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A Role for SKN-1/Nrf in Pathogen Resistance and Immunosenescence in Caenorhabditis elegans

Figure 3

The pathogen response-specific TIR-1 and p38 MAPK PMK-1 are required for SKN-1 activation upon P. aeruginosa infection.

(A) Representative epifluorescence microscopic images showing the expression of Pgcs-1::GFP in pmk-1(km25) mutants as well as in the p38 MAPK phosphatase vhp-1(RNAi), and the Toll/IL-1 resistance (TIR) domain protein tir-1(RNAi) animals in response to P. aeruginosa infection. L3 larvae were exposed to PA14 for 24 hours. Microscopic images are representatives from 3 independent experiments. (B) Quantification of reporter expression from data shown on panel (A) completed with data of control animals fed by OP50 for 24 h. (C) Quantification of SKN-1 nuclear translocation in tir-1(RNAi) L3 larvae upon 5 h PA14 exposure. Representative epifluorescence images of tir(RNAi) L3 larvae are shown in Figure S3. Please note that data in Figure 2B and 3C were derived from the same set of experiments. (D) Suggested model of SKN-1 activation during P. aeruginosa infection. Upon exposure to PA14, the TIR-1/PMK-1 pathway is indispensable but insufficient to elicit SKN-1 transactivation. We propose a second, unknown factor/pathway that is required to activate SKN-1. Whether the two pathways act in parallel or consecutively is unclear. Solid arrows indicate a direct, while dashed arrows indicate an indirect/unknown connection. EV: empty vector RNAi.

Figure 3

doi: https://doi.org/10.1371/journal.ppat.1002673.g003