Worm Breeder's Gazette 13(5): 22 (February 1, 1995)
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.
Department of MCD Biology, University of Colorado, Boulder
The gene let-60 ras plays a key role in a genetic pathway that specifies the vulva cell fate. Loss of function (lf) mutations of let-60 cause Vul (and therefore is egg laying defective), in which all of the VPCs take on the hyperdermal cell fate. Hyperactive mutations or gain of function (gf) of let-60 cause Muv, in which more than three VPCs are differentiated to become vulva cells. Ras is used to transmit cell growth signals in many organisms from yeast to human. Studying the role of let-60 ras pathway in C. elegans will help in understanding the Ras signal transduction pathway in other organisms. How the lef-60 ras pathway is negatively controlled is not well understood. For example, we don't know how the kinases downstream of let-60 ras are kept inactive. To isolate the negative regulators downstream of let-60 ras, we have screened and isolated suppressors that revert the Vul phenotype caused by a let-60 ras dominant-negative (dn) mutation. Seven different genes are identified from fourteen recessive extragenic suppressors. The preliminary mapping and complementation results of nine recessive extragenic suppressors are shown below The suppression of let-60 (dn) by ku105 is not allele specific since ku105 can suppress three different let-60 (dn) alleles: sy94, syl01,and syl00. ku105 homozygous suppress let-60(dn) better than ku105/Df, indicating that ku105 is possibly a recessive antimorph. Since previous genetic study suggests that the let-60 ras (dn) mutation decreases the pathway's activity (thus leading to the vulvaless phenotype), potential suppressors are expected to increase or restore the normal activity of the pathway.