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.