Worm Breeder's Gazette 9(3): 49
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.
I told you earlier that X-chromosome duplications suppress X-linked hypomorphs in regions they do not duplicate. For example, a duplication including unc-20+ will suppress lin-15 (n765), a hypomorph at least 20 map units away from the nearest gene duplicated. This suggests that X-chromosome expression is elevated by X-duplications in 2X animals, a suggestion that has been directly confirmed by assaying transcription of cloned genes (Casson and Meyer, last newsletter). The suppression in 2X animals is both size and dose-dependent; large duplications suppress better in general than small duplications, and two copies of a duplication suppress better than one copy. With the possible exception of a duplication of dpy-22+, which suppresses better than expected based on its size, the suppression does not seem to be especially dependent on the region of the X duplicated; not all regions of the X have been tested. The same result is found in both 1X males and 1X hermaphrodites (produced by her-l(e1520)), and again the amount of suppression is dependent on size and dose (in one case, for the latter), but not on the region duplicated. However, XO hermaphrodites are not suppressed as well as XX hermaphrodites, suggesting that X expression is not elevated as much in XO as in XX animals. I'll assume that suppression of X-linked hypomorphs reflects elevated X expression; so far, the data support that. The suppression is enhanced by the X-dependent dpy mutation dpy-21, which elevates overall X expression: a Dp/+; dpy-21 strain is a better suppressor than either the duplication or dpy-21 alone in both 1X and 2X animals. This is probably true for two other X-dependent dpy's, dpy- 26 and dpy-27, but the data are not so complete. Some time ago, I found (with Bill Wood) that dpy-21 and certain large X duplications interacted to make 1X animals intersexual. The fact that dpy-21 and X- duplications each elevate X expression in 1X animals leads to a hypothesis that the intersexuality of these strains is due to overexpressing some !one or many) particular X-linked gene products involved in sex determination. One contradictory result was that the duplication of dpy-22+, which has very high X expression, is not intersexual in dpy-21 strains. Another problem now arises. A dpy-26: l is a normal male, but with high X expression, as high or higher than mnDp25/+; dpy-21, which is (at least sometimes) intersexual. This argues against the hypothesis that X expression alone is responsible for the intersexuality of Dp/+: dpy- 21 XO animals, and suggests that the duplication affects sexual development in a way that dpy-21 and dpy-26 do not; perhaps the duplications affect genes that dpy-21 doesn't affect strongly, or perhaps the duplications provide some non-expressed elements that affect sexual development. I have also been looking at maternal effects on X expression by using XO hermaphrodites. The data don't form a coherent whole yet, but the general conclusion is that the progeny of XO mothers do not suppress hypomorphs as well as the progeny of XX mothers do. The effect is especially pronounced in the XO progeny of XO mothers.