Worm Breeder's Gazette 9(1): 69

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Another random walk along the sex determination pathway

J. Hodgkin

Figure 1

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 
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.

Figure 1