contested - the weight sits with the supporting side
refutedsupported
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Source [2] notes that certain XO mice can develop as fertile females, while other sources discuss male development associated with sex-reversal factors, leaving the claim about fertile XO males unconfirmed by the complete source text.
An autosomally inherited condition is described in the mouse which causes genetic females to develop as phenotypic males. XX males are phenotypically normal with the exception of small testes, which, in the adult, are devoid of germ cells. During late fetal and early postnatal development, male-type germ cells are present but progressively become lost, so that none is present by 10 days of age. XO males are also phenotypically normal, but spermatogenesis is active in the testis, and spermatozoa are produced. Cytological evidence of a Y-autosome translocation was completely lacking, and it is proposed that an autosomal dominant gene mutation, analogous to that found in other mammalian species, is responsible for the sex reversal.
McLaren & Monk (1982) and Cattanach et al. (1982) reported that T(X; 16)16H/X Sxr mice, in which the X chromosome bearing Sxr is the inactivated X chromosome, can develop as fertile females. By mating such females to X/Y Sxr males it has been possible to produce mice homozygous for Sxr. Two X Sxr/Y Sxr males were identified which together fathered 141 sons and 1 daughter. The single daughter proved to be XO, indicating a non-disjunctional event with neither paternal sex chromosome being transmitted. It is concluded that X Sxr/ Y Sxr mice are viable and fertile, and that all their progeny, provided they receive a paternal sex chromosome, develop as males.
IT is generally considered that the Y chromosome is necessary for the development of the mammalian testis and the consequent male phenotype. Exceptions occasionally occur in man and other animals, where a male phenotype is associated with an apparently normal female karyotype. In some instances it has been possible to show that such “sex reversal” has an autosomal genetic basis. Although this might imply that the Y chromosome is not a prerequisite of maleness, it has not been excluded that a small male-determining region of the Y may have been translocated to an autosome without producing a recognisable karyotypic change1 (reviewed in ref. 2). The best studied case of male development with an apparently female karyotype is provided by the Sxr mutant in the mouse. This autosomal dominant condition causes both XX and XO mice to develop as males, although germ cells are absent in Sxr,XX animals and spermatogenesis is impaired in Sxr,XO mice. Sxr,XY males have a slightly reduced testis size but are usually fertile. Cytological scrutiny of mitotic and meiotic chromosomes (including chromosome banding) has revealed no evidence for a Y–autosome translocation, although a small translocation undetectable by the methods used cannot be ruled out (reviewed in ref. 2). This situation can now be investigated using serological methods for detecting H–Y (histocompatibility–Y) antigen on the surface of mouse sperm3 and male epidermal cells4. These techniques have provided further evidence tha
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