The male tail of C. elegans is a specialised structure consisting of a cuticular fan in which are embedded 18 symmetrically placed mechanosensory sensilla called rays, which each have distinct characteristics due to their morphology, position and neurotransmitter usage. The
mab-2 mutation causes loss of both the V and T cell derived rays1. We have found this mutation to be allelic with a
rnt-1 knockout and to be rescued by the cosmid B0414 which contains
rnt-1. We will further analyse the ray phenotype by lineage analysis using suitable markers. In addition, mutations appear to be temperature sensitive for sterility and an intestinal mitotic defect. It is interesting that a
rnt-1::gfp reporter construct has been shown previously to be expressed in the intestine as well as seam cells2 so lending support to the hypothesis that both the ray loss and intestinal phenotypes may be caused by mutation of
rnt-1.Initial attempts at cloning
mab-2 involved screening genes mapping to the same region by feeding RNAi (Chromosome I feeding library was a gift from J. Ahringer). As a result of the screen two genes which phenocopied
mab-2 mutants were identified. In light of our subsequent identification of
mab-2, it is interesting to find that 3 genes giving a virtually identical ray loss phenotype are located within a 0.21 cM region of LGI.The two novel Mab genes are situated in a putative operon and so are presumably co-regulated. Do worm operons represent functional cassettes of genes as in bacteria? The common RNAi phenotypes of these two co-regulated genes imply interesting co-functionality. Further support for their co-functionality is provided by the fact that homologues of these two genes plus another in the operon are involved in rRNA processing in yeast. In addition, orthologues of one of these Mab genes and another gene in the operon are thought to modulate the Notch signalling pathway in mammals. We are in the process of investigating the possibility that these functions are conserved in C. elegans.References: 1) Hodgkin, J. Genetics (1983) 103: 43-64; 2) Nam S, Jin YH, Li QL, Lee KY, Jeong GB, Ito Y, Lee J, Bae SC. Mol Cell Biol. (2002) 22(2):547-54.