Worm Breeder's Gazette 9(3): 52
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.
We are continuing to study two loci, sup-26 III and sup-27 V, both of which are defined by semidominant EMS-induced mutations that suppress the Tra and Egl phenotypes resulting from the semidominant allele her- l(n695) (see WBG, Vol. 9, No. 1, p. 70 and Vol. 9, No. 2, p. 97). Neither sup-26 (n1091 or ct49) nor sup-27 (n1092 or n1102) mutations alone appear to affect XX or XO animals. In addition, these mutations do not appear to suppress the Tra phenotypes resulting from the null (O) mutations in either tra-1(e1099) or tra-2(e1095) XX animals, suggesting that the sup mutations suppress the effects of her- l(n695) by acting upstream of tra-2 in the regulatory pathway of sex- determining genes. Here we report further results bearing on the action of sup-26 III. Using a weak allele of tra-2 [n1106, which we will refer to as tra-2(w)], Villeneuve and Meyer (WBG, Vol. 9, No. 1, p. 78) have presented evidence that an egl-16 mutation leads to a decrease in tra-2 expression. They showed that tra-2(w);egl-16(n485) XX animals are sterile or visibly sexually transformed, while both single mutant XX strains are fertile Egl hermaphrodites (see Table below). However this enhancement of tra-2(w) by egl-16(n485) is eliminated by the presence of a her-l(O) mutation (e1520); a tra-2(w); her-1(0);egl-16(n485) XX strain is a fertile Egl hermaphrodite. This result indicates that the egl-16 effect on tra-2(w) in the double mutant requires a functional her-l gene, and therefore suggests that egl-16 regulates her-l: the egl-16 defect causes inappropriately high her-l expression, which in turn represses tra-2. We have obtained comparable evidence regarding the effects of sup- 26 mutations. First, we have shown that sup-26(n1091) also eliminates the enhancement of the tra-2(w) phenotype by egl-16(n485); a tra-2(w);sup- 26(n1091);egl- 16(n485) XX strain is a fertile Egl hermaphrodite. This result indicates that the sup-26 mutation can suppress the effect of inappropriate her-l expression not only in strains carrying her-l(n695) , but also in a strain carrying the her-l(+) allele. Second, a sup-26 mutation efficiently suppresses the Egl phenotype resulting from tra-2( w) in tra-2(w);sup-26 XX animals, although it has no apparent effect on the Tra phenotype of tra-2(0) XX animals (see Table below). [A sup- 26 mutation does not affect the phenotype resulting from an egl-16 mutation; sup-26(n1091);egl-16(n485) XX animals are Egl hermaphrodites, a phenotype similar to that observed by Villeneuve and Meyer for her- l(O);egl-16(n485) XX animals (WBG Vol. 9, No. 1, p. 78)]. The two instances of suppression above can be explained by increased tra-2 activity resulting from the sup-26 mutation. This increase could be caused either by repression of her-l activity, or by a direct effect on tra-2. Consistent with (but not proof of) the effect being on her-l is an additional finding, that the her-l(O) mutation also suppresses the Egl phenotype resulting from tra-2(w) in tra-2(w);her- 1(0) XX animals, although the suppression is not as strong as that seen in tra- 2(w);sup-26(n1091) XX animals. Possibly arguing against the effect being on her-l is the fact that the sup-26 effects are observed in XX animals, where the her-l(+) gene has often been assumed to be 'off'. However, there is no strong evidence for this assumption. Our results can be explained if the her-l gene is partially 'on' in her- l(n695) XX animals, slightly 'on' in her-l(+) XX animals, and 'off' in sup-26(n1091);her-1(n695) and sup-26(n1091);her-1(+) XX animals. According to this interpretation, the sup-26 mutations act by repressing her-l activity, consistent with a role for sup-26 as a regulator of her-l in XX animals. {Figure 1}