Baessler Keith A, Lee Younjoo, Sampson Nicole S
Biochemistry and Structural Biology Graduate Program, Stony Brook University, Stony Brook, NY 11794, USA.
ACS Chem Biol. 2009 May 15;4(5):357-66. doi: 10.1021/cb900013d.
We investigated the role of beta(1) integrin in mammalian fertilization and the mode of inhibition of fertilinbeta-derived polymers. We determined that polymers displaying the Glu-Cys-Asp peptide from the fertilinbeta disintegrin domain mediate inhibition of mammalian fertilization through a beta(1) integrin receptor on the egg surface. Inhibition of fertilization is a consequence of competition with sperm binding to the cell surface, not activation of an egg-signaling pathway. The presence of the beta(1) integrin on the egg surface increases the rate of sperm attachment but does not alter the total number of sperm that can attach or fuse to the egg. We conclude that the presence of beta(1) integrin enhances the initial adhesion of sperm to the egg plasma membrane and that subsequent attachment and fusion are mediated by additional egg and sperm proteins present in the beta(1) integrin complex. Therefore, the mechanisms by which sperm fertilize wild-type and beta(1) knockout eggs are different.
我们研究了β(1)整合素在哺乳动物受精过程中的作用以及抑制受精素β衍生聚合物的方式。我们确定，展示来自受精素β解整合素结构域的Glu-Cys-Asp肽的聚合物通过卵表面的β(1)整合素受体介导对哺乳动物受精的抑制作用。受精抑制是与精子结合到细胞表面竞争的结果，而非激活卵信号通路。卵表面β(1)整合素的存在增加了精子附着的速率，但不改变能够附着或融合到卵上的精子总数。我们得出结论，β(1)整合素的存在增强了精子对卵质膜的初始黏附，并且随后的附着和融合由β(1)整合素复合物中存在的其他卵和精子蛋白介导。因此，精子使野生型卵和β(1)敲除卵受精的机制是不同的。
