Lawlor David W, Tezara Wilmer
Plant Sciences, Centre for Crop Improvement, Rothamsted Research, Harpenden, Herts, UK.
Ann Bot. 2009 Feb;103(4):561-79. doi: 10.1093/aob/mcn244. Epub 2009 Jan 19.
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.
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.
水分亏缺（WD）通过降低气孔对二氧化碳的导度（g(s)）和光合代谢潜力（A(pot)）来降低光合速率（A）。关于光强和实验方法，对g(s)和A(pot)的相对重要性以及它们如何受WD影响进行了综述。
随着WD的加剧，A随着g(s)的下降而降低。在生长和WD期间的低光照条件下，A受二氧化碳浓度升高的刺激，表明代谢（A(pot)）未受损，但在高光照下A不受刺激，表明受到抑制。在给定的细胞间二氧化碳浓度（C(i)）下，A降低，表明代谢受损（A(pot)）。随着WD加剧，C(i)以及可能的叶绿体二氧化碳浓度（C(c)）先降低后升高，同时平衡二氧化碳浓度也如此。对C(c)和内部（叶肉）导度（g(i)）的估计被认为是不确定的。直到非常严重的WD时，光合系统活性才会受到影响，此时仍维持电子（e(-)）传递（ET）和还原剂含量。低A与维持或降低的光呼吸（PR）一起，为e(-)提供了较小的汇，导致能量转导过度激发。尽管非光化学猝灭（NPQ）增加，但过量的能量和e(-)会导致活性氧（ROS）的产生。有证据表明ROS会损害ATP合酶，从而使ATP含量随着WD而逐渐降低。ATP的减少限制了卡尔文循环中RuBP的产生，进而限制了A(pot)。Rubisco活性不太可能决定A(pot)。蔗糖合成受到底物缺乏和酶调节受损的限制。随着WD的发展，PR相对于光呼吸（R(L)）降低，线粒体消耗还原剂并合成ATP。在低A条件下随着WD加剧，R(L)会增加C(i)和C(c)。本综述强调了光强的影响，考虑了技术，并建立了一个WD条件下光合代谢的定性模型，该模型解释了许多观察结果：提出了可检验的假设。
