We have been analyzing an X-linked dominant suppressor of the semidominant allele
her-1(
n695)V, which causes incomplete masculinization of XX animals (Trent et al., 1983, Genetics 104:619). The suppressor, called
ct31, was isolated from the F1 progeny of gamma-ray mutagenized
n695 worms. Two- and three-factor mapping data show that
ct31 is closely linked to
unc-9 X. So far at least three phenotypes of
ct31 have been identified. First, this mutation dominantly suppresses the Tra and Egl phenotypes of
n695. Second,
ct31 homozygotes are Dpy.
ct31/+ heterozygotes are of variable length ranging from that of the homozygous Dpy to wild type.
ct31 males are short and have abnormal tail structures. Third, recent evidence suggests that
ct31 dominantly lowers X-chromosome expression in hermaphrodites but not in males. To investigate the effect of
ct31 on X-chromosome expression, strains were constructed that carry
ct31 and an X-linked hypomorph, lin- 15
(n765). Mutations in
lin-15 result in a Muv phenotype with one to six ventral protrusions (blips) (Ferguson and Horvitz, 1985, Genetics 110: 17). The penetrance of this allele varies at different temperatures as well as with the level of X- chromosome expression (P. Meneely, E. Ferguson, and W.B. Wood, manuscript in preparation). A mutation causing an increase in X- chromosome expression in a
lin-15(
n765) background will suppress the Muv phenotype (decrease the penetrance), while a mutation causing a decrease in X-chromosome expression will enhance the Muv phenotype ( increase the penetrance). The data in Table 1 show that
ct31 enhances the penetrance of the
lin-15(
n765) Muv phenotype in hermaphrodites but not in males. An increase in penetrance is also seen in
ct31/+;
n765 hermaphrodites. One interpretation of these data is that
ct31 lowers X-chromosome expression. Strains carrying
ct31 and other X linked hypomorphs will be constructed to test this interpretation. We have independently isolated two other X-linked
n695 suppressors, which result in phenotypes similar to those seen with
ct31. Since
ct31 males will not mate, complementation tests have not been done to ask if these three mutations are allelic. Over an eight-month period at least five strains carrying
ct31 and two strains carrying one of the other Dpy suppressors have spontaneously reverted to wild-type length. The
ct31 mutation could not be recovered from the
ct31 revertants, suggesting that they did not result from an extragenic event. The X chromosome from a revertant strain acted as a wild-type chromosome when made heterozygous with
ct31. Two of these revertants tested no longer suppressed her- 1
(n695) or affected the penetrance of
lin-15(
n765) at 16 C. An attempt to isolate EMS induced alleles of
ct31 was unsuccessful after screening 13,000 F1 progeny of
her-1(
n695). Since
ct31 was isolated after gamma-ray mutagenesis and spontaneously reverts to wild-type phenotype at a high frequency, it may be an unstable chromosomal rearrangement. The dominant
ct31 phenotype contrasts strikingly with the recessive phenotype resulting from egl- 16 (
n485) (Anne Villeneuve and Barbara Meyer, WBG, Vol. 9, no. 9).
ct31 has a feminizing effect and seems to lower X-chromosome expression while
egl-16(
n485) has a masculinizing effect and increases X-chromosome expression. Differences in map position rule out the possibility that the two mutations could be allelic (Anne Villeneuve and Barbara Meyer, personal communication). Therefore,
ct31 may represent one of several loci on the X chromosome involved in interpreting the X-chromosome-to-autosome ratio in the control of sex determination and dosage compensation. [See Figure 1]