Mutations in
dpy-21,
dpy-27, and
dpy-28 cause XX animals to be dumpy and/or inviable, while XO animals remain essentially unaffected. It has been demonstrated that these mutations result in the over-expression of X-linked genes in XX animals (Meyer and Casson Cell 47:871 1986, Meneely and Wood Genetics 117:25 1987, DeLong, Casson and Meyer Genetics 117:657 1987). Recently we have discovered a powerful screen for the isolation of mutations in genes, such as
dpy-21,
dpy-27, and
dpy-28, that are involved in the execution of the hermaphrodite mode of dosage compensation. Mutations in
xol-1 cause the aberrant invocation of the hermaphrodite mode of dosage compensation in XO animals; the resulting under-expression of the single X chromosome in these animals causes them to die as embryos (see L. Miller, WBG
v10 n1; L Miller, this WGB) . Mutations which disrupt the hermaphrodite mode of dosage compensation result in the rescue of
xol-1 XO animals. By reverting the
xol-1 XO lethality we isolated mutations in a number of genes that are required for the proper execution of the hermaphrodite mode of dosage compensation. Among the many suppressors isolated were 14 new alleles of
dpy-21 (3 of which are suppressible by
sup-7(
st5), and another 2 of which were isolated in a mutator strain), 1 new allele of
dpy26, and 5 new alleles of
dpy-27 (1 of which is suppressible by sup- 7
(st5)). In addition, we isolated a single allele of a new gene, dpy- 29, which maps to the
unc-61 of LG V. Homozygous
dpy-29(
y100) XX progeny of heterozygous mothers are dumpy; homozygous progeny of homozygous mothers are inviable, with rare dumpy escapers. This lethality is cold sensitive: at 20 C the viability of XX animals in homozygous
dpy-29(
y100) strains is 3.4%; at 15 C it is 0.6%. XO animals appear unaffected. By the
lin-14 assay, we have shown that
dpy-29(
y100) suppresses the
lin-14 phenotype in XX animals to a degree equivalent to that seen with
dpy-21,
dpy-27, or
dpy-28 mutations. In
dpy-29 this suppression is seen in the homozygous progeny of heterozygous mothers. No suppression is seen in
dpy-29 XO animals. Thus
dpy-29(
y100) results in sex-specific over-expression of X-linked genes. The phenotypes of
dpy-29 are essentially identical with those seen in dpy- 27, in that
dpy-29(
y100) does not promote X-chromosome nondisjunction as do mutations in
dpy-26 and
dpy-28. We have previously constructed
dpy-27;
dpy-28;
dpy-28 double mutant animals, and shown that these animals are about as viable as the single mutants. Preliminary results from the construction of
dpy-27;
dpy-29 suggest that these animals are also about as viable as the single mutant. We interpret this to mean that
dpy-29, as well as
dpy-26, involved in a common process, which we believe to be the execution of the hermaphrodite mode of dosage compensation. Finally, given the number of alleles of these genes in existence, it is possible that additional genes in this class exist. Thus we are continuing our
xol-1 XO reversion screen to identify both more alleles of
dpy-26,
dpy-28, and
dpy-29 as well as any additional new genes in this class.