Behavior of ACRBP-deficient mouse sperm in the female reproductive tract
Behavior of ACRBP-deficient mouse sperm in the female reproductive tract
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DOI：
10.1262/jrd.2018-137
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发表时间：
2019-04-01
影响因子：
1.8
通讯作者：
Baba, Tadashi
中科院分区：
文献类型：
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作者：
Nagashima, Kiyoshi;Usui, Tomoyuki;Baba, Tadashi
ACRBP是一种位于精子顶体的前顶体蛋白结合蛋白，缺乏ACRBP的基因敲除小鼠由于顶体的异常形成而表现出男性生育力低下。在这项研究中，为了阐明导致低生育力表型的机制，我们研究了ACRBP缺陷小鼠精子在雌性生殖道中的行为。当对交配后迁移到子宫和输卵管的精子进行计数时，交配后小鼠输卵管中ACRBP缺陷精子的数量明显较少。然而，从输卵管中回收的ACRBP缺陷精子具有形态正常的头部形状，并保持正常的运动能力。重要的是，ACRBP缺陷精子成功获得未受精卵母细胞的能力显着降低。这些数据表明，ACRBP缺陷小鼠的雄性生育力低下可能归因于顶体反应的不完全性，而不是精子从子宫迁移到输卵管的障碍。
Gene-knockout mice lacking ACRBP, a proacrosin-binding protein localized in the acrosome of sperm, have been shown to exhibit male subfertility, owing to abnormal formation of the acrosome. In this study, to elucidate the mechanism contributing to the subfertility phenotype, we examined the behavior of ACRBP-deficient mouse sperm in the female reproductive tract. When sperm that had migrated into the uterus and oviduct after mating were counted, the number of ACRBP-deficient sperm was noticeably smaller in the oviduct of mice post mating. However, ACRBP-deficient sperm recovered from the oviduct possessed morphologically normal head shape and retained normal motility. Importantly, ACRBP-deficient sperm displayed a marked reduction in the ability to successfully gain access to unfertilized oocytes. These data suggest that male subfertility of ACRBP-deficient mice may be attributed to incompleteness of the acrosome reaction rather than impairment in sperm migration from the uterus to the oviduct.