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.

Is sup-26 a Regulator of her-1?

J. Manser, C. Trent and W.B. Wood

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}