We are interested in understanding how a complex organ of the correct size, shape, and function is generated. To address this, we are studying formation of the C. elegans gonad. We have identified the
sys-1 gene that is required for hermaphrodite gonad development, but is not essential for male gonad development. Hermaphrodites that are homozygous for
sys-1(
q544) , a putative null allele, exhibit two interesting defects. First, they lack distal tip cells, and the cells that normally make distal tip cells can generate extra anchor cells (Miskowski et al., 2001). This phenotype is similar to that described for mutants in the Frizzled homolog,
lin-17 . (Sternberg and Horvitz, 1988). Second, they fail to form the somatic gonadal primordium during late L2, which rearranges cells into a prepattern of the adult organ. To gain insight into the mechanism by which
sys-1 acts, we have pursued cloning of the
sys-1 gene. The
sys-1 locus was mapped near
fog-3 on LGI by three-factor mapping and deficiency analysis. In that region, a gene was identified that rescues the
sys-1 mutant phenotype and mimics the
sys-1(
q544) defect by RNAi. This gene encodes a novel, cytoplasmic protein. A putative C. briggsae homolog of this gene has been identified; it is over 50% identical to its C. elegans counterpart at the amino acid level. We are currently investigating the function of the C. briggsae gene by RNAi. Using the sequence similarity between C. briggsae and C. elegans , we are deleting the most conserved regions from the C. elegans gene and testing the activity of these reconstructed genes by transformation rescue. We hope that this analysis will help elucidate the function of this novel protein. Miskowski, J.A. et al. (2001) Dev Biol 230: 61-73. Sternberg, P.W. and Horvitz, H.R. (1988) Dev Biol 130: 67-73.