Figure 4

Molecular validation of weak gene interactions. (A) Ranking of interaction strength shows the distribution of phenotypic influence of deletion mutants. Some physiologically relevant hits (for example, UBC7/QRI8) fell below our clustering thresholds of >10 or <-16 (blue and green shading, respectively); the related components, CUE1 and RPN4, were on the cusp of our threshold but were still functionally relevant. (B) The cue1-Δ0 and rpn4-Δ0 strains showed deletion suppressor phenotypes specific for yor1-ΔF (at right), since the single mutant (that is, in the context of wild-type Yor1) did not affect oligomycin resistance. (C) By pulse-chase analysis, Yor1-ΔF turnover was reduced in the cue1-Δ0 and rpn4-Δ0 backgrounds relative to the wild-type background. Maturation of a control protein, Gas1, was unaffected. (D) Quantification of three replicates of the experiment shown in Figure 2B; error bars represent standard deviation.