Abstract
LINDSTEN et al. suggested that the locus controlling the Xga sex-linked red-cell antigen was on the short arm of the X chromosome1 on the basis of a study of two women with a presumptive isochromosome for the long arm of the X (Xqi) and a normal X chromosome. Both were Xg(a −), but their fathers were Xg(a +), and it seemed that the paternal Xga allele for the dominant Xg(a +) character had not been transmitted to them. Because the abnormal Xs of the two patients lacked the short arms, it seemed that the Xg locus could be on the short arms of the X. But this interpretation rested on the evidence of paternity and on two assumptions: first, that the 45,X cells, present in both subjects (both were mosaics with a 45,X cell line), were not responsible for the observed genetic exception; and second, that the Xg locus escaped2–4 the alleged preferential inactivation of structurally abnormal X chromosomes, in which case a paternal Xga allele should manifest its presence if the locus were on the long arm of the X.
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POLANI, P., ANGELL, R., GIANNELLI, F. et al. Evidence that the Xg Locus is Inactivated in Structurally Abnormal X Chromosomes. Nature 227, 613–616 (1970). https://doi.org/10.1038/227613a0
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DOI: https://doi.org/10.1038/227613a0
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