Department of Cell Research and Immunology, Tel Aviv University, Ramat Aviv, Israel.
Biochem J. 2011 Nov 1;439(3):433-42. doi: 10.1042/BJ20111010.
EHDs [EH (Eps15 homology)-domain-containing proteins] participate in different stages of endocytosis. EHD2 is a plasma-membrane-associated EHD which regulates trafficking from the plasma membrane and recycling. EHD2 has a role in nucleotide-dependent membrane remodelling and its ATP-binding domain is involved in dimerization, which creates a membrane-binding region. Nucleotide binding is important for association of EHD2 with the plasma membrane, since a nucleotide-free mutant (EHD2 T72A) failed to associate. To elucidate the possible function of EHD2 during endocytic trafficking, we attempted to unravel proteins that interact with EHD2, using the yeast two-hybrid system. A novel interaction was found between EHD2 and Nek3 [NIMA (never in mitosis in Aspergillus nidulans)-related kinase 3], a serine/threonine kinase. EHD2 was also found in association with Vav1, a Nek3-regulated GEF (guanine-nucleotide-exchange factor) for Rho GTPases. Since Vav1 regulates Rac1 activity and promotes actin polymerization, the impact of overexpression of EHD2 on Rac1 activity was tested. The results indicated that wt (wild-type) EHD2, but not its P-loop mutants, reduced Rac1 activity. The inhibitory effect of EHD2 overexpression was partially rescued by co-expression of Rac1 as measured using a cholera toxin trafficking assay. The results of the present study strongly indicate that EHD2 regulates trafficking from the plasma membrane by controlling Rac1 activity.
EH 结构域蛋白(EH (Eps15 homology)-domain-containing proteins)参与胞吞作用的不同阶段。EHD2 是一种与质膜相关的 EHD,调节从质膜的运输和回收。EHD2 在核苷酸依赖的膜重塑中起作用,其 ATP 结合域参与二聚化,形成一个膜结合区。核苷酸结合对于 EHD2 与质膜的结合很重要,因为无核苷酸的突变体(EHD2 T72A)无法结合。为了阐明 EHD2 在胞吞作用中的可能功能,我们试图利用酵母双杂交系统阐明与 EHD2 相互作用的蛋白质。发现 EHD2 与 Nek3 [NIMA( Aspergillus nidulans 中的 never in mitosis)相关激酶 3]之间存在新的相互作用,Nek3 是一种丝氨酸/苏氨酸激酶。EHD2 还与 Vav1 相关,Vav1 是一种 Nek3 调节的 Rho GTPases 的鸟嘌呤核苷酸交换因子(guanine-nucleotide-exchange factor)。由于 Vav1 调节 Rac1 活性并促进肌动蛋白聚合,因此测试了过表达 EHD2 对 Rac1 活性的影响。结果表明,wt(野生型)EHD2,但不是其 P 环突变体,降低了 Rac1 活性。用霍乱毒素运输测定法测量时,用 Rac1 共表达部分挽救了 EHD2 过表达的抑制作用。本研究的结果强烈表明,EHD2 通过控制 Rac1 活性来调节从质膜的运输。