Testis structure in the sys (symplastic spermatids) mouse.
Testis structure in the sys (symplastic spermatids) mouse.
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sys（共生精子细胞）小鼠的睾丸结构。
DOI：
10.1002/aja.1001920206
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
MacGregor,GR
中科院分区：
文献类型：
--
作者：
Russell,LD;Hikim,AP;Overbeek,PA;MacGregor,GR
研究了带有隐性插入突变的小鼠睾丸的结构和发育异常。纯合子（sys/sys）男性由于精子发生异常导致无精子症而不育。精子发生的主要中断发生在连接圆形精子细胞的细胞间桥过早打开，导致共质体形成时。共质体含有多达285个核。共质体内精子细胞的发育在精子细胞核开始伸长之前或之后被阻止。共质体退化，似乎被支持细胞和小管内巨噬细胞吞噬。此外，还观察到年轻的圆形精子细胞和精母细胞的变性。精母细胞变性在某些小管中是实质性的，并使它们除了基底室细胞之外的细胞耗尽。支持细胞异常是突出的，包括细胞内空泡化，圆形精子细胞周围缺乏顶端突起，变性和偶尔脱落。虽然也可以看到基底膜的重叠和内折，但这并不常见。这种类型首先出现在19日龄至22日龄的动物身上。青春期前动物的睾丸组织学存在相当大的变异性;一些显示退化的粗线期精母细胞，几乎没有支持细胞空泡，而另一些显示空泡，没有明显升高的退化精母细胞数量。尽管本研究尚未揭示受插入失活事件影响的原代细胞类型，但支持细胞的异常可能是生殖细胞变性的原因，因为通常认为支持细胞的缺陷可导致主要生殖细胞异常，但反之亦然。
Testes of mice with the recessive insertional mutation termedsymplastic spermatids (sys)were assessed for structural and developmental abnormalities. Homozygous (sys/sys) males are infertile due to an abnormality in spermatogenesis leading to azoospermia. The major interruption to spermatogenesis occurs when the intercellular bridges that connect round spermatids open prematurely resulting in the formation of symplasts. Symplasts contain as many as 285 nuclei. Development of spermatids within symplasts is arrested just before, or just after, elongation of the spermatid nuclei begins. Symplasts degenerate and appear to be phagocytized by Sertoli cells and by intratubular macrophages. In addition, degeneration of young round spermatids and also spermatocytes occasionally is observed. Spermatocyte degeneration is substantial in some tubules and leaves them depleted of cells other than basal compartment cells. Sertoli cell abnormalities are prominent and include intracellular vacuolation, absence of apical processes surrounding round spermatids, degeneration, and occasional sloughing. Although reduplication and infolding of the basal lamina is also seen, this does not appear as a common phenomenon. Thesysphenotype is first manifest in animals between 19 days and 22 days of age. Considerable variability is seen in testis histology of prepubertal animals; some display degenerating pachytene spermatocytes and virtually no Sertoli cell vacuoles, while others display vacuoles without apparent elevated numbers of degenerating spermatocytes. Although this study has not revealed the primary cell type(s) affected by the insertional inactivation event, it is possible that the abnormalities in the Sertoli cells are responsible for germ cell degeneration as it is generally recognized that deficits in the Sertoli cell can result in major germ cell abnormalities but not vice versa.