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  • 1
    Electronic Resource
    Electronic Resource
    Chichester [u.a.] : Wiley-Blackwell
    Developmental Genetics 7 (1986), S. 109-116 
    ISSN: 0192-253X
    Keywords: Sxr ; pseudomale ; masculinization ; Jost's principle ; Life and Medical Sciences ; Genetics
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: The genetic factor Sxr causes sex reversal of chromosomally female (XX or XO) mice to phenotypic maleness by inducing development of testes that produce androgens. It has been considered that these sex-reversed animals, called pseudomales, confirm the principle originally developed by Jost that adequate androgenization produces normal phenotypic maleness in mammals, irrespective of chromosomal sex. However, wepreviously discovered that the epididymis of sex-reversed XX mice (pseudomales of genotype XXSxr) lacks EH 9 cells (epididymal head, cell type No. 9, the principal cell' of the initial segment). The purpose of the present study was to determine whether cell type EH 9 of XXSxr pseudomales is replaced by a principal cell of a different appearance, or whether the initial segment itself is actually absent. We made serial sections of entire epididymal heads and did microdissections to unravel the highly coiled epididymal duct. Using these two approaches, we studied the sequence of epididymal segments, and estimated lengths of the relevant portion of the epididymal duct; we found that the initial segment of XXSxr pseudomales is truly absent. This is the first report of a mutant genotype causing absence of a segment of the epididymis. The XXSxr mutant appears to be an exception to Jost's principle. This finding shows that, even in full androgenization, male phenotype may not always be independent of chromosomal sex.
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  • 2
    Electronic Resource
    Electronic Resource
    Chichester [u.a.] : Wiley-Blackwell
    Developmental Genetics 8 (1987), S. 11-15 
    ISSN: 0192-253X
    Keywords: testicular feminization ; androgen induction ; meiosis inducing substance ; Life and Medical Sciences ; Genetics
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: The sex-linked recessive gene Tfm in the mouse produces a condition of testicular feminization (androgen insensitivity syndrome, AIS) in hemizygotes, comparable to the condition of the same name in humans. The murine mutant was originally believed to have no derivatives of the mesonephric duct system (MDS), and this absence was ascribed to dependence of these derivatives on androgens for survival. However, microscopical epi-didymides, retia testes, and vasa deferentia were identified in these animals in our laboratory. These micro-organs may play a role in meiosis induction in Tfm/Y animals. The present study was designed to determine whether survival of these organs is due to retention of an ability to respond to androgens, or whether they are unique amongst MDS derivatives in being independent of androgens.Previous studies in our laboratory demonstrated that the enzyme β-glucuronidase (βG) is androgen sensitive in the epididymis of the normal mouse. In the present investigation we used this enzyme as a marker to study androgen sensitivity in the microscopical epididymides of Tfm/Y hemizygotes and in the epididymides of control +/Y litter-mate brothers. Both mutant and control animals were studied with and without exogenous androgen stimulation.Tfm/Y hemizygotes demonstrated low levels of diffuse, cytoplasmic βG activity that appears to be unresponsive to exogenous androgen stimulation. In light of our previous studies, this distribution of βG reaction products suggests some degree of androgen sensitivity. The survival of these micro-organs and their partial androgen sensitivity may be related to the role of the MDS in inducing meiosis.
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  • 3
    ISSN: 0192-253X
    Keywords: Zinc finger Y ; sex reversed ; epididymis ; sex differentiation ; Life and Medical Sciences ; Genetics
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: The presence of the mutation Sex reversed (Sxr), a copy of a Y-chromosomal segment that gets transferred to an X chromosome, causes the resulting XXSxr mice to develop as apparent males. However, several features of male sexual development are abnormal in these animals. The testes are small and aspermatogenic, and the epididymides lack the initial segment. Testes and epididymides show abnormalities of extracellular matrix. In this study we examined transcription of the conserved Y chromosomal gene Zfy, which has an X-chromosomal homologue (Zfx). Northern blotting showed Zfy to be expressed in the testes of XXSxr animals, except for those that carry the coat-marker gene Tabby (Ta), despite the lack of germ cells in XXSxr mice. Reverse transcription polymerase chain reaction (RT-PCR) studies detected Zfy in mRNA in testes even when Ta was present. RT-PCR also demonstrated Zfy transcription in epididymides of normal males, though not in XXSxr mice. Previous authors reported an absence of Zfy transcription in XXSxr testes; Zfy transcription in normal testes has been ascribed to germ cells. Our observation indicates that this idea requires re-evaluation. The occurrence of Zfy transcription in the normal epididymis is similarly a novel finding that may help explain those aspects of epididymal development that occur in the absence of androgen. © 1994 Wiley-Liss, Inc.
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