New genes that interact with lin-35 Rb to negatively regulate the let-60 ras pathway in Caenorhabditis elegans.
Previous studies have shown that a synthetic multivulva phenotype results from mutations in genes that antagonize the ras-mediated intercellular signaling system responsible for vulval induction in Caenorhabditis elegans. Synthetic multivulva mutations define two classes of genes, A and B, and a mutation in a gene of each class is required to produce the multivulva phenotype. The ectopic vulval tissue in multivulva animals is generated by vulval precursor cells that in the wild type do not generate vulval tissue. One of the class B synthetic multivulva genes, lin-35, encodes a protein similar to the retinoblastoma (Rb) protein. In this article, we describe the isolation and characterization of 50 synthetic multivulva mutations, the identification of new components of both the class A and class B lin-35 Rb pathways, and the cloning of lin-52, a class B gene that may have a conserved role in Rb-mediated signaling.
Department of Biology, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
Jeffrey H
JH
Thomas
Craig J
CJ
Ceol
Hillel T
HT
Schwartz
H Robert
HR
Horvitz
D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics* / Q000378:metabolism; D029742:Caenorhabditis elegans Proteins; D015536:Down-Regulation; D005786:Gene Expression Regulation; D009154:Mutation; D012097:Repressor Proteins / Q000235:genetics*; D018631:ras Proteins / Q000235:genetics*
D029742:Caenorhabditis elegans Proteins; D012097:Repressor Proteins; C116485:lin-35 protein, C elegans; C066646:let-60 protein, C elegans; D018631:ras Proteins