Hill Kirsti, Krugmann Sonja, Andrews Simon R, Coadwell W John, Finan Peter, Welch Heidi C E, Hawkins Phillip T, Stephens Len R
Inositide Laboratory, The Babraham Institute, Babraham Research Campus, Cambridge CB2 4AT, United Kingdom.
J Biol Chem. 2005 Feb 11;280(6):4166-73. doi: 10.1074/jbc.M411262200. Epub 2004 Nov 15.
P-Rex1 is a guanine-nucleotide exchange factor (GEF) for the small GTPase Rac. We have investigated here the mechanisms of stimulation of P-Rex1 Rac-GEF activity by the lipid second messenger phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5)P3) and the Gbetagamma subunits of heterotrimeric G proteins. We show that a P-Rex1 mutant lacking the PH domain (DeltaPH) cannot be stimulated by PtdIns(3,4,5)P3, which implies that the PH domain confers PtdIns(3,4,5)P3 regulation of P-Rex1 Rac-GEF activity. Consistent with this, we found that PtdIns(3,4,5)P3 binds to the PH domain of P-Rex1 and that the DH/PH domain tandem is sufficient for PtdIns(3,4,5)P3-stimulated P-Rex1 activity. The Rac-GEF activities of the DeltaPH mutant and the DH/PH domain tandem can both be stimulated by Gbetagamma subunits, which infers that Gbetagamma subunits regulate P-Rex1 activity by binding to the catalytic DH domain. Deletion of the DEP, PDZ, or inositol polyphosphate 4-phosphatase homology domains has no major consequences on the abilities of either PtdIns(3,4,5)P3 or Gbetagamma subunits to stimulate P-Rex1 Rac-GEF activity. However, the presence of any of these domains impacts on the levels of basal and/or stimulated P-Rex1 Rac-GEF activity, suggesting that there are important functional interactions between the DH/PH domain tandem and the DEP, PDZ, and inositol polyphosphate 4-phosphatase homology domains of P-Rex1.
P-Rex1是小GTP酶Rac的鸟嘌呤核苷酸交换因子(GEF)。我们在此研究了脂质第二信使磷脂酰肌醇(3,4,5)-三磷酸(PtdIns(3,4,5)P3)和异源三聚体G蛋白的Gβγ亚基刺激P-Rex1 Rac-GEF活性的机制。我们发现,缺乏PH结构域的P-Rex1突变体(DeltaPH)不能被PtdIns(3,4,5)P3刺激,这意味着PH结构域赋予了PtdIns(3,4,5)P3对P-Rex1 Rac-GEF活性的调节作用。与此一致的是,我们发现PtdIns(3,4,5)P3与P-Rex1的PH结构域结合,并且DH/PH结构域串联足以实现PtdIns(3,4,5)P3刺激的P-Rex1活性。DeltaPH突变体和DH/PH结构域串联的Rac-GEF活性都可以被Gβγ亚基刺激,这表明Gβγ亚基通过与催化性DH结构域结合来调节P-Rex1活性。缺失DEP、PDZ或肌醇多磷酸4-磷酸酶同源结构域对PtdIns(3,4,5)P3或Gβγ亚基刺激P-Rex1 Rac-GEF活性的能力没有重大影响。然而,这些结构域中的任何一个的存在都会影响基础和/或刺激后的P-Rex1 Rac-GEF活性水平,这表明P-Rex1的DH/PH结构域串联与DEP、PDZ和肌醇多磷酸4-磷酸酶同源结构域之间存在重要的功能相互作用。