Worm Breeder's Gazette 13(3): 104 (June 1, 1994)
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 positions precisely flanking the center of the somatic gonad Several apparent let-60 loss-of-function mutations cause defects in SM migration. We have previously described two such alleles, let-60 ( n1046 ku48 )and let-60 ( n1046 ku75 ),which are intragenic revertants of let-60 ( n1046 gf)WBG 13(1)]. We sequenced these alleles and found that they contain identical or very similar lesions to those in the previously described loss-of-function alleles let-60 ( n2022 )and let-60 ( n2021 )[Beitel, Clark and Horvitz 1990]. In vulva development, n1046 gfcauses a Muv phenotype, n2022 or n2021 causes a partial Vul phenotype, while n1046 ku48 or n1046 ku75 is wild type (i.e. the gain of function and loss of function mutations mutually suppress each other). However, with respect to SM migration, both n2022 and n2021 homozygotes (like n1046 homozygotes), are wild-type. Therefore, the SM migration phenotype in our intragenic revertants must require the presence of both n1046 and either ku48 or ku75 in cis. A low penetrance SM migration defect also is seen when n1046 is placed in trans to either n2022 or n2021 .These complex genetic interactions between n1046 and other let-60 mutations raise questions as to the nature of the n1046 allele with respect to SM migration.
let-60 ( n1046 )also displays interesting genetic interactions with mutations in other genes affecting SM migration. Although let-60 ( n1046 )does not suppress the SM migration defects of either egl-15 ( n484 )or sem-5 ( n1779 ),it does partially suppress egl-17 ( e1313 )and egl-17 ( n1377 ). Iet-60 ( n1046 )also enhances the weak SM migration defect caused by mutations in lin-45 raf, sur-1 MAPK, or sur-3 .From these results, we think that the ras pathway normally plays some role in regulating SM migration, although the nature of that role is not yet clear.
We isolated two apparent gain-of-function mutations in sur-3 as semidominant suppressors of the let-60 ( n1046 gf)Muv phenotype. sur-3 ( ku68 )also enhances the Vul and/or Let phenotypes caused by weak alleles of let-60 and lin-45 ,but does not cause any vulval defects in a wild-type background. sur-3 ( ku68 )causes a weak posterior displacement (or possibly randomization) of SM positions. Double mutants between sur-3 ( ku68 )and either egl-15 ( n484 )or egl-17 ( n1377 )have strongly randomized SM positions, similar to what is seen when the gonad is ablated in egl-15 or egl-17 mutants [Stern and Horvitz, 1991]. Gonad ablation experiments in sur-3 , let-60 and various double mutant animals may help to clarify the roles of these genes in regulating SM migration.
We are currently screening for sur-3 loss-of-function mutations. We have also cloned the sur-3 gene by transformation rescue in order to begin a molecular characterization of sur-3 .
Stern, M. J. and Horvitz, H. R. (1990). Development 113, 797-803.