Peterson Francis C, Deng Qing, Zettl Markus, Prehoda Kenneth E, Lim Wendell A, Way Michael, Volkman Brian F
Department of Biochemistry, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
J Biol Chem. 2007 Mar 16;282(11):8446-53. doi: 10.1074/jbc.M609902200. Epub 2007 Jan 16.
The WASP-interacting protein (WIP) targets WASP/WAVE proteins through a constitutive interaction with an amino-terminal enabled/VASP homology (EVH1) domain. Parallel investigations had previously identified two distinct N-WASP binding motifs corresponding to WIP residues 451-461 and 461-485, and we determined the structure of a complex between WIP-(461-485) and the N-WASP EVH1 domain (Volkman, B. F., Prehoda, K. E., Scott, J. A., Peterson, F. C., and Lim, W. A. (2002) Cell 111, 565-576). The present results show that, when combined, the WIP-(451-485) sequence wraps further around the EVH1 domain, extending the interface observed previously. Specific contacts with three WIP epitopes corresponded to regions of high sequence conservation in the verprolin family. A central polyproline motif occupied the canonical binding site but in a reversed orientation relative to other EVH1 complexes. This interaction was augmented in the amino- and carboxyl-terminal directions by additional hydrophobic contacts involving WIP residues 454-459 and 475-478, respectively. Disruption of any of the three WIP epitopes reduced N-WASP binding in cells, demonstrating a functional requirement for the entire binding domain, which is significantly longer than the polyproline motifs recognized by other EVH1 domains.
WASP相互作用蛋白(WIP)通过与氨基末端Enabled/VASP同源(EVH1)结构域的组成性相互作用靶向WASP/WAVE蛋白。此前的平行研究已鉴定出两个不同的与WIP残基451 - 461和461 - 485相对应的N - WASP结合基序,并且我们确定了WIP - (461 - 485)与N - WASP EVH1结构域之间复合物的结构(Volkman, B. F., Prehoda, K. E., Scott, J. A., Peterson, F. C., and Lim, W. A. (2002) Cell 111, 565 - 576)。目前的结果表明,当结合在一起时,WIP - (451 - 485)序列进一步围绕EVH1结构域缠绕,扩展了先前观察到的界面。与三个WIP表位的特异性接触对应于verprolin家族中高序列保守区域。一个中央多聚脯氨酸基序占据了典型结合位点,但相对于其他EVH1复合物其方向相反。这种相互作用分别通过涉及WIP残基454 - 459和475 - 478的额外疏水接触在氨基末端和羧基末端方向上增强。破坏三个WIP表位中的任何一个都会降低细胞中N - WASP的结合,这表明整个结合结构域具有功能需求,该结构域明显长于其他EVH1结构域识别的多聚脯氨酸基序。