In C. elegans two TGFb signaling mechanisms, the Sma/Mab and the dauer pathways, have been described. In the Sma/Mab pathway, the common type II serine/threonine kinase receptor, DAF-4, signals with the type I receptor, SMA-6, and its putative ligand, DBL-1. However, in the dauer pathway, DAF-4 functions with a different type I receptor, DAF-1, and ligand, DAF-7. These distinct receptor-ligand complexes can then transduce signals to the downstream effectors, the Smads, specific for that particular pathway. Mutations in any one of the components of the Sma/Mab pathway leads to small body size, male tail ray abnormalities and crumpled spicules. We have previously shown that the small genes are epistatic to the gene
lon-2, mutants of which are longer than wild type. Further analysis shows that
dbl-1 (see abstract by Suzuki et al.) is epistatic to
lon-2. To identify new members of the Sma/Mab pathway, we have undertaken a screen designed to suppress the
lon-2 mutation. We have screened 9,000 genomes and identified several mutations capable of suppressing the long phenotype to either that of wild type or small body size. Complementation tests show that we have identified several existing components of the pathway including alleles of
sma-2,
sma-3,
sma-4 (Smads),
sma-6 (type I receptor) and
dbl-1 (ligand). In addition, we have identified two mutations which may be allelic to
sma-10, previously identified in our lab (in an F2 screen for Smas) as a mutant that exhibits a small body size with male tail fusion patterns similar to those seen in other small mutants. The isolation of these two putative
sma-10 alleles from the
lon-2 suppressor screen support the involvement of
sma-10 in the small pathway. We are currently in the process of cloning
sma-10 to characterize its role in determining body size and patterning of the male tail.