Department of Cell Biology and Cell Dynamics Program, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Cytoskeleton (Hoboken). 2010 Jun;67(6):346-64. doi: 10.1002/cm.20449.
Supervillin, the largest member of the villin/gelsolin/flightless family, is a peripheral membrane protein that regulates each step of cell motility, including cell spreading. Most known interactors bind within its amino (N)-terminus. We show here that the supervillin carboxy (C)-terminus can be modeled as supervillin-specific loops extending from gelsolin-like repeats plus a villin-like headpiece. We have identified 27 new candidate interactors from yeast two-hybrid screens. The interacting sequences from 12 of these proteins (BUB1, EPLIN/LIMA1, FLNA, HAX1, KIF14, KIFC3, MIF4GD/SLIP1, ODF2/Cenexin, RHAMM, STARD9/KIF16A, Tks5/SH3PXD2A, TNFAIP1) co-localize with and mis-localize EGFP-supervillin in mammalian cells, suggesting associations in vivo. Supervillin-interacting sequences within BUB1, FLNA, HAX1, and MIF4GD also mimic supervillin over-expression by inhibiting cell spreading. Most new interactors have known roles in supervillin-associated processes, e.g. cell motility, membrane trafficking, ERK signaling, and matrix invasion; three (KIF14, KIFC3, STARD9/KIF16A) have kinesin motor domains; and five (EPLIN, KIF14, BUB1, ODF2/cenexin, RHAMM) are important for cell division. GST fusions of the supervillin G2-G3 or G4-G6 repeats co-sediment KIF14 and EPLIN, respectively, consistent with a direct association. Supervillin depletion leads to increased numbers of bi- and multi-nucleated cells. Cytokinesis failure occurs predominately during early cytokinesis. Supervillin localizes with endogenous myosin II and EPLIN in the cleavage furrow, and overlaps with the oncogenic kinesin, KIF14, at the midbody. We conclude that supervillin, like its interactors, is important for efficient cytokinesis. Our results also suggest that supervillin and its interaction partners coordinate actin and microtubule motor functions throughout the cell cycle.
超级微丝蛋白是微丝丝束蛋白/凝胶蛋白/无翅型家族中最大的成员,是一种调节细胞运动各个步骤的外周膜蛋白,包括细胞铺展。大多数已知的相互作用蛋白结合在其氨基(N)端。我们在这里表明,超级微丝蛋白的羧基(C)端可以模拟为从凝胶蛋白样重复序列加上微丝蛋白样头部延伸的超级微丝蛋白特异性环。我们已经从酵母双杂交筛选中鉴定出 27 个新的候选相互作用蛋白。从这 12 个蛋白质的相互作用序列(BUB1、EPLIN/LIMA1、FLNA、HAX1、KIF14、KIFC3、MIF4GD/SLIP1、ODF2/Cenexin、RHAMM、STARD9/KIF16A、Tks5/SH3PXD2A、TNFAIP1)中,有 12 个在哺乳动物细胞中与 EGFP-超级微丝蛋白共定位并发生定位错误,提示其在体内存在关联。BUB1、FLNA、HAX1 和 MIF4GD 中的超级微丝蛋白相互作用序列也通过抑制细胞铺展模拟超级微丝蛋白的过度表达。大多数新的相互作用蛋白在超级微丝蛋白相关过程中具有已知的作用,例如细胞运动、膜运输、ERK 信号和基质侵袭;三个(KIF14、KIFC3、STARD9/KIF16A)具有驱动蛋白马达结构域;而五个(EPLIN、KIF14、BUB1、ODF2/cenexin、RHAMM)对细胞分裂很重要。超级微丝蛋白 G2-G3 或 G4-G6 重复的 GST 融合物分别与 KIF14 和 EPLIN 共沉淀,这与直接关联一致。超级微丝蛋白耗竭导致双核和多核细胞数量增加。有丝分裂失败主要发生在早期有丝分裂过程中。超级微丝蛋白与内源性肌球蛋白 II 和 EPLIN 在分裂沟中定位,并与致癌驱动蛋白 KIF14 在中体处重叠。我们得出的结论是,超级微丝蛋白与它的相互作用蛋白一样,对于有效的有丝分裂很重要。我们的结果还表明,超级微丝蛋白及其相互作用伙伴在整个细胞周期中协调肌动蛋白和微管马达功能。