Figure 5. DAF‐16/FOXO is required for increased resistance to bacterial pathogens in long‐lived mitochondrial mutants.

• A
  A deletion of daf‐16 completely abolishes the increased resistance to bacterial pathogens in isp‐1 mutants. P‐value indicates the significance of difference between red and purple lines. Three biological replicates per strain were performed.
• B, C
  While daf‐16 RNAi effectively decreases the expression of DAF‐16 target genes (B, sod‐3, dod‐3, mtl‐1, ftn‐1, icl‐1, sodh‐1), it does not affect the expression of any of the innate immunity genes (C, T24B8.5, K08D8.5, F55G11.8, clec‐65, clec‐67, dod‐22, Y9C9A.8, and C32H11.4). This indicates that DAF‐16 is not required for expression of innate immune signaling pathway target genes in isp‐1 mutants. daf‐16 expression was knocked down using RNAi beginning at the L4 stage of the parental generation. RNA was isolated from six biological replicates at the young adult stage of the experimental generation. RNA from the six biological replicates was pooled for RNA sequencing.

Data information: Statistical significance in panel A was assessed using log‐rank test.

Source data are available online for this figure.