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 (
n1046ku75 ),have a similar SM migration defect. The
let-60 (
n1046k48 )and
let-60 (
n1046ku75 )alleles were isolated in an ongoing screen for non-Muv revertants of
let-60 (
n1046gf). 64% of
let-60 (
n1046ku48 )homozygotes die as young larvae; 64% of the survivors are Egl (n=238). Only 2% of
let-60 (
n1046ku75 )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 (
sy94dn)/+.We are currently sequencing the
let-60 (
n1046ku48 )and
let-60 (
n1046ku75 )mutant alleles to identify their lesions. SM migration appears normal in
let-60 (
n1046gf)mutants. However, we have found that
let-60 (
n1046gf)can partially suppress the SM migration defect of
egl-17 (
e1313)animals. We did not see any effect of
let-60 (
n1046gf)on the SM migration defects of
egl-15 (
n484)or
sem-5 (
n1779)animals.