Multiple signalling pathways are involved in the response of C. elegans to infection by the fungus Drechmeria coniospora. They include the
p38 MAPK and DAF-2 pathways, as well as a non-canonical TGF-beta pathway. They all modulate the expression of genes encoding antimicrobial peptides such as NLP-29. Transgenic worms carrying a reporter construct with GFP under the control of the
nlp-29 promoter show an increased fluorescence following Drechmeria infection, but also upon injury and under conditions of osmotic stress (see abstracts by Pujol et al., Zugasti et al.). In a screen for nipi (no induction of peptide after Drechmeria infection) mutants that did not show any expression of GFP upon infection (Pujol et al., Ziegler et al.), we also identified mutants with an unusually high level of constitutive GFP expression (peni=peptide expression no infection). Seven mutants (
fr7-
fr13) of this class were obtained from an EMS screen of 10,000 F1 worms. They presumably correspond to loss of function mutations in negative regulators or gain of function mutations in positive regulators. Despite the high constitutive level of
pnlp-29::gfp expression, infection does induce a further increase in fluorescence as measured by the UBI Biosort. We used a pgpdh-1::gfp reporter, kindly provided by Todd Lamitina, to assay for an osmotic stress response and
pcnc-2::gfp that is induced only by infection (see Zugasti et al.), to establish whether the different mutants affected an infection-specific pathway. Whereas two of the mutants (
fr10 and
fr13) also showed an increased expression of pgpdh-1::gfp and can therefore be assigned to part of the osmotic stress response, one mutant (
fr8) exhibited an high level of
pcnc-2::gfp expression and is therefore a candidate for a gene involved in an anti-fungal innate immunity pathway. Progress towards identifying this mutant will be presented.