Parsons Maddy, Monypenny James, Ameer-Beg Simon M, Millard Thomas H, Machesky Laura M, Peter Marion, Keppler Melanie D, Schiavo Giampietro, Watson Rose, Chernoff Jonathan, Zicha Daniel, Vojnovic Borivoj, Ng Tony
Randall Centre, King's College London, 3rd Floor, New Hunt's House, Guy's Medical School Campus, London SE1 1UL, United Kingdom.
Mol Cell Biol. 2005 Mar;25(5):1680-95. doi: 10.1128/MCB.25.5.1680-1695.2005.
While a significant amount is known about the biochemical signaling pathways of the Rho family GTPase Cdc42, a better understanding of how these signaling networks are coordinated in cells is required. In particular, the predominant subcellular sites where GTP-bound Cdc42 binds to its effectors, such as p21-activated kinase 1 (PAK1) and N-WASP, a homolog of the Wiskott-Aldritch syndrome protein, are still undetermined. Recent fluorescence resonance energy transfer (FRET) imaging experiments using activity biosensors show inconsistencies between the site of local activity of PAK1 or N-WASP and the formation of specific membrane protrusion structures in the cell periphery. The data presented here demonstrate the localization of interactions by using multiphoton time-domain fluorescence lifetime imaging microscopy (FLIM). Our data here establish that activated Cdc42 interacts with PAK1 in a nucleotide-dependent manner in the cell periphery, leading to Thr-423 phosphorylation of PAK1, particularly along the lengths of cell protrusion structures. In contrast, the majority of GFP-N-WASP undergoing FRET with Cy3-Cdc42 is localized within a transferrin receptor- and Rab11-positive endosomal compartment in breast carcinoma cells. These data reveal for the first time distinct spatial association patterns between Cdc42 and its key effector proteins controlling cytoskeletal remodeling.
虽然我们对Rho家族GTP酶Cdc42的生化信号通路已经有了大量了解,但仍需要更好地理解这些信号网络在细胞中是如何协调的。特别是,结合了GTP的Cdc42与其效应蛋白(如p21激活激酶1(PAK1)和维斯科特-奥尔德里奇综合征蛋白的同源物N-WASP)结合的主要亚细胞位点仍未确定。最近使用活性生物传感器进行的荧光共振能量转移(FRET)成像实验表明,PAK1或N-WASP的局部活性位点与细胞周边特定膜突出结构的形成之间存在不一致。本文展示的数据通过多光子时域荧光寿命成像显微镜(FLIM)证明了相互作用的定位。我们的数据表明,活化的Cdc42在细胞周边以核苷酸依赖的方式与PAK1相互作用,导致PAK1的苏氨酸-423磷酸化,特别是沿着细胞突出结构的长度。相比之下,与Cy3-Cdc42发生FRET的大多数GFP-N-WASP定位于乳腺癌细胞中转铁蛋白受体和Rab11阳性的内体区室。这些数据首次揭示了Cdc42与其控制细胞骨架重塑的关键效应蛋白之间不同的空间关联模式。