Worm Breeder's Gazette 15(2): 48 (February 1, 1998)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
Waksman Institute, Rutgers University, 190 Frelinghuysen Road, Piscataway, NJ 08854-8020
In C. elegans, two well described TGFb signaling mechanisms, the Sma/Mab and the dauer pathways, have been described. Both pathways share a common type II serine-threonine kinase receptor, DAF-4, which transmits each TGFb signal by associating with different type I receptors, SMA-6 or DAF-1. These distinct receptor complexes can then transduce signals sent by the ligand 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.Previously, we have identified several novel mutants from a screen done in our lab based on small body size. This analysis reveals five new loci - sma-9, sma-10, sma-11, sma-12 and sma-13. All of them are phenotypically small, similar to sma-2, -3, -4, -6 and daf-4 mutants, and complement these existing TGFb signaling components. We are focusing on sma-10 because male tail fusion patterns are similar to those seen in other small mutants. Interestingly, sma-9 has a similar mutant phenotype (C. Savage-Dunn, personal communication). These two genes may represent general TGFb signaling components or regulators. We are currently in the process of cloning sma-10 to identify its role in TGFb signaling.