PTR-15 is one of 24 C. elegans proteins with homology to the Hedgehog receptor Patched. PTC and PTR proteins carry both sterol-sensing and RND domains; previous work (Zugasti et al. 2005) showed that several of the PTR proteins are involved in molting. However, RNAi knockdown of
ptr-15 revealed no obvious defect. Whole Genome Sequencing has now revealed that a mutation in a pathogen-sensitivity gene,
bus-13 (
e2710), is a missense alteration in
ptr-15. The
bus-13 mutant was isolated by virtue of its resistance to the surface pathogen Microbacterium nematophilum.
bus-13 mutants also show variable alterations in staining with multiple fluorescent lectins (Gravato-Nobre et al. 2005). Response of
bus-13 to other surface pathogens is unusual. Most bus mutants are killed by either of two complementary Leucobacter strains (Verde1 and Verde2), but not both. In contrast,
bus-13 mutants are rapidly killed by both. The lethal sensitivity to Verde1 provides an excellent assay for
ptr-15 activity: a transgene expressing
ptr-15(+) allows
bus-13 mutants to grow well in the presence of Verde1, confirming that
bus-13 is the same as
ptr-15. Many genes affecting the cuticle surface display seam-cell expression (Gravato-Nobre et al. 2011). Surprisingly, the intestine and pharynx, and not the seam cells, are the main sites of expression of a
ptr-15p::
ptr-15::rfp operon rescuing construct. A C-terminal translational fusion construct also exhibited some gut expression, but failed to rescue. Further translational constructs are in progress. Also surprisingly, selection for mutations that allow
bus-13 to grow on Verde1 failed to yield mutations in any of the known and expected Verde1-resistance loci (~ 8 genes); instead, an apparent intragenic partial revertant of
bus-13 was obtained. Similarly, selection for mutations that would allow
bus-13 to grow on Verde2 did not yield many mutations in the expected Verde-2 resistance loci (~ 20 genes). These observations suggest that the pathogen-susceptibility of the
ptr-15/bus-13 mutant is unusual and distinct from that of most other surface-affecting genes.