| First Author | Lee CH | Year | 2001 |
| Journal | Genesis | Volume | 30 |
| Issue | 1 | Pages | 7-11 |
| PubMed ID | 11353512 | Mgi Jnum | J:69946 |
| Mgi Id | MGI:2135815 | Doi | 10.1002/gene.1026 |
| Citation | Lee CH, et al. (2001) Low levels of Sry transcripts cannot be the sole cause of B6-Y(TIR) sex reversal. Genesis 30(1):7-11 |
| abstractText | 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. Copyright 2001 Wiley-Liss, Inc. |
