Worm Breeder's Gazette 13(3): 38 (June 1, 1994)
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.
In many organisms, different sexes have different numbers of X chromosomes. Dosage compensation functions to normalise the level of X-linked expression between the sexes. In C. elegans, XX diploids develop as hermaphrodites and XO diploids develop as males. A set of autosomal genes, dpy-21 , dpy-26 ,etc. function to normalise X-linked expression, probably by down regulating X-linked transcription in XX hermaphrodites, but not in XO males. XX animals carrying mutations in any of these (dpy genes are Dpy or inviable, whereas XO animals are virtually wild-type in phenotype. Thus, it has been speculated that the dosage compensation dpy genes function primarily in XX, but not XO animals [for review, see Villeneuve and Meyer (1990). Adv. Genet. 27: 117].
I have characterised the phenotype of a novel class of tra-7 (eg, for enhanced gain-of-function) feminising alleles in XO animals and have detected a potential interaction between the sex determination and dosage compensation pathways. The tra-2 (eg) alleles were originally isolated by J. Hodgkin in a selection for XO feminising mutations that enhance the activity of tra-2 ( e2046 gf). XO tra-2 ( e2531 eg e2046 gf) animals are transformed from male into female. To genetically characterise the phenotype of XO animals that carry only the tra-2 ( e2531 eg) mutation and not the tra-2 ( e2046 gf) mutation, I have isolated an intragenic recombinant that carries only the tra-2 ( e2531 eg,) mutation. XO animals that carry the tra-2 ( e2531 eg) mutation are transformed from male into hermaphrodite. Although XO tra-2 ( e2531 eg) animals are fertile hermaphrodites, the mean brood size is only 9.9 ± 7.6, of which only 0-1 animals develop into adults (n=6). Nomarski inspection of the germ line of XO tra-2 ( e2531 eg) hermaphrodites indicates that many of the oocytes are aberrant in morphology, possibly explaining the low fertility. To test the possibility that dosage compensation might be incorrectly activated during gametogenesis in XO mothers, I constructed a tra-2 ( e2531 eg); dpy-26 ( n199 )strain and counted broods from (m-z-) XO hermaphrodites. Surprisingly, the fertility of XO tra-2 ( e2531 eg); dpy-26 ( n199 )is dramatically improved. The mean brood size of XO tra-2 ( e2531 eg);dpy/-26( n199 )hermaphrodites is increased to 204 ± 17.4, 1/4 of which develop into wild-type adults and 3/4 are Dpy or inviable (n=6). These results have led me to speculate that there may be an interaction between the sex determination and dosage compensation pathways that occurs during gametogenesis. Thus, although dosage compensation mechanisms are normally not active in XO animals, they may be detrimentally activated during gametogenesis, if the germline is feminised. This phenomenon does not appear to be limited to XO tra-2 (eg)) Hermaphrodites, because it has previously been reported that XO her-1 (lf); dpy-26 ( n199 )hermaphrodites are more fertile than XO her-1 (lf)hermaphrodites Hodgkin (1983), MGG 192:452]. I am currently testing how the dosage compensation dpy genes interact with other XO feminising genes in the sex determination pathway.