首页> 外文期刊>Biology of Reproduction: Offical Journal of the Society for the Study of Reproduction >Expression of transgenic PPP1CC2 in the testis of Ppp1cc-null mice rescues spermatid viability and spermiation but does not restore normal sperm tail ultrastructure, sperm motility, or fertility.
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Expression of transgenic PPP1CC2 in the testis of Ppp1cc-null mice rescues spermatid viability and spermiation but does not restore normal sperm tail ultrastructure, sperm motility, or fertility.

机译:在无Ppp1cc小鼠的睾丸中表达转基因PPP1CC2可以挽救精子的生存能力和精子,但不能恢复正常的精子尾部超微结构,精子活力或生育能力。

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摘要

Two isoforms of phosphoprotein phosphatase 1, PPP1CC1 and PPP1CC2, are translated from alternatively spliced transcripts of a single gene, Ppp1cc, and differ only at their extreme C-termini. While PPP1CC1 expression is almost ubiquitous, PPP1CC2 is largely restricted to testicular germ cells and mature spermatozoa. Targeted deletion of Ppp1cc leads to sterility of -/- males due to a combination of gross structural defects in developing spermatids resulting in apoptosis and faulty spermiation. Because PPP1CC2 is the only PP1 isoform that demonstrates high-level expression in wild-type meiotic and postmeiotic male germ cells, we have tested whether its loss in Ppp1cc-/- males is largely responsible for manifestation of this phenotype by expressing PPP1CC2 transgenically in the testis of Ppp1cc-/- mice (rescue mice). Herein, we demonstrate that PPP1CC2 expression in the Ppp1cc-/- testis is antiapoptotic, thus reestablishing spermatid development and spermiation. However, because aberrant flagellar morphogenesis is incompletely ameliorated, rescue males remain infertile. Because these results suggest that expression of PPP1CC2 in developing germ cells is essential but insufficient for normal spermatogenesis to occur, appropriate spatial and temporal expression of both PPP1CC isoforms in the testis during spermatogenesis appears to be necessary to produce structurally normal fertility-competent spermatozoa.
机译:磷蛋白磷酸酶的两种同工型,即PPP1CC1和PPP1CC2,是从单个基因Ppp1cc的可变剪接转录本中翻译得到的,仅在其极端C末端不同。尽管PPP1CC1的表达几乎无处不在,但PPP1CC2很大程度上限于睾丸生殖细胞和成熟的精子。 Ppp1cc的靶向缺失导致-/-雄性不育,这是由于发育中的精子的总体结构缺陷的组合导致凋亡和精子功能不良。由于PPP1CC2是唯一在野生型减数分裂和减数分裂后的雄性生殖细胞中表现出高水平表达的PP1亚型,因此我们通过在转基因动物中转基因表达PPP1CC2来测试其在Ppp1cc-/-雄性中的丢失是否在很大程度上负责了该表型的表现。 Ppp1cc-/-小鼠(营救小鼠)的睾丸。在本文中,我们证明PPP1CC2在Ppp1cc-/-睾丸中的表达是抗凋亡的,从而重新建立了精子的发育和精子。但是,由于异常鞭毛形态发生没有得到完全改善,因此营救的雄性仍然不育。因为这些结果表明,在发育中的生殖细胞中PPP1CC2的表达是必不可少的,但不足以使正常的精子发生发生,因此在精子发生过程中睾丸中两种PPP1CC亚型的适当时空表达似乎对于产生结构上正常的能育精子是必要的。

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