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.
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 males! 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).