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Michael D. Griswold, Editorial: What Can Spermatogonial Transplants Teach Us about Male Reproductive Biology?, Endocrinology, Volume 141, Issue 3, March 2000, Pages 857–858, https://doi.org/10.1210/endo.141.3.7430
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In this issue of Endocrinology, there is a rapid communication by Mahato et al. (1) that addresses the issue of estrogen action directly on germinal cells in the testis. The authors transplanted germ cells from the testis of the estrogen receptor α (ERα) knockout mice into the seminiferous tubules of germ cell-depleted wild-type mice. The germ cells carrying the knockout mutation underwent qualitatively normal spermatogenesis, and the recipients were fertile. Offspring derived from some of the recipient mice were shown by coat color and PCR to be derived from sperm carrying the disrupted gene for the ERα.
The transplantation of testicular germ cells from a donor to recipient of the same or a closely related species was pioneered in the laboratory of Dr. Ralph Brinster at the University of Pennsylvania (2–4). The initial reports on the successful transplants from donor mice and rats into recipient mice generated a great deal of interest and excitement from both basic and clinical scientists. In the technique developed in Brinster’s laboratory, mixed germ cells, including an unknown number of spermatogonial stem cells, are introduced into the lumen of the seminiferous tubules. To initiate spermatogenesis, some of the stem cells introduced into the tubular lumen had to negotiate through Sertoli-Sertoli junctions to the basal lamina. This was a novel concept to most reproductive scientists because there was no reason to predict that this type of relocalization of germ cells could occur. Brinster and Avarbock (1994) also showed in mating experiments that the bacterial marker LacZ gene in transplanted cells that developed into sperm was passed to successive generations (2). This report also described how transplantation was successful when the endogenous germ cells in the recipient animals were reduced or eliminated using the chemotherapeutic agent, busulfan. At the levels used, busulfan does not kill all endogenous spermatogonia, but some stem cells remain and will reinitiate spermatogenesis in the recipient. Because a busulfan-treated recipient testis will simultaneously develop spermatogenesis via the transplanted spermatogonia and via endogenous stem cells, a genetic or morphological marker is required to identify the sperm arising from the transplanted stem cells.
