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Immune genes are under intense, pathogen-induced pressure, which causes these genes to diversify over evolutionary time and become species-specific. Through a forward genetic screen we recently described a  C .  elegans -specific gene called  pals-22  to be a repressor of “Intracellular Pathogen Response” or IPR genes. Here we describe  pals-25 , which, like  pals-22 , is a species-specific gene of unknown biochemical function. We identified  pals-25  in a screen for suppression of  pals-22  mutant phenotypes and found that mutations in  pals-25  suppress all known phenotypes caused by mutations in  pals-22 . These phenotypes include increased IPR gene expression, thermotolerance, and immunity against natural pathogens, including  Nematocida parisii  microsporidia and the Orsay virus. Mutations in  pals-25  also reverse the reduced lifespan and slowed growth of  pals-22  mutants. Transcriptome analysis indicates that  pals-22  and  pals-25  control expression of genes induced not only by natural pathogens of the intestine, but also by natural pathogens of the epidermis. Indeed, in an independent forward genetic screen we identified  pals-22  as a repressor and  pals-25  as an activator of epidermal defense gene expression. In summary, the species-specific  pals-22  and  pals-25  genes act as a switch to regulate a program of gene expression, growth, and defense against diverse natural pathogens in  C .  elegans .

Antagonistic paralogs control a switch between growth and pathogen resistance in C. elegans