Rajmohan Rajamuthiah, Meng Lei, Yu Shangjuan, Thanabalu Thirumaran
School of Biological Sciences, Nanyang Technological University, Singapore 637551, Republic of Singapore.
Biochem Biophys Res Commun. 2006 Apr 7;342(2):529-36. doi: 10.1016/j.bbrc.2006.01.160. Epub 2006 Feb 8.
Wiskott-Aldrich syndrome is caused by alterations in the Wiskott-Aldrich syndrome protein (WASP) and several of these mutations affect WASP's interaction with WIP (WASP-interacting protein), suggesting that loss of interaction between WASP and WIP is causal to the disease. Las17p is the yeast homologue of WASP and las17Delta strain is unable to grow at 37 degrees C. We show that Human WASP suppresses the growth defect of Saccharomyces cerevisiae las17Delta strain, only in the presence of WIP. WIP mediates cortical localisation of WASP as well as stabilise WASP in yeast cells. Mutations which affected WASP-WIP interaction abolished WASP's ability to suppress the growth defect of las17Delta strain. We have demonstrated that WASP-WIP is an active complex and WASP's ability to suppress the growth defect of las17Delta strain is dependent on the presence of a functional Arp2/3 activating domain of WASP and also the Verprolin domain (V) of WIP.
威斯科特-奥尔德里奇综合征由威斯科特-奥尔德里奇综合征蛋白（WASP）的改变引起，其中一些突变影响WASP与WIP（WASP相互作用蛋白）的相互作用，这表明WASP与WIP之间相互作用的丧失是该疾病的病因。Las17p是WASP的酵母同源物，las17Δ菌株在37℃下无法生长。我们发现，只有在WIP存在的情况下，人WASP才能抑制酿酒酵母las17Δ菌株的生长缺陷。WIP介导WASP在酵母细胞中的皮质定位并稳定WASP。影响WASP-WIP相互作用的突变消除了WASP抑制las17Δ菌株生长缺陷的能力。我们已经证明，WASP-WIP是一个活性复合物，WASP抑制las17Δ菌株生长缺陷的能力取决于WASP功能性Arp2/3激活结构域的存在以及WIP的维普洛林结构域（V）。
