Mahmoud Shima, Planes María Dolores, Cabedo Marc, Trujillo Cristina, Rienzo Alessandro, Caballero-Molada Marcos, Sharma Sukesh C, Montesinos Consuelo, Mulet José Miguel, Serrano Ramón
Instituto de Biología Molecular y Celular de Plantas, Universidad Politécnica de Valencia-Consejo Superior de Investigaciones Científicas, Spain.
FEBS Lett. 2017 Jul;591(13):1993-2002. doi: 10.1002/1873-3468.12673. Epub 2017 Jun 14.
We have identified in yeast a connection between two master regulators of cell growth: a biochemical connection involving the TORC1 protein kinase (which activates protein synthesis, nutrient uptake, and anabolism) and a biophysical connection involving the plasma membrane proton-pumping H -ATPase Pma1 (which drives nutrient and K uptake and regulates pH homeostasis). Raising the temperature to nonpermissive values in a TOR thermosensitive mutant decreases Pma1 activity. Rapamycin, a TORC1 inhibitor, inhibits Pma1 dependent on its receptor Fpr1 and on the protein phosphatase Sit4, a TORC1 effector. Mutation of either Sit4 or Tco89, a nonessential subunit of TORC1, decreases proton efflux, K uptake, intracellular pH, cell growth, and tolerance to weak organic acids. Tco89 does not affect Pma1 activity but activates K transport.
一种是涉及TORC1蛋白激酶的生化联系（该激酶激活蛋白质合成、营养物质摄取和合成代谢），另一种是涉及质膜质子泵H⁺-ATPase Pma1的生物物理联系（该泵驱动营养物质和钾的摄取并调节pH稳态）。在TOR温度敏感突变体中将温度升高到非允许值会降低Pma1活性。雷帕霉素是一种TORC1抑制剂，它通过其受体Fpr1和TORC1效应器蛋白磷酸酶Sit4来抑制Pma1。Sit4或TORC1的非必需亚基Tco89发生突变会降低质子外流、钾摄取、细胞内pH、细胞生长以及对弱有机酸的耐受性。Tco89不影响Pma1活性，但会激活钾转运。
