Juvenile spermatogonial depletion (js']jsd) mutant seminiferous tubules are capable of supporting transplanted spermatogenesis

被引:51
作者
Boettger-Tong, HL
Johnston, DS
Russell, LD
Griswold, MD
Bishop, CE
机构
[1] Baylor Coll Med, Dept Obstet & Gynecol, Houston, TX 77030 USA
[2] Baylor Coll Med, Dept Mol Genet, Houston, TX 77030 USA
[3] Washington State Univ, Dept Mol Biosci, Pullman, WA 99164 USA
[4] Washington State Univ, Ctr Reprod Biol, Pullman, WA 99164 USA
[5] So Illinois Univ, Sch Med, Dept Physiol, Carbondale, IL 62901 USA
关键词
gametogenesis; processes; spermatogenesis; testes;
D O I
10.1095/biolreprod63.4.1185
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
In mice, the juvenile spermatogonial depletion (jsd) mutation results in a single wave of spermatogenesis followed by failure of type A spermatogonial stem cells to repopulate the testis, rendering male animals sterile. It is not clear whether the defect in jsd resides in a failure of the somatic component to support spermatogenesis or in a failure that is intrinsic to the mutant's germ cells. To determine if the jsd intratesticular environment is capable of supporting spermatogenesis, germ cell transplantation experiments were performed in which C57BL/6 ROSA germ cells were transplanted into jsd recipients. To determine if jsd spermatogonia are able to develop in a permissive seminiferous environment, jsd germ cells were transplanted into W/W-v and busulfan-treated C57BL/6 animals. The data demonstrate that up to 7 mo after transplantation of normal germ cells, jsd seminiferous tubules are capable of supporting spermatogenesis. In contrast, when jsd germ cells were transplanted into busulfan-treated C57BL/6 testis, or into testis of W/W-v mice, no jsd-derived spermatogenesis was observed. The data support the hypothesis that the jsd phenotype is due to a defect in the germ cells themselves, and not in the intratubular environment.
引用
收藏
页码:1185 / 1191
页数:7
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