Worm Breeder's Gazette 10(1): 130

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.

y63 Suppresses the Dosage Compensation But Not the Sex Determination Effects of sdc-1(n485)

A. Villeneuve and B. Meyer

We have isolated a dominant suppressor of sdc-1(n485) that maps 
between lin-14 and unc-9 on the X chromosome.  This mutation, called 
y63, suppresses the dosage compensation effects of sdc-1 (n485).
Specifically, while sdc-1(n485) XX hermaphrodites are Egl, slightly 
Dpy, and have protruding vulvae, phenotypes that correlate with 
elevated levels of X-linked gene expression, most y63 sdc-1(n485) XX 
hermaphrodites are wild-type in length, non-Egl, and have normal 
vulvae.  (Both sdc-1(n485) and y63 sdc-1(n485) XO animals are wild-
type males) .  Secondly, while xol-1(y9) 5) XO 
animals live, xol-1(y9) y63 sdc-1(n485) XO animals die .  According to 
the current model, the XO specific lethality caused by xol-1 mutations 
is due to inappropriate expression of the XX mode of dosage 
compensation in XO animals; sdc-1 mutations suppress xol-1 by shifting 
dosage compensation back toward the XO mode (Miller et al., WBG this 
issue).  The simplest interpretation of this result, then, is that y63 
suppresses the dosage compensation defect caused by sdc-1(n485), 
thereby preventing suppression of xol-1(y9).  Thirdly, while dpy-28(y1)
; 5) XX animals die even at 15 C, a temperature 
normally permissive for dpy-28 (y1) (Plenefisch and Meyer, WBG, this 
issue), dpy-28(y1); y63 sdc-1(n485) XX animals can survive.  We are 
currently testing directly whether X-specific mRNA levels are restored 
to wild-type in y63 sdc-1(n485) XX animals.
By contrast, y63 does not suppress the sexual transformation 
phenotypes caused by sdc-1(n485).  First, as in sdc-1(n485) strains, 
occasional XX pseudomales occur in y63 sdc-1(n485) strains.  Second, 
the enhancement of sexual transformation seen when sdc-1 (n485) is 
placed in trans to a deficiency of the locus or in combination with a 
weak allele of tra-2 (Villeneuve and Meyer, Cell 48:25-37) is likewise 
not suppressed by y63.  Moreover, XX pseudomales of genotype y63 sdc-1(
n485) / + mnDf1 or tra-2(n1106); y63 sdc-1(n485) are wild-type in 
length and have better male tail morphology than their non-y63 
counterparts, which are short and have abnormal bursae due to the 
dosage compensation disruption.  Finally, y63 also does not suppress 
enhancement of the sdc-1(n485) e by xol-1(y9).
Approximately 10-15% of xol-1(y9) X animals 
develop as pseudomales, all of which are unable to mate presumably due 
in part to the sdc-1 dosage compensation defect; because this defect 
is alleviated by y63, the triple mutant strain xol-1(y9) y63 sdc-1(
n485) actually produces some XX mating 
y63 has no obvious phenotype by itself in either XX or XO animals.  
We are currently testing whether it can suppress other alleles of sdc-
1 and/or mutations in other dosage compensation genes.
In addition to analyzing this and other sdc-1 suppressors, we have 
been isolating more sdc-1 alleles in order to obtain new classes of 
sdc-1 mutations and to define the null phenotype.  So far an EMS 
complementation screen of 34,000 chromosomes has yielded eight new 
alleles and one deficiency; seven of these alleles appear similar to 
sdc-1 (n485), and the eighth, recently isolated, is as yet not well 
characterized.  Two additional alleles, one of which is strongly 
temperature sensitive, have been isolated as suppressors of xol-1(y9).