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. 2016 Jan 27;6(3):541–549. doi: 10.1534/g3.115.025650

Figure 4.

Figure 4

Endogenous hyperactivation of p38 MAPK innate immune responses protects nematodes from bacterial infection and delays the development of wild-type nematodes. In both (A) and (B), wild-type animals were grown on RNAi bacteria expressing the empty vector L4440 (Wild-type), or a construct designed to knockdown nsy-1 [nsy-1(RNAi)]. nsy-1(ums8) animals, were grown in parallel on RNAi bacteria expressing the empty vector L4440 [nsy-1(ums8)], or a construct designed to knockdown nsy-1 [nsy-1(ums8) + nsy-1(RNAi)]. (A) P. aeruginosa pathogenesis assays were performed on RNAi-treated animals of the indicated genotypes. The difference in P. aeruginosa susceptibility between wild-type and nsy-1(ums8) animals is significant, as is the survival difference between nsy-1(ums8) and nsy-1(ums8) + nsy-1(RNAi) (P < 0.001). Data are representative of two biological replicates. The sample sizes for this experiment are: wild-type (115), nsy-1(RNAi) (122), nsy-1(ums8) (111), and nsy-1(ums8) + nsy-1(RNAi) (133) (B) The development of RNAi-treated animals of the indicated genotypes to the L4 larval stage or older was recorded. The data are the average of three plates, with error bars showing the standard deviation between plates. The sample sizes for this experiment are: wild-type + L4440 (1,200), wild-type + nsy-1(RNAi) (1179), nsy-1(ums8) + L4440 (956), and nsy-1(ums8) + nsy-1(RNAi) (1010). Data are representative of two biological replicates. * P < 0.001.