The pattern of X chromosome inactivation in X autosome translocation carries in a herd of Limousin-Jersey crossbred cattle was studied using the reverse banding technique consisting of 5-bromodeoxyuridine incorporation and acridine orange staining and autoradiography on cultures of solid tissues and blood samples exposed to tritiated thymidine. The late-replicating X chromosome was noted to be the normal X in strikingly high proportions of cells in cultures of different tissues from all translocation carriers. It is suggested that the predominance of cells in which the normal X is inactivated may be the result of a post-inactivation selection process. Such a selection process during the prenatal life favouring cells in which the genes of the normal X chromosome remain unexpressed in translocation carrier females may be the mechanism that helps these conceptuses escape the adverse effects of functional aneuploidy. Based on the observation that the translocation carriers of this line of cattle are exclusively females and that there is a higher than expected rate of pregnancy loss, it is also postulated that the altered X chromosome may be lethal to all male conceptuses and to some of their female counterparts.
In two kittens from the same litter with spina bifida and meningocoele the phenotypic male was found to have a normal 38XY chromosome complement whilst the phenotypic female had a 37XO chromosome complement. It was concluded that the spina bifida condition was due to the manx ancestry and not to the 37XO karyotype. The possible effect of the XO complement in cats is discussed.
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