pH, abscisic acid and the integration of metabolism in plants under stressed and non‐stressed conditions. II. Modifications in modes of metabolism induced by variation in the tension on the water column and by stress

The hydrolysis of ATP 4− by the plasmalemma and tonoplast H + /ATPases and \({\mathrm{P_{2}O}_{7}^{4{-}}}\) by the tonoplast pyrophosphatase results in the export of a proton to the apoplast or vacuole with \({\mathrm{HOPO}_{3}^{2{-}}}\) remaining in the cytoplasm. As the enzymes that synthesize ATP 4− require \({\mathrm{{(}HO{)}_{2}PO}_{2}^{{-}}}\) as a substrate it is proposed that protons are an essential substrate for ATP 4− synthesis. Thus, the entry of protons to the cytoplasm by sym‐ and antiports will control the rate of ATP 4− synthesis. Evidence is adduced that plants control the tension on the water column by removing water to or from the ‘cellular reservoir’ and guard cells by generating osmotic gradients. Schemes are presented that propose a series of metabolic changes that result in a seamless transition through the following states: (1) the import of K + , Cl − and water from the apoplast to the vacuole, the K + being admitted to the cytoplasm via a Ca 2+ ‐activated K + −H + symport and the water via a Ca 2+ ‐activated aquaporin; (2) the continued import of K + and water from the apoplast to the vacuole with the concomitant export of protons and the synthesis of malate from glucose in the cytoplasm for importation into the vacuole; (3) when the tension on the water column is optimal, respiration and photosynthesis is maximal resulting in biosynthetic reactions and growth; (4) when tension on the water column increases, K + , Cl − and water are exported from the vacuole to the apoplast; (5) the continued export of K + and water from the vacuole to the apoplast with malate for export being synthesized in the cytoplasm; the export of K + resulting in the acidification of the vacuole; and (6) a further increase in tension results in the deactivation of the plasmalemma H + /ATPase by a further increase in cytoplasmic Ca 2+ which also indirectly activates the alternative oxidase. It is suggested that mitochondrial pyruvate is partly oxidized by the TCA cycle and is partly exported to the cytoplasm where it is carboxylated to form malate 1− for continued export to the apoplast. K + is transferred from the vacuole to the apoplast, the K + being replaced by protons from the export of mitochondrial pyruvate. The maintenance of the tonoplast electrochemical gradient is thought to result in an increase in the pH of the apoplast which may cause the hydrolysis of abscisic acid precursors with the resulting abscisic acid opening Ca 2+ channels so that the above events are reinforced. (7) This mode is proposed to continue by the metabolism of glucose to four phosphoenolpyruvate, three of which are carboxylated to malate 1− for continued export to the apoplast with K + from the vacuole, the ‘stress‐tolerant quiescent state’.