Worm Breeder's Gazette 9(1): 69
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.
1. Supermales (3A;1X) are viable, but very thin and pale. Madl and Herman (Genetics 93: 393 (1979)) tentatively inferred that 3A;1X animals are inviable, from the fact that 'HFM' (4A;3X) tetraploid hermaphrodites crossed with diploid (2A;1X) males produced relatively few matroclinous male progeny. A different cross, which generates 3A;1X animals more explicitly, has been carried out using unc-1(e1598) (a dominant sex-linked marker) and him-8(e1489), which causes frequent X chromosome nondisjunction. When 2A;2X hermaphrodites homozygous for these two mutations are crossed with 4A; 2X males, viable non-Unc male progeny are produced. These must be 3A; 1X animals produced by the fertilization of 1A;OX eggs by 2A;1X sperm. Fewer than the predicted number of 3A;1X animals are obtained, and there is some embryonic lethality, but most of the supermales survive. They grow slowly, and are pale, thin and slightly long. Some have abnormal male tail anatomy but many are normal and make sperm. So far none has mated successfully, in contrast to 3A;2X males, which are often fertile. It appears that C. elegans is viable at X/A ratios ranging from 0.33 (3A;1X) to 1.5 (2A;3X), though possibly not beyond this range. 2. Synergistic maternal effects for fem mutations Homozygous fem-3 females crossed with wild-type males yield a fraction of abnormal fem-3/+ XO male progeny, which have abnormal gonads and sometimes rudimentary vulval development. Most of the fem- 3/+ XO animals are normal males, and fem-3/+ XO males derived from fem- 3/+ XY mothers are always normal. Therefore this result is due to an inadequate contribution of fem-3(+) product from the mother, rather than to haplo-insufficiency. A related effect is seen among the fem- 3/+ XX progeny of fem-3 mothers, some of which are female rather than hermaphrodite. The maternal insufficiency effect on both XX and XO progeny is exacerbated by the presence of mutations in the other fem genes (using putative null alleles in each of the three genes) : [See Figure 1] These results indicate that the maternal contributions of fem gene products are important, perhaps to maintain tra-1 activity in a repressed state during early embryogenesis. In the absence of the repression, tra-1 hyperactivity may sometimes (but apparently not always) lead to irreparable feminization of both XX and XO progeny, which develop as females and abnormal males respectively.