Overexpression of c-<I>myc</I> induces apoptosis at the prophase of meiosis of rat primary spermatocytes Export

@article{citeulike:1597791, abstract = {Transgenic rats expressing the rat c-myc gene under the control of the human metallothionein II A promoter were produced. We found that the female transgenic rats were fertile, but that the male transgenic rats were sterile. Atrophy of the seminiferous tubules and depletion of sperm were observed in the sterile male testes. The expression of differential stage-specific mRNAs, including those of the c-kit receptor proto-oncogene, meiotic heat-shock protein 70 gene, acrosin gene, and transition protein 1 gene, was analyzed by the reverse transcriptase-polymerase chain reaction during spermatogenesis. The results suggested that spermatogenesis in these sterile rats were arrested at the prophase of meiosis in the primary spermatocytes. We found that apoptotic DNA fragmentation occured in primary spermatocytes of the sterile transgenic rats. These results suggest that overexpression of the c-myc gene induces apoptosis at the prophase meiosis of the primary spermatocytes thereby causing male sterility in the c-myc transgenic rats. {\copyright} Wiley-Liss, Inc.}, address = {YS New Technology Institute, Inc., Shimotsuga-gun, Tochigi; Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan}, author = {Kodaira, Kunihiko and Takahashi, Ri-Ichi and Hirabayashi, Masumi and Suzuki, Takashige and Obinata, Masuo and Ueda, Masatsugu}, citeulike-article-id = {1597791}, citeulike-linkout-0 = {http://dx.doi.org/10.1002/(SICI)1098-2795(199612)45:4%3C403::AID-MRD1%3E3.0.CO;2-V}, citeulike-linkout-1 = {http://www3.interscience.wiley.com/cgi-bin/abstract/71778/ABSTRACT}, doi = {10.1002/(SICI)1098-2795(199612)45:4%3C403::AID-MRD1%3E3.0.CO;2-V}, journal = {Molecular Reproduction and Development}, keywords = {apoptosis, c-myc, meiosis, primary\_spermatocytes, prophase, rat, spermatocytes, testis}, number = {4}, pages = {403--410}, posted-at = {2007-08-28 04:59:58}, priority = {2}, title = {Overexpression of c-<I>myc</I> induces apoptosis at the prophase of meiosis of rat primary spermatocytes}, url = {http://dx.doi.org/10.1002/(SICI)1098-2795(199612)45:4%3C403::AID-MRD1%3E3.0.CO;2-V}, volume = {45}, year = {1996} }

TY - JOUR ID - citeulike:1597791 L3 - citeulike-article-id:1597791 N2 - Transgenic rats expressing the rat c-myc gene under the control of the human metallothionein II A promoter were produced. We found that the female transgenic rats were fertile, but that the male transgenic rats were sterile. Atrophy of the seminiferous tubules and depletion of sperm were observed in the sterile male testes. The expression of differential stage-specific mRNAs, including those of the c-kit receptor proto-oncogene, meiotic heat-shock protein 70 gene, acrosin gene, and transition protein 1 gene, was analyzed by the reverse transcriptase-polymerase chain reaction during spermatogenesis. The results suggested that spermatogenesis in these sterile rats were arrested at the prophase of meiosis in the primary spermatocytes. We found that apoptotic DNA fragmentation occured in primary spermatocytes of the sterile transgenic rats. These results suggest that overexpression of the c-myc gene induces apoptosis at the prophase meiosis of the primary spermatocytes thereby causing male sterility in the c-myc transgenic rats. © Wiley-Liss, Inc. IS - 4 JF - Molecular Reproduction and Development AD - YS New Technology Institute, Inc., Shimotsuga-gun, Tochigi; Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan EP - 410 TI - Overexpression of c-<I>myc</I> induces apoptosis at the prophase of meiosis of rat primary spermatocytes VL - 45 SP - 403 KW - apoptosis KW - c-myc KW - meiosis KW - primary_spermatocytes KW - prophase KW - rat KW - spermatocytes KW - testis AU - Kodaira, Kunihiko AU - Takahashi, Ri-Ichi AU - Hirabayashi, Masumi AU - Suzuki, Takashige AU - Obinata, Masuo AU - Ueda, Masatsugu PY - 1996/// UR - http://dx.doi.org/10.1002/(SICI)1098-2795(199612)45:4%3C403::AID-MRD1%3E3.0.CO;2-V ER -