Figure 3. Disruption of the p38‐mediated innate immune signaling pathway markedly ablates extended longevity of long‐lived mitochondrial mutants.

• A–H
  To examine the role of the p38‐mediated innate immune signaling pathway in the long lifespan of the nuo‐6 and isp‐1 mitochondrial mutants, we crossed the long‐lived mitochondrial mutants to worms with mutations in nsy‐1, sek‐1, pmk‐1, and atf‐7(gof). In each case, mutation of genes involved in p38‐mediated innate immunity signaling markedly reduces the lifespan of the long‐lived mitochondrial mutant but has little or no impact on wild‐type lifespan. In panel G, we utilized pmk‐1 RNAi instead of the pmk‐1 mutation because of the close proximity of isp‐1 and pmk‐1 on the same chromosome. EV indicates empty vector. The lifespan results for panels A, B, D, E, F, and H were performed in a single parallel experiment. Results are from a minimum of three biological replicates per strain.

Data information: Statistical significance for survival plots was determined with the log‐rank test. P‐values indicate significance between red and purple lines. Control strains are shown in multiple panels for direct comparison.

Source data are available online for this figure.