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The caption to Figure 3 as published was incorrect. The correct caption appears below. Fig. 3. O 2 concentrations radially through 90-mm non-aerenchymatous, primary root of maize in 1% agar with shoots exposed to 21% O 2 (top curve) and 10% O 2 (bottom curve); the tracks were taken at 70 mm from the root-shoot junction (from Figure 6 of Armstrong et al. 1993). Temperature was 25°C. E indicates epidermis. O 2 concentrations were measured using a micro-platinum electrode and are presented as percentage O 2 in a gas phase at equilibrium with the solution.Abstract. Anoxia can be one consequence of waterlogging and submergence of plants. Anoxia in plant tissues reduces the rate of energy production by 65-97% compared with the rate in air. Thus, adaptation to anoxia always includes coping with an energy crisis. Tolerance to anoxia is relevant to wetland species, rice cultivation and transient waterlogging of other agricultural and horticultural crops. This perspective, in two parts, examines mechanisms of anoxia tolerance in plants. Part 1 covers anoxia tolerance in terms of growth and survival, the interaction of anoxia tolerance with other environmental factors, and the development of anoxic cores within plant tissues. Equally importantly, Part 1 also examines anaerobic carbohydrate catabolism (principally ethanolic fermentation in plants) and its regulation. We put forward two modes of anoxia tolerance, one based on reduced rates of anaerobic carbohydrate catabolism and the other on accelerated rates (Pasteur effect). Further, Part 1 examines mechanisms of post-anoxic injury. In Part 2 (Greenway and Gibbs, manuscript in preparation) we consider flow of the limited amount of energy produced under anoxia to processes essential for cell survival. We show that acclimation to anoxia in plants involves integration of a set of sophisticated characteristics, as a consequence of which the habitat within the anoxic cell is a very different world to that of the aerobic cell.

Anoxia in plant tissues results in an energy crisis (Gibbs and Greenway 2003). How anoxia-tolerant tissues cope with such an energy crisis is relevant not only to anoxia tolerance, but also to adverse conditions in air that cause an energy crisis.To survive an energy crisis, plant cells need to reduce their energy requirements for maintenance, and also direct the limited amount of energy produced during anaerobic catabolism to the energy-consuming processes that are critical to survival.We postulate that during anoxia, reductions in ion fluxes and protein turnover achieve economies in energy consumption. Processes receiving energy from the limited supply available under anoxia include synthesis of anaerobic proteins and energy-dependent substrate transport. Energy would also be required for maintenance of membrane integrity and for regulation of cytoplasmic pH (pHcyt). We suggest that a moderate decrease in the set point of pHcyt, from approximately 7.5 to approximately 7.0 is an acclimation to the energy crisis in anoxia-tolerant tissues. This decrease in the set point of pHcyt would favour metabolism of acclimative value, such as reduction in protein synthesis and stimulation of ethanolic fermentation. During anoxia lasting several days, a proportion of the scarce energy produced may need to be spent to mitigate the acidifying effect on pHcyt arising from fluxes of undissociated organic acids across the tonoplast as a consequence of high concentrations of organic acids in the vacuole. Increases in vacuolar pH (pHvac), with concomitant decreases in the vacuolar concentrations of undissociated acids, would mitigate such an 'acid load' on the cytoplasm. We present evidence that a preferential engagement of V-PPiases, over that of V-ATPases, may direct energy flow at the tonoplast to maintain pHcyt.We conclude that the likely causes of death under anoxia are firstly, a decrease in pHcyt below 7.0. Cytoplasmic acidosis occurs in several anoxia-intolerant tissues and may contribute to their death. Such adverse decreases in pHcyt can be mitigated by the biochemical pH stat. Secondly, deterioration in membrane selectivity culminating in loss of membrane integrity would be fatal. We suggest these two causes are not mutually exclusive but may act in concert.

Enzymes which are affected by the addition of inorganic salts during in vitro assay were extracted from salt-sensitive Phaseolus vulgaris, salt-tolerant Atriplex spongiosa, and Salicornia australis and tested for sensitivity to NaCl. In each case malate dehydrogenase, aspartate transaminase, glucose 6-phosphate dehydrogenase, and isocitrate dehydrogenase showed NaCl responses similar to those found for commercially available crystalline enzymes from other organisms. Enzymes extracted from plants grown in saline cultures showed no important changes in specific activity or salt sensitivity. Interaction of pH optima and NaCl concentrations suggests that enzymes may differ in the way they respond to salt treatment.

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