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Low levels of Sry transcripts cannot be the sole cause of B6‐Y TIR sex reversal
Author(s) -
Lee ChungHae,
Taketo Teruko
Publication year - 2001
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/gene.1026
Subject(s) - testis determining factor , biology , y chromosome , sex reversal , gonad , autosome , x chromosome , sexual differentiation , genetics , microbiology and biotechnology , gene , endocrinology
Summary: Sry , a single‐copy gene on the Y‐chromosome, triggers the fetal gonad to begin testis differentiation in mammals. On the other hand, mutation or absence of Sry results in ovary differentiation and the female phenotype. However, cases of XY sex reversal in the presence of wild‐type Sry exist in mice and man. One such example is the B6‐Y TIR mouse, whose autosomes and X‐chromosome are from the C57BL/6J mouse (an inbred strain of Mus musculus molossinus ), whereas the Y‐chromosome is from a Mus musculus domesticus mouse originating in Tirano, Italy. The B6‐Y TIR mouse never develops normal testes and instead develops ovaries or ovotestes in fetal life. It has been suggested that low levels of Sry transcription may account for the aberrant testis differentiation in the B6‐Y TIR mouse. In this study, however, we observed relatively low levels of Sry transcripts not only in B6‐Y TIR but also in B6 mice, which develop normal testes. We conclude that low dosage of Sry transcripts cannot be the sole cause of sex reversal in the B6‐Y TIR gonad. genesis 30:7–11, 2001. © 2001 Wiley‐Liss, Inc.