The cumulative genetic evidence continues to support the proposal that
dpy-29, like
sdc-1 and
sdc-2, is required in XX animals for the proper control of both sex determination and dosage compensation. However, unlike the sdc genes, the dosage compensation and sex- determination functions of
dpy-29 appear to be independently mutable. Furthermore, null or near null alleles of
dpy-29 do not normally masculinize XX animals, rather, the cryptic Tra phenotype can only be seen in certain genetic backgrounds. The tra V mutations, which cause recessive masculinization of XX animals, appear to result from loss of only the sex-determination function of the gene. One
dpy-29 allele appears to disrupt only the dosage-compensation function, the remaining
dpy-29 alleles appear to disrupt both gene functions.
dpy-29 is required for the XX mode of dosage compensation. Mutations in
dpy-29 result in recessive XX-specific dumpiness and XX- specific maternal effect lethality; the lethality ranges from 72% to 98%. Phenotypically, mutations in
dpy-29 resemble mutations in the dosage compensation dpy genes
dpy-26, he
lin-14 assay we have shown that mutations in
dpy-29 result in elevated levels of X-linked gene expression. Like other mutations that disrupt the XX mode of dosage compensation, mutations in
dpy-29 rescue
xol-1 XO animals.
dpy-29 is required for hermaphrodite sexual development.
dpy-29 differs from the dosage compensation dpy genes in two ways: 1)
dpy-29 mutations, like
sdc-1 and
sdc-2 mutations, suppress the lethality of
xol-1 XO animals, resulting in rescued animals that are male. By contrast,
dpy-26, s suppress the lethality of
xol-1 XO animals but result in rescued animals that are hermaphrodite. 2)
dpy-29 mutations also differs from
dpy-26, s in their effects on the sexual phenotype of 2X:3A animals.
dpy-29(
y100) 2X:3A animals, like dpy(+) 2X:3A animals, are usually male; by contrast,
dpy-26, imals are feminized. The masculinizing effect of
dpy-29 mutations can be seen directly when placed in trans to tra
(y52).
dpy-29/tra V XX animals range from 0 to 99% masculinized, depending on the
dpy-29 allele. This masculinization is specific to mutations in these two genes;
dpy-29 mutations show no dominant masculinization with mutations in
tra-1 or
tra-2. tra V mutations show no dominant masculinization with mutations in
dpy-26,
dpy-28, nodpy-29 rs to act upstream of
her-1.
her-1(+) is required for the masculinization of tra V XX animals and for the masculinization of
dpy-29/tra V XX animals. This result, combined with the observation that
dpy-29 mutations suppress the XO- specific lethality of
xol-1 mutations, indicates that
dpy-29 acts at the same point of the sex-determination pathway as
sdc-1 and
sdc-2.The dosage-compensation and the sex- determination functions of
dpy-29 are independently mutable. The extent of masculinization of the
dpy-29 alleles is unrelated to the strength of the dosage compensation defect, which is measured by extent of the XX-specific maternal-effect lethality. For example, both
dpy-29(
y144) and
dpy-29(
y100) have the same level of maternal- effect lethality (97%), however 99% of
dpy-29(
y144)/tra V animals are masculinized, whereas only 3% of
dpy-29(
y100)/tra V animals are masculinized. By a cis-trans test,
dpy-29 and tra V mutations are in the same gene. Three independent tra V
dpy-29 mutants were obtained by inducing dpy- 29 mutations on a tra V chromosome (two different tra V alleles were used). All three double mutants are phenotypically indistinguishable from strong
dpy-29 mutations: XX animals are fully hermaphrodite and exhibit a strong maternal-effect lethality (96% - 98%). We have evidence that the original tra V mutation is still present in two of the double mutants. For one double mutant, a Tra non-Dpy recombinant was obtained after screening 17,000 progeny of tra V
dpy-29/+ mothers. In another double mutant, the
dpy-29 mutation was shown to be suppressible by
sup-7(
st5). The tra V
dpy-29; ed animals are pseudomales, in contrast to the tra V
dpy-29 mutant animals which, when viable, are hermaphrodites.