Figure EV2. Disruption of genes involved in the p38‐mediated innate immune signaling pathway abolishes the extended longevity of long‐lived mitochondrial mutants independently of bacterial proliferation.

Quantification of nuo‐6 and isp‐1 lifespan on non‐proliferating bacteria revealed that their long lifespan is independent of bacterial proliferation. Similarly, lifespan extension in nuo‐6 and isp‐1 mutants is completely dependent on having a function p38‐mediated innate immune signaling pathways as deletion of nsy‐1, sek‐1, or atf‐7(gof) completely prevented the increase in lifespan in long‐lived nuo‐6 and isp‐1 mutants. Lifespans were performed in liquid culture with worms fed ad libitum. Bacteria proliferation was prevented through treatment with cold and antibiotics. All strains were tested in a single parallel experiment. Two biological replicates per strain were measured with a total of at least 274 animals per strain.

Data information: Statistical significance for survival plots was determined with the log‐rank test. P‐value indicates significance of difference between blue and purple lines. Control strains are shown in multiple panels for direct comparison.

Source data are available online for this figure.