Srivastava J, Barreiro G, Groscurth S, Gingras A R, Goult B T, Critchley D R, Kelly M J S, Jacobson M P, Barber D L
Department of Cell and Tissue Biology, University of California, San Francisco, CA 94143, USA.
Proc Natl Acad Sci U S A. 2008 Sep 23;105(38):14436-41. doi: 10.1073/pnas.0805163105. Epub 2008 Sep 9.
Actin filament binding by the focal adhesion (FA)-associated protein talin stabilizes cell-substrate adhesions and is thought to be rate-limiting in cell migration. Although F-actin binding by talin is known to be pH-sensitive in vitro, with lower affinity at higher pH, the functional significance of this pH dependence is unknown. Because increased intracellular pH (pH(i)) promotes cell migration and is a hallmark of metastatic carcinomas, we asked whether it increases FA remodeling through lower-affinity talin-actin binding. Talin contains several actin binding sites, but we found that only the COOH-terminal USH-I/LWEQ module showed pH-dependent actin binding, with lower affinity and decreased maximal binding at higher pH. Molecular dynamics simulations and NMR of this module revealed a structural mechanism for pH-dependent actin binding. A cluster of titratable amino acids with upshifted pK(a) values, including His-2418, was identified at one end of the five-helix bundle distal from the actin binding site. Protonation of His-2418 induces changes in the conformation and dynamics of the remote actin binding site. Structural analyses of a mutant talin-H2418F at pH 6.0 and 8.0 suggested changes different from the WT protein, and we confirmed that actin binding by talin-H2418F was relatively pH-insensitive. In motile fibroblasts, increasing pH(i) decreased FA lifetime and increased the migratory rate. However, expression of talin-H2418F increased lifetime 2-fold and decreased the migratory rate. These data identify a molecular mechanism for pH-sensitive actin binding by talin and suggest that FA turnover is pH-dependent and in part mediated by pH-dependent affinity of talin for binding actin.
黏着斑(FA)相关蛋白踝蛋白与肌动蛋白丝的结合可稳定细胞与底物的黏附,并且被认为是细胞迁移的限速步骤。虽然已知踝蛋白与F-肌动蛋白的结合在体外对pH敏感,在较高pH下亲和力较低,但这种pH依赖性的功能意义尚不清楚。由于细胞内pH值(pH(i))升高会促进细胞迁移,并且是转移性癌的一个标志,我们研究了它是否通过降低踝蛋白-肌动蛋白的结合亲和力来增加黏着斑重塑。踝蛋白包含多个肌动蛋白结合位点,但我们发现只有COOH末端的USH-I/LWEQ模块显示出pH依赖性肌动蛋白结合,在较高pH下亲和力较低且最大结合量减少。该模块的分子动力学模拟和核磁共振揭示了pH依赖性肌动蛋白结合的结构机制。在远离肌动蛋白结合位点的五螺旋束一端,鉴定出一组pK(a)值上移的可滴定氨基酸簇,包括His-2418。His-2418的质子化会诱导远端肌动蛋白结合位点的构象和动力学发生变化。对pH 6.0和8.0条件下的突变体踝蛋白-H2418F进行结构分析,结果表明其变化与野生型蛋白不同,并且我们证实踝蛋白-H2418F与肌动蛋白的结合相对不依赖于pH。在运动的成纤维细胞中,升高pH(i)会缩短黏着斑寿命并提高迁移速率。然而,踝蛋白-H2418F的表达使黏着斑寿命增加了2倍,并降低了迁移速率。这些数据确定了踝蛋白对pH敏感的肌动蛋白结合的分子机制,并表明黏着斑更新是pH依赖性的,部分由踝蛋白结合肌动蛋白的pH依赖性亲和力介导。