Skip to main content
. 2010 Aug 26;6(8):e1001075. doi: 10.1371/journal.ppat.1001075

Figure 7. Genetic interactions between swan-1 and mbk-1/DYRK to regulate Pnhr-57::GFP expression and resistance to P. aeruginosa fast killing.

Figure 7

A, B. Bacterially mediated RNAi was used to decrease expression of individual DYRK homologs in C. elegans, and the effects on Pnhr-57::GFP expression was determined by protein blots. The bars show mean values from 3 replicate experiments; error bars represent standard errors. ** p<0.01. A. In swan-1(ok267), vhl-1(ok161) double mutants, mbk-1 RNAi significantly decreased expression of the reporter, but RNAi for the other DYRK homologs did not change Pnhr-57::GFP levels relative to the empty vector control. B. In egl-9(sa307) animals, RNAi for the DYRK homologs tested had no effect on Pnhr-57::GFP. C, D. The mbk-1(pk1389) deletion mutation suppressed Pnhr-57::GFP expression in swan-1(ok267), vhl-1(ok161) double mutant animals (C) and in swan-1(ok267) animals expressing stabilized HIF-1(P621G) protein (D). E, F. The mbk-1(pk1389) mutation suppressed resistance to P. aeruginosa PAO1 in swan-1(ok267) animals. In these experiments, HIF-1 protein was stabilized by either the vhl-1(ok161) loss-of-function mutation (E) or the HIF-1(P621) stabilizing mutation (F). Each experiment was repeated at least three times with 30–50 animals for each strain. The error bars represent standard errors. *: p<0.05; **: p<0.01. These data are presented in tabular format in Text S1.