pell@boulder.Colorado.EDU (Anthony Pelletier) (04/02/88)
In article <367@nancy.UUCP> straney@msudoc.UUCP (Ronald W. DeBry) writes: ><1988Mar31.124839.9957@utzoo.uucp> rising@utzoo.uucp (Jim Rising) writes: > >>Higher early (pre-natal; juvenile) mortality may be due to >>deleterious recessives on the X--for which the males are "homozygous." > >Mammals accomplish dosage compensation by completely shutting off one X. >This happens early, at about the 8 or 16 cell stage (another guess - I >could look it up, but that will spoil the fun for those who want to >flame me for getting my facts wrong :-) ). It *is* about the same time >that the zygote's own genes get turned on. It could still be that some >of the deleterious effects are lessened in females, since only half of >her cells will be hemizygous for the recessive allele, but you'd have to >do some more to convince me of that. > >>--Jim Rising >Ron DeBry Dept. of Zoology Michigan State University I think I can convince you of that. It turns out that you can kill (or remove) half the cells of a developing mammal at least through the blastula stage and the thing develops fine. So in the case of cell-lethal X mutations, at X inactivation, half the cells in the female embryo die with no ill effects. In the hemizygous male, the embryo obviously dies (note, this does not address infant mortality). For non-cell-lethal mutations on the X, the female is mosaic (often, if the mutant cells are less fit than the wt, they make up a smaller portion of the organism). So you get interesting things like: no sweat pores on parts of the body and calico cats. -tony