Worm Breeder's Gazette 13(1): 77 (October 1, 1993)
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.
The sel-1 gene may participate in several different cell fate decisions mediated by lin-12 or glp-1 (Sundaram & Greenwald, Genetics, in press). Mutations in the sel-1 gene were found to suppress multiple lin-12 ( n676 n930 )associated defects, enhance lin-12 gain of function defects, and suppress the maternal effect lethal glp-1 allele e2142 .None of the alleles originally studied display phenotypes in a wild type background. We are continuing the characterization of the sel-1 gene by determining its null phenotype, molecular nature, and cellular focus.
Gene dosage studies indicated that existing sel-1 mutations are reduction or loss of function alleles (Sundaram & Greenwald, Genetics, in press). Since sel-1 alleles were originally identified by reverting the egg laying defect of a lin-12 hypomorph, sel-1 (0)alleles would not have been obtained if they caused an Egl, sterile, or lethal phenotype. We therefore performed a noncomplementation screen for sel-1 (0) alleles based on the observation that sel-1 /Dfsuppresses glp-1 ( e2142 )but sel-1 /+does not. Our preliminary analysis of 10,500 chromosomes screened after EMS mutagenesis indicates that we have isolated two new sel-1 alleles. Both new alleles suppress lin-12 and glp-1 ,and display no other obvious phenotype. This information combined with the gene dosage studies indicates that the sel-1 null phenotype is probably wild type.
We mapped sel-1 to a position between the cloned polymorphism arP5 and the cloned gene lin-25 (Tuck & Greenwald, WBG 12(5):49). This interval of about 200kb is completely covered by overlapping cosmid clones. We tested clones from this interval for sel-1 gene activity by two assays. First, we found that cosmids C06C11 and T17C2 complement the suppression of glp-1 ( e2142 )when coinjected with a dpy-20 (+)marker. Curiously, no complementation occurred with arrays formed with the rol-6 (d)marker. Second, we found that a 10kb HindIII subclone from C06C11 complements suppression of lin-12 ( n676 n930 )as well as suppression of glp-1 ( e2142 ).We are currently sequencing our smallest rescuing clone of 6.8kb, and isolating cDNAs derived from this region.