2), confirming the phenotype of nourseothricin resistance, whereas all the other mutants behaved the same as the wild-type strain.
These data are now shown in Figure 2 figure supplement 1, which shows that the different mutants behave the same.
The SsrADD mutant behaved like the wild type strain during exposure to chloramphenicol, amoxicillin and paraquat (Fig. 6).
Figure 6D shows that slx4Δ cells reproducibly showed slightly more sensitivity than wild-type cells in the higher UV dose range, and that the saw1Δ slx4Δ double mutant behaved like the saw1Δ single mutant.
Again, the kinase-deficient HIPK1D315N mutant behaved like the wild type protein.
Interestingly, we found that the ΔNp63 α-K193E mutant behaved as the wild-type ΔNp63 α protein on both promoters (Fig. 5C), suggesting that the K193E mutation selectively alters ΔNp63 α transcriptional activity.
The double Δ pkaA Δ snfA deletion mutant behaved like the wild-type strain, secreting a similar amount of cellulases in the presence of avicel as the sole carbon source.
Most likely, the suppression is mediated through the loss of the Hos2 HDAC as the deletion of hos2 in the S2A mutant behaved similarly to the S5A mutant.
