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X‐Linked testicular feminization in the mouse as a non‐inducible regulatory mutation of the Jacob‐Monod type
Author(s) -
Ohno Susumu,
Lyon Mary F.
Publication year - 1970
Publication title -
clinical genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 102
eISSN - 1399-0004
pISSN - 0009-9163
DOI - 10.1111/j.1399-0004.1970.tb01627.x
Subject(s) - testicular feminization , feminization (sociology) , endocrinology , medicine , kidney , biology , testosterone (patch) , locus (genetics) , dihydrotestosterone , alcohol dehydrogenase , mutation , gene , genetics , androgen , enzyme , hormone , biochemistry , sociology , social science , androgen receptor , prostate cancer , cancer
Testosterone and 5 α‐dihydrotestosterone normally induce alcohol dehydrogenase (ADH) production in the mouse kidney. The following results suggest that the X‐linked testicular feminization ( T fm ) mutation in the mouse is a non‐inducible mutation of a repressive regulatory gene locus. Eleven affected X Tfm Y mice and 3 X Tfm X + heterozygous females, as well as their normal sibs, were challenged with 10 mg of either testosterone or 5α‐dihydrotestosterone and killed 5 days later. Kidney ADH of normal sibs were in the fully induced state, while no detectable kidney ADH activity was found in X Tem Y. In accordance with the X‐inactivation hypothesis, individual kidneys of heterozygous females showed extremely variable degrees of inducibility of kidney ADH.