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Follicle-Stimulating Hormone Is Indispensable for the Last Spermatogonial Mitosis Preceding Meiosis Initiation in Newts (Cynops pyrrhogaster)¹

^a Department of Materials and Life Science, Graduate School of Science and Technology, ^b Department of Biological Science, Faculty of Science, Kumamoto University, Kumamoto 860-8555, Japan

We previously reported that mammalian FSH induced differentiation of secondary spermatogonia into primary spermatocytes in organ culture of newt testicular fragments, whereas in medium lacking FSH primary spermatocytes never appeared. Here, we investigated why spermatogonia fail to form primary spermatocytes in the absence of FSH. Spermatogonia maintained proliferative activity and viability at about half the level of those cultured in the presence of FSH, progressed into the seventh generation, but became moribund during the G2/M phase. Thus, the eighth generation of spermatogonia never appeared, suggesting that cell death is the chief reason why primary spermatocytes fail to form in the absence of FSH. The presence of Dmc1, a molecular marker for the spermatocyte stage, confirmed our microscopic observations that spermatogonia differentiated into primary spermatocytes in the presence of FSH. Thus, FSH is indispensable for the completion of the last spermatogonial mitosis, a prerequisite for the conversion of germ cells from mitosis to meiosis. Because prolactin induced apoptosis in spermatogonia during the seventh generation, we propose that a checkpoint exists for the initiation of meiosis in the seventh generation whereby spermatogonia enter meiosis when the concentration ratio of FSH to prolactin is high but fail to do so when the ratio is low.

First decision: 2 July 2001.

¹ This work was supported by a Grant-in-Aid for Science Research (12680718) from the Ministry of Education, Science, Sports, and Culture of Japan; and by Special Coordination Funds for Promoting Science and Technology.

² Correspondence: Shin-ichi Abé, Department of Materials and Life Science, Graduate School of Science and Technology, Kumamoto University, Kurokami 2-39-1, Kumamoto 860-8555, Japan. FAX: 81 96 342 3437; abeshin{at}gpo.kumamoto-u.ac.jp

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