Expression of TEX101, regulated by ACE, is essential for the production of fertile mouse spermatozoa
Expression of TEX101, regulated by ACE, is essential for the production of fertile mouse spermatozoa
复制标题
DOI：
10.1073/pnas.1222166110
复制
发表时间：
2013-05-14
影响因子：
11.1
通讯作者：
Okabe, Masaru
中科院分区：
文献类型：
--
作者：
Fujihara, Yoshitaka;Tokuhiro, Keizo;Okabe, Masaru
正常形状、数量和活力的精子的形成不足以满足雄性幼崽的繁殖。精子必须具备良好的受精能力。我们发现，睾丸表达基因101(Tex 101)突变的男性产生的精子外观正常，但不具备受精能力，并伴有精子膜上去整合素和金属肽酶结构域3(ADAM3)的缺失。研究还发现，精子上TEX101的存在受血管紧张素转换酶(ACE)的调节。ACE去除GPI锚定蛋白TEX101是产生可育精子所必需的，而ACE的功能并不依赖于其众所周知的肽酶活性。TEX101作为一种独特的ACE特异性底物的发现，可能为生产期待已久的男性避孕药提供一个潜在的靶点。
Formation of spermatozoa of normal shape, number, and motility is insufficient for the male siring of pups. The spermatozoa must be accompanied by sound fertilizing ability. We found that males with disrupted testis-expressed gene 101 (Tex101) produce normal-looking but fertilization-incompetent spermatozoa, which were accompanied by a deficiency of a disintegrin and metallopeptidase domain 3 (ADAM3) on sperm plasma membrane. It was also found that the existence of TEX101 on spermatozoa was regulated by angiotensin-converting enzyme (ACE). The removal of GPI-anchored protein TEX101 by ACE was essential to produce fertile spermatozoa, and the function of ACE was not depending on its well-known peptidase activity. The finding of TEX101 as a unique specific substrate for ACE may provide a potential target for the production of an awaited contraceptive medicine for men.