Background: Water deficit (WD) decreases photosynthetic rate (A) via decreased stomatal conductance to CO(2) (g(s)) and photosynthetic metabolic potential (A(pot)). The relative importance of g(s) and A(pot), and how they are affected by WD, are reviewed with respect to light intensity and to experimental approaches.
Scope and conclusions: With progressive WD, A decreases as g(s) falls. Under low light during growth and WD, A is stimulated by elevated CO(2), showing that metabolism (A(pot)) is not impaired, but at high light A is not stimulated, showing inhibition. At a given intercellular CO(2) concentration (C(i)) A decreases, showing impaired metabolism (A(pot)). The C(i) and probably chloroplast CO(2) concentration (C(c)), decreases and then increases, together with the equilibrium CO(2) concentration, with greater WD. Estimation of C(c) and internal (mesophyll) conductance (g(i)) is considered uncertain. Photosystem activity is unaffected until very severe WD, maintaining electron (e(-)) transport (ET) and reductant content. Low A, together with photorespiration (PR), which is maintained or decreased, provides a smaller sink for e(-)(,) causing over-energization of energy transduction. Despite increased non-photochemical quenching (NPQ), excess energy and e(-) result in generation of reactive oxygen species (ROS). Evidence is considered that ROS damages ATP synthase so that ATP content decreases progressively with WD. Decreased ATP limits RuBP production by the Calvin cycle and thus A(pot). Rubisco activity is unlikely to determine A(pot). Sucrose synthesis is limited by lack of substrate and impaired enzyme regulation. With WD, PR decreases relative to light respiration (R(L)), and mitochondria consume reductant and synthesise ATP. With progressing WD at low A, R(L) increases C(i) and C(c). This review emphasises the effects of light intensity, considers techniques, and develops a qualitative model of photosynthetic metabolism under WD that explains many observations: testable hypotheses are suggested.