Department of Reproductive Biology, National Center for Child Health and Development, 2-10-1 Okura, Setagaya, Tokyo 157-8535, Japan.
Sci Rep. 2011;1:68. doi: 10.1038/srep00068. Epub 2011 Aug 19.
When a sperm and an oocyte unite upon fertilization, their cell membranes adhere and fuse, but little is known about the factors regulating sperm-oocyte adhesion. Here we explored the role of β-catenin in sperm-oocyte adhesion. Biochemical analysis revealed that E-cadherin and β-catenin formed a complex in oocytes and also in sperm. Sperm-oocyte adhesion was impaired when β-catenin-deficient oocytes were inseminated with sperm. Furthermore, expression of β-catenin decreased from the sperm head and the site of an oocyte to which a sperm adheres after completion of sperm-oocyte adhesion. UBE1-41, an inhibitor of ubiquitin-activating enzyme 1, inhibited the degradation of β-catenin, and reduced the fusing ability of wild-type (but not β-catenin-deficient) oocytes. These results indicate that β-catenin is not only involved in membrane adhesion, but also in the transition to membrane fusion upon fertilization.
当精子和卵子在受精时结合,它们的细胞膜会黏附并融合,但对于调节精子-卵子黏附的因素知之甚少。在这里,我们探讨了β-连环蛋白在精子-卵子黏附中的作用。生化分析显示,E-钙黏蛋白和β-连环蛋白在卵子中和精子中都形成复合物。当β-连环蛋白缺陷的卵子与精子受精时,精子-卵子黏附受到损害。此外,β-连环蛋白的表达在精子-卵子黏附完成后,从精子头部和附着精子的卵子部位减少。UBE1-41,一种泛素激活酶 1 的抑制剂,抑制了β-连环蛋白的降解,并降低了野生型(而非β-连环蛋白缺陷型)卵子的融合能力。这些结果表明,β-连环蛋白不仅参与了膜黏附,而且还参与了受精时向膜融合的转变。