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首页> 外文期刊>Molecular and Cellular Biology >Asthenozoospermia in Mice with Targeted Deletion of the Sperm Mitochondrion-Associated Cysteine-Rich Protein (Smcp) Gene
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Asthenozoospermia in Mice with Targeted Deletion of the Sperm Mitochondrion-Associated Cysteine-Rich Protein (Smcp) Gene

机译：精子线粒体相关的半胱氨酸丰富蛋白（Smcp）基因的靶向删除的小鼠弱精子症。

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The sperm mitochondria-associated cysteine-rich protein (SMCP) is a cysteine- and proline-rich structural protein that is closely associated with the keratinous capsules of sperm mitochondria in the mitochondrial sheath surrounding the outer dense fibers and axoneme. To investigate the function of SMCP, we generated mice with a targeted disruption of the gene Smcp by homologous recombination. Homozygous mutant males on a mixed genetic background (C57BL/6J × 129/Sv) are fully fertile, while they are infertile on the 129/Sv background, although spermatogenesis and mating are normal. Homozygous Smcp?/? female mice are fertile on both genetic backgrounds. Electron microscopical examination demonstrated normal structures of sperm head, mitochondria, and tail. In vivo experiments with sperm of Smcp?/? 129/Sv mice revealed that the migration of spermatozoa from the uterus into the oviduct is reduced. This result is supported by the observation that sperm motility as determined by the computer-assisted semen analysis system (CASA) is significantly affected as compared to wild-type spermatozoa. In vitro fertilization assays showed that Smcp-deficient spermatozoa are able to bind to the oocyte but that the number of fertilized eggs is reduced by more than threefold relative to the wild-type control. However, removal of the zona pellucida resulted in an unaffected sperm-egg fusion which was monitored by the presence of pronuclei and generation of blastocyts. These results indicate that the infertility of the male Smcp?/? mice on the 129/Sv background is due to reduced motility of the spermatozoa and decreased capability of the spermatozoa to penetrate oocytes.
机译：精子线粒体相关的富含半胱氨酸的蛋白（SMCP）是富含半胱氨酸和脯氨酸的结构蛋白，与围绕外部致密纤维和轴突的线粒体鞘中的精子线粒体的角质胶囊紧密相关。为了研究SMCP的功能，我们产生了通过同源重组靶向破坏 Smcp 基因的小鼠。混合遗传背景（C57BL / 6J×129 / Sv）上的纯合突变体雄性完全受精，而在129 / Sv背景上不育，尽管精子发生和交配是正常的。纯合子 Smcp ？/？ 雌性小鼠在两种遗传背景下均能繁殖。电子显微镜检查显示精子头，线粒体和尾巴的正常结构。对129 / Sv小鼠的 Smcp ？/？ 精子进行的体内实验表明，精子从子宫向输卵管的迁移减少了。与野生型精子相比，计算机辅助精液分析系统（CASA）所确定的精子运动力受到显着影响的观察结果支持了这一结果。体外受精试验表明， Smcp 缺陷型精子能够与卵母细胞结合，但受精卵的数量相对于野生型对照减少了三倍以上。然而，透明带的去除导致未受影响的精卵融合，其通过前核的存在和胚泡的产生来监测。这些结果表明在129 / Sv背景下雄性 Smcp ？/？ 小鼠的不育是由于精子运动力降低和精子渗透能力降低所致。卵母细胞。

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