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}