Arrest of spermatogonial differentiation in jsd/jsd, Sl17H/Sl17H, and cryptorchid mice

Arrest of spermatogonial differentiation in jsd/jsd, Sl17H/Sl17H, and cryptorchid mice
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DOI:
10.1095/biolreprod61.3.842
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发表时间:
1999-09-01
影响因子:
3.6
通讯作者:
Nishimune, Y
Nishimune, Y
中科院分区:
生物学2区
文献类型:
--
作者:
de Rooij, DG;Okabe, M;Nishimune, Y

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隐睾C57 BI小鼠和JSD/JSD和SI 17 H/SI 17 H突变小鼠的生精停滞的性质通过研究整个生精小管来确定。在所有三种类型的小鼠中,实际上只发现了A型精原细胞,拓扑学上排列在1至16个(很少更多)细胞的克隆中。这些克隆大小是典型的未分化精原细胞。这些细胞位于2个以上细胞链中的比例(50-70%)与正常上皮中上皮阶段VII-VIII中所见的比例相当。结果表明,在这三种小鼠中,精子发生均发生在未分化的A型精原细胞,特别是A(al)型精原细胞分化为第一代分化型精原细胞A1时停止,剩余的A型精原细胞增殖,但未出现精原细胞聚集,同时发生了精原细胞凋亡。所有大小的精原细胞克隆都发生了凋亡,但有相对较多的大的凋亡克隆,这表明当它们变大时,这些克隆变得更加脆弱。与正常上皮细胞相比,在所有三种类型的小鼠中,都存在奇数克隆,不包含2(n)个细胞,以及在同一细胞质中存在2个或更多个精原细胞核的团块。这表明缺乏完整性的精原细胞克隆,也观察到在其他情况下与基底membrane.It的细胞相对缺乏的结论是未分化的精原细胞的分化,在所有三种类型的小鼠以及维生素A缺乏的动物,是一个相当脆弱的点,在生精发育途径。
The nature of the spermatogenic arrest in cryptorchid C57BI mice and in jsd/jsd and SI17H/SI17H mutant mice was identified by studying whole mounts of seminiferous tubules. In all three types of mice, virtually only A spermatogonia were found, topographically arranged in clones of 1 to 16 (rarely more) cells. These clonal sizes are typical for undifferentiated spermatogonia. The proportion of these cells lying in chains of more than 2 cells (50-70%) was comparable to that seen in epithelial stages VII-VIII in the normal epithelium. It is concluded that in all three types of mice, spermatogenesis is arrested at the point where the undifferentiated A spermatogonia, specifically A(al) spermatogonia, differentiate into the first generation of the differentiating-type spermatogonia, the A1 spermatogonia.The remaining A spermatogonia were proliferating, but no accumulation of spermatogonia was present, as spermatogonial apoptosis also took place. Spermatogonial clones of all sizes were seen to undergo apoptosis, but there were relatively many large apoptotic clones, indicating that the clones became more vulnerable when they became larger.In contrast to what is seen in the normal epithelium, odd-numbered clones, not composed of 2(n) cells, were present, as well as clumps of 2 or more spermatogonial nuclei in the same cytoplasm, in all three types of mice. This indicates a lack of integrity of spermatogonial clones, also observed in other situations with a relative paucity of cells on the basal membrane.It is concluded that the differentiation of the undifferentiated spermatogonia, affected in all three types of mice as well as in vitamin A-deficient animals, is a rather vulnerable point in the spermatogenic developmental pathway.