• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell motility and the cytoskeleton >Further studies on knockout mice lacking a functional dynein heavy chain (MDHC7). 2. A developmental explanation for the asthenozoospermia.
【24h】

Further studies on knockout mice lacking a functional dynein heavy chain (MDHC7). 2. A developmental explanation for the asthenozoospermia.

机译：对缺乏功能性动力蛋白重链（MDHC7）的基因敲除小鼠的进一步研究。 2.对弱精子症的发育解释。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Male mice had been previously generated in which the inner dynein arm heavy chain 7 gene (MDHC7) was disrupted. MDHC7(-/-) animals show asthenozoospermia and are sterile. Very few of their spermatozoa can achieve forward progression, but for those that can, we add here the information (1) that the three-dimensional aspects of their movement are normal; (2) that their maximum velocity is less than that of wild-type controls; and (3) that they are entirely unable to penetrate media of raised viscosity (25-4,000 cP). However, the large majority of the spermatozoa can achieve only a low amplitude vibration. In these sperm we find, using electron microscopy, that the outer dense fibres retain attachments to the inner surface of the mitochondria. Such attachments are present in normal epididymal mouse spermatozoa but are broken down as soon as the sperm become motile on release from the epididymis. The attachments are presumed to be essential during midpiece development and, afterwards, to require a threshold level of force to loosen them and so permit the sliding displacements necessary for normal bending. We presume that the disruption of the inner dynein arm heavy chain gene, MDHC7, means that there is insufficient force to overcome the attachments, for all but a few spermatozoa. Cell Motil. Cytoskeleton 61:74-82, 2005. (c) 2005 Wiley-Liss, Inc.
机译：先前已经产生了雄性小鼠，其中内部动力动力臂重链7基因（MDHC7）被破坏。 MDHC7（-/-）动物表现出弱精子症并且是不育的。他们的精子很少能向前发展，但对于那些精子，我们在这里添加以下信息：（1）他们运动的三维方面是正常的; （2）它们的最大速度小于野生型对照的最大速度; （3）它们完全无法渗透粘度升高（25-4,000 cP）的介质。但是，绝大多数的精子只能达到低振幅的振动。在这些精子中，我们使用电子显微镜发现，外部致密纤维保留了与线粒体内表面的附着。此类附件存在于正常附睾小鼠的精子中，但一旦精子从附睾中释放出来，它们就开始活动。假定附件在中间件​​开发过程中是必不可少的，然后需要一个阈值的力才能使其松开，从而允许正常弯曲所必需的滑动位移。我们认为，内部动力蛋白重链基因MDHC7的破坏意味着除少数精子外，没有足够的力来克服附着力。细胞动力。 Cytoskeleton 61：74-82，2005.（c）2005 Wiley-Liss，Inc.

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号