Worm Breeder's Gazette 13(1): 76 (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.
During the L2 stage in the hermaphrodite, the two sex myoblasts (SMs) migrate from the posterior to their final positions laterally flanking the center of the somatic gonad. Precise positioning of the SMs depends on a signal(s) from a subset of somatic gonad cells (Thomas, Stern and Horvitz 1990). In egl-15 , egl-17 ,or sem-5 mutants, the SM migrations terminate prematurely; therefore the final positions of the SMs are more posterior than normal (Stern and Horvitz 1991; Clark, Stern and Horvitz 1992). We have found that two let-60 mutants, let60 ( n1046 ku48 )and let-60 ( n1046 ku75 ),have a similar SM migration defect.
The let-60 ( n1046 k48 )and let-60 ( n1046 ku75 )alleles were isolated in an ongoing screen for non-Muv revertants of let-60 ( n1046 gf). 64% of let-60 ( n1046 ku48 )homozygotes die as young larvae; 64% of the survivors are Egl (n=238). Only 2% of let-60 ( n1046 ku75 )homozygotes die as larvae; 82% of the survivors are Egl (n=156). Both mutants have essentially wild-type vulval lineages, but the SMs are often displaced posteriorly. We believe that the SM migration defect is a loss-of-function phenotype because (l) the defect is fully recessive; (2) the defect is also seen in heterozygotes with a previously described let-60 (lf)allele; and (3) the defect is also seen (albeit more weakly) in animals of genotype let-60 ( sy94 dn)/+.We are currently sequencing the let-60 ( n1046 ku48 )and let-60 ( n1046 ku75 )mutant alleles to identify their lesions.
SM migration appears normal in let-60 ( n1046 gf)mutants. However, we have found that let-60 ( n1046 gf)can partially suppress the SM migration defect of egl-17 ( e1313 )animals. We did not see any effect of let-60 ( n1046 gf)on the SM migration defects of egl-15 ( n484 )or sem-5 ( n1779 )animals.