Kametaka Satoshi, Mattera Rafael, Bonifacino Juan S
Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Building 18T/Room 101, National Institutes of Health, Bethesda, MD 20892, USA.
Mol Cell Biol. 2005 Sep;25(18):7988-8000. doi: 10.1128/MCB.25.18.7988-8000.2005.
The Golgi-localized, Gamma-ear-containing, Arf-binding (GGA) proteins are monomeric clathrin adaptors that mediate the sorting of transmembrane cargo at the trans-Golgi network and endosomes. Here we report that one of these proteins, GGA3, becomes transiently phosphorylated upon activation of the epidermal growth factor (EGF) receptor. This phosphorylation takes place on a previously unrecognized site in the "hinge" segment of the protein, S368, and is strictly dependent on the constitutive phosphorylation of another site, S372. The EGF-induced phosphorylation of S368 does not require internalization of the EGF receptor or association of GGA3 with membranes. This phosphorylation can be blocked by inhibitors of both the mitogen-activated protein kinase and phosphatidylinositol 3-kinase pathways that function downstream of the activated EGF receptor. Phosphorylation of GGA3 on S368 causes an increase in the hydrodynamic radius of the protein, indicating a transition to a more asymmetric shape. Mutation of S368 and S372 to a phosphomimic aspartate residue decreases the association of GGA3 with membranes. These observations indicate that EGF signaling elicits phosphorylation events that regulate the association of GGA3 with organellar membranes.
高尔基体定位、含γ耳、Arf结合(GGA)蛋白是单体网格蛋白衔接蛋白,介导跨膜货物在反式高尔基体网络和内体中的分选。在此我们报告,这些蛋白之一GGA3在表皮生长因子(EGF)受体激活后会发生瞬时磷酸化。这种磷酸化发生在该蛋白“铰链”区一个先前未被识别的位点S368上,并且严格依赖于另一个位点S372的组成性磷酸化。EGF诱导的S368磷酸化不需要EGF受体内化或GGA3与膜的结合。这种磷酸化可被在活化的EGF受体下游起作用的丝裂原活化蛋白激酶和磷脂酰肌醇3激酶途径的抑制剂阻断。GGA3在S368上的磷酸化导致该蛋白的流体动力学半径增加,表明其转变为更不对称的形状。将S368和S372突变为模拟磷酸化的天冬氨酸残基会降低GGA3与膜的结合。这些观察结果表明,EGF信号传导引发磷酸化事件,从而调节GGA3与细胞器膜的结合。