Yeast Physiology Group, Department of Genetics and Microbiology, Facultad de Biología, Universidad de Murcia, 30071, Murcia, Spain.
Instituto de Biología Funcional y Genómica (IBFG), Consejo Superior de Investigaciones Científicas/Departamento de Microbiología y Genética, Universidad de Salamanca, 37007, Salamanca, Spain.
Sci Rep. 2017 Jul 20;7(1):6057. doi: 10.1038/s41598-017-06053-x.
The final step in post-translational processing of Ras and Rho GTPases involves methylation of the prenylated cysteine residue by an isoprenylcysteine-O-carboxyl methyltransferase (ICMT). ICMT activity is essential for cell growth and development in higher eukaryotes, and inhibition of GTPase methylation has become an attractive target in cancer therapy to inactivate prenylated oncoproteins. However, the specificity and dynamics of the GTPase methylation process remain to be fully clarified. Notably, cells lacking Mam4, the ICMT ortholog in the fission yeast Schizosaccharomyces pombe, are viable. We have exploited this feature to analyze the role of methylation on GTPase localization and function. We show that methylation differentially affects GTPase membrane localization, being particularly relevant for plasma membrane tethering and downstream signaling of palmitoylated and farnesylated GTPases Ras1 and Rho2 lacking C-terminal polybasic motifs. Indeed, Ras1 and Rho2 cysteine methylation is required for proper regulation of differentiation elicited by MAPK Spk1 and for stress-dependent activation of the cell integrity pathway (CIP) and its main effector MAPK Pmk1. Further, Mam4 negatively regulates TORC2 signaling by a cross-inhibitory mechanism relying on Rho GTPase methylation. These results highlight the requirement for a tight control of GTPase methylation in vivo to allow adequate GTPase function.
Ras 和 Rho GTPases 翻译后加工的最后一步涉及异戊烯基半胱氨酸-O-羧基甲基转移酶(ICMT)对 prenylated cysteine 残基的甲基化。在高等真核生物中,ICMT 活性对于细胞生长和发育至关重要,并且抑制 GTPase 甲基化已成为癌症治疗中失活 prenylated 癌蛋白的有吸引力的靶标。然而,GTPase 甲基化过程的特异性和动力学仍有待充分阐明。值得注意的是,裂殖酵母 Schizosaccharomyces pombe 中 ICMT 的同源物 Mam4 缺失的细胞是可行的。我们利用这一特征来分析甲基化对 GTPase 定位和功能的作用。我们表明,甲基化对 GTPase 的膜定位有差异影响,特别是对于 palmitoylated 和 farnesylated GTPases Ras1 和 Rho2 的质膜锚定和下游信号转导具有重要意义,这些 GTPases 缺乏 C 端多碱性基序。事实上,Ras1 和 Rho2 半胱氨酸甲基化对于 MAPK Spk1 引发的分化的适当调节以及应激依赖性细胞完整性途径(CIP)及其主要效应物 MAPK Pmk1 的激活是必需的。此外,Mam4 通过依赖 Rho GTPase 甲基化的交叉抑制机制负调控 TORC2 信号。这些结果强调了在体内对 GTPase 甲基化进行严格控制以允许适当的 GTPase 功能的必要性。