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Submitted on March 11, 2002
Accepted on July 23, 2002
1 Department of Physiology, Institute of Biomedicine (P.S., M.M., J.P., I.H., M.P.), and Turku Graduate School of Biomedical Sciences (P.S., J.P.), University of Turku, Kiinamyllynkatu 10, FIN-20520 Turku, Finland; Institute of Reproductive Medicine of the University (T.G.C., C.-H.Y.), D-48129 Münster, Germany; and Reproduction & Development Research Group (J.D.), Blaise Pascal University, CNRS UMR 6547 -GEEM, 24 Avenue des Landais Aubière, France
* To whom correspondence should be addressed. E-mail: matti.poutanen{at}utu.fi.
We have generated two transgenic mouse lines (GPX5-Tag1, and -Tag2) by expressing the Simian Virus 40 large and small T-antigens (SV40 Tag) under a 5 kb promoter of the murine glutathione peroxidase 5 (GPX5) gene. In GPX5-Tag1 mice, with high level of Tag expression, severe dysplasia was found in the epididymis and seminal vesicles. These mice developed also adrenal and prostate tumors and spermatogenesis was distrupted. In GPX5-Tag2 mice, with lower level of Tag expression, the only histological change was the slightly hyperplastic epithelium in the initial segment of the epididymidis and in the seminal vesicles. Despite normal mating behaviour these mice were infertile. The most conspicuous feature of the sperm was angulation of the flagellum, which appeared during epididymal transit, probably due to the observed reduction in the osmotic pressure of cauda epididymidal fluid. The angulation did not affect the motility or kinematic parameters of the sperm, but they were also incapable of fertilization in vitro. The lack of expression of several genes specific for the initial segment suggests that in the GPX5-Tag2 mice the transgene expression bring about a differentiation arrest in this part of epididymis. This novel mouse line provides a model for epididymal dysfunction leading to defects in post-testicular sperm maturation and infertility.
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