Innate immunity in the nematode worm Caenorhabditis elegans involves two genes: PMK-1 and DAF-16, which is up-regulated by the insulin/insulin-like growth factor tyrosine kinase DAF-2. Worms carrying loss-of-function mutations in pmk-1 are more sensitive to pathogens, whereas daf-2 null mutants are more resistant. Troemel et al. have shown that the pathogen resistance observed in daf-2 mutants requires a functional PMK-1 gene and that PMK-1 works either downstream or in parallel with DAF-2. However, the downstream targets of the two genes do not overlap. Detailed analyses of pathogen resistance suggest that PMK-1, unlike DAF-16, is specific to the immune response required for pathogen response, whereas the DAF-2 DAF-16 pathway appears to play a less precise role in immunity. Thus, at least two separate pathways contribute to innate immunity in C. elegans. -- LMZ
PloS Genet. 2, 10.1371/journal.pgen.0020183.eor (2006).
