Worm Breeder's Gazette 15(1): 52 (October 1, 1997)
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.
|1||Dept. of Biology, Queens College, CUNY, Flushing, NY 11367.|
|2||Waksman Institute, Rutgers University, Piscataway, NJ 08855.|
We are interested in identifying new components of the TGFb pathway. Analysis of the sma-2, sma-3, and sma-4 genes revealed that they are Smads, which appear to be the primary TGFb signal transducers. They share mutant phenotypes with a subset of phenotypes exhibited by mutations in daf-4. Interestingly, daf-4 is involved in sending two signals, the dauer signal, and the Small/Mab signal. Each of these pathways utilizes a unique set of Smads. Our primary approach has been a series of genetic screens for mutations that are similar to mutations in daf-4, a TGF type II receptor. Since four genes in the Small/Mab pathway mutate to a small body size, we have hypothesized that other genes in the pathway might mutate to similar phenotypes. We have screened 17,000 genomes for additional Small mutants. Most mutants are now mapped and complemented. In this screen, we expected to find a ligand and a type I receptor for the Small/Mab pathway, since these components were not identified when the search began. Three alleles of sma-6 have been obtained in this screen, which we previously identified as a new type I receptor in this pathway. We have also generated an allele of dbl-1, a ligand for the Small/Mab pathway (see abstracts by Y. Suzuki and B. Wood). Of the remaining Sma mutants, there are five loci which are of continued interest, because of their classical Sma phenotype and the presence of multiple alleles. Two non-allelic loci from this group also have fusions of tail rays, in patterns similar to mutations of other small loci. The genes corresponding to these loci are being cloned and further characterized.