The fungal pathogen Drechmeria coniospora infects C. elegans and elicits an innate immune response mediated, in part, by the induction of antimicrobial peptides in the epidermis. The signaling pathways controlling this phenomenon remain to be fully characterized. In this issue of Virulence, Couillault and colleagues use both proteomics and genetics to discover an unexpected role for the unfolded protein response (UPR) target chaperone BiP/GRP78/hsp-3 in the control of fungal infection-induced antimicrobial peptide expression in C. elegans. Although the expression of
hsp-3 is regulated by the UPR, Couillault and colleagues describe a novel signaling role for this BiP/GRP78 homolog.