Fig. 1.
Regulations of sugar catabolism, fermentation, glycolysis, and major amino acid metabolism associated with NAD(P)+ regeneration and ATP production in terrestrial and wetland plants under O2-deficient conditions. Blue arrows and letters indicate the reactions and enzymes in the up-regulated pathways when the mitochondrial electron transport and the TCA-cycle flux decrease under O2-deficient conditions. Red letters indicate the regeneration of NAD(P)+ from NAD(P)H. In rice plants, the blue pathways contribute to their tolerance to long-term O2 deficiency compared with the terrestrial plants. Some wetland plants such as rice also have a high ability to optimally regulate the pyruvate level by activation of pyrophosphate (PPi)-dependent phosphofructokinase (PFK-PPi) and pyruvate phosphate dikinase (PPDK) that consume PPi instead of ATP for energy conservation. Besides glycolysis, PPi is consumed to regulate the cytosolic pH by the tonoplast H+-pumping pyrophosphatase (H+-PPiase) instead of H+-ATPase in wetland plants. Although two independent pathways for sucrose degradation contribute to the regulation of glycolytic flux in both terrestrial and wetland plants, the UDP-dependent sucrose synthase (SuSy) pathway is regarded as energetically more advantageous for survival under O2-deficient conditions than the invertase (INV) pathway because here, PPi is utilized instead of ATP. Sugar supply to glycolysis through starch mobilization is observed in species with developed storage organs such as tuber, rhizome, and endosperm. In NAD(P)H regeneration during the metabolisms of 2-oxoglutarate and glutamate associated with γ-aminobutyric acid (GABA) production, the glutamate dehydrogenase (GDH) pathway without ATP consumption is more efficient in energy consumption than the NAD(P)H-dependent glutamine: 2-oxoglutarate aminotransferase (GOGAT) pathway with ATP consumption. The accumulation of some amino acids such as GABA, alanine, and glutamate play an important role in avoiding carbohydrate loss not only during O2-deficient conditions but also during the recovery phase of re-oxygenation after hypoxia/anoxia. Alanine accumulation by alanine aminotransferase (AlaAT) can operate non-circular TCA-cycle and gluconeogenesis under O2 deficiency and re-oxygenation. Abbreviations are as follows: ADH, alcohol dehydrogenase; AlaAT, alanine aminotransferase; ALDH, acetaldehyde dehydrogenase; AspAT, aspartate aminotransferase; CoASH, coenzyme A; FK, fructokinase; GABA-T, GABA transaminase; GAD, glutamate decarboxylase; GHBDH, γ-aminobutyrate dehydrogenase; Glucose-1-P, glucose-1-phosphate; GS, glutamine synthetase; HXK, hexokinase; LDH lactate dehydrogenase; MDH, malate dehydrogenase; PCK, phosphoenolpyruvate carboxykinase; PDC, pyruvate decarboxylase; PDH; pyruvate dehydrogenase; PEPC, phosphoenolpyruvate carboxylase; PFK, ATP-dependent phosphofructokinase; PFK-PPi, PPi-dependent phosphofructokinase; PGI, phosphoglucoisomerase; PGM, phosphoglucomutase; Pi, phosphate; PK, pyruvate kinase; PPDK, pyruvate Pi dikinase; SSADH, succinate semialdehyde dehydrogenase; Starch Pase, starch phosphorylase; TCA, tricarboxylic acid; UDP, uridine diphosphate; UGPPase, UDP-glucose pyrophosphorylase; UTP, uridine triphosphate