Instituto de Biología Molecular y Celular de Plantas, Universidad Politécnica de Valencia-Consejo Superior de Investigaciones Científicas, Camino de Vera, Valencia, Spain.
Plant J. 2012 May;70(4):704-16. doi: 10.1111/j.1365-313X.2012.04921.x. Epub 2012 Mar 6.
Intracellular pH must be kept close to neutrality to be compatible with cellular functions, but the mechanisms of pH homeostasis and the responses to intracellular acidification are mostly unknown. In the plant Arabidopsis thaliana, we found that intracellular acid stress generated by weak organic acids at normal external pH induces expression of several chaperone genes, including ROF2, which encodes a peptidyl-prolyl cis-trans isomerase of the FK506-binding protein class. Loss of function of ROF2, and especially double mutation of ROF2 and the closely related gene ROF1, results in acid sensitivity. Over-expression of ROF2 confers tolerance to intracellular acidification by increasing proton extrusion from cells. The activation of the plasma membrane proton pump (H(+) -ATPase) is indirect: over-expression of ROF2 activates K(+) uptake, causing depolarization of the plasma membrane, which activates the electrogenic H(+) pump. The depolarization of ROF2 over-expressing plants explains their tolerance to toxic cations such as lithium, norspermidine and hygromycin B, whose uptake is driven by the membrane potential. As ROF2 induction and intracellular acidification are common consequences of many stresses, this mechanism of pH homeostasis may be of general importance for stress tolerance.
细胞内 pH 值必须保持接近中性，以适应细胞功能，但 pH 值稳态的机制和细胞内酸化的反应大多未知。在植物拟南芥中，我们发现正常外部 pH 值下弱有机酸产生的细胞内酸应激诱导包括 ROF2 在内的几个伴侣基因的表达，ROF2 编码 FK506 结合蛋白类的肽基脯氨酰顺反异构酶。ROF2 的功能丧失，特别是 ROF2 和密切相关的基因 ROF1 的双突变，导致对酸敏感。ROF2 的过表达通过增加质子从细胞中排出，赋予细胞对细胞内酸化的耐受性。质膜质子泵（H(+) -ATPase）的激活是间接的：ROF2 的过表达激活 K(+) 摄取，导致质膜去极化，从而激活电致质子泵。ROF2 过表达植物的去极化解释了它们对毒性阳离子（如锂、腐胺和 Hygromycin B）的耐受性，这些阳离子的摄取是由膜电位驱动的。由于 ROF2 的诱导和细胞内酸化是许多应激的常见后果，这种 pH 值稳态机制可能对应激耐受性具有普遍重要性。
