Worm Breeder's Gazette 10(2): 23

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.

dpy-29: Yet Another XX-specific Lethal

John Plenefisch, Martha Soto, Leslie DeLong and Barbara Meyer

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.