Avenson Thomas J, Cruz Jeffrey A, Kramer David M
Institute of Biological Chemistry, 289 Clark Hall, Washington State University, Pullman, WA 99164-6340, USA.
Proc Natl Acad Sci U S A. 2004 Apr 13;101(15):5530-5. doi: 10.1073/pnas.0401269101. Epub 2004 Apr 2.
Energy-dependent exciton quenching, or q(E), protects the higher plant photosynthetic apparatus from photodamage. Initiation of q(E) involves protonation of violaxanthin deepoxidase and PsbS, a component of the photosystem II antenna complex, as a result of lumen acidification driven by photosynthetic electron transfer. It has become clear that the response of q(E) to linear electron flow, termed "q(E) sensitivity," must be modulated in response to fluctuating environmental conditions. Previously, three mechanisms have been proposed to account for q(E) modulation: (i) the sensitivity of q(E) to the lumen pH is altered; (ii) elevated cyclic electron flow around photosystem I increases proton translocation into the lumen; and (iii) lowering the conductivity of the thylakoid ATP synthase to protons (g(H+)) allows formation of a larger steady-state proton motive force (pmf). Kinetic analysis of the electrochromic shift of intrinsic thylakoid pigments, a linear indicator of transthylakoid electric field component, suggests that, when CO(2) alone was lowered from 350 ppm to 50 ppm CO(2), modulation of q(E) sensitivity could be explained solely by changes in conductivity. Lowering both CO(2) (to 50 ppm) and O(2) (to 1%) resulted in an additional increase in q(E) sensitivity that could not be explained by changes in conductivity or cyclic electron flow associated with photosystem I. Evidence is presented for a fourth mechanism, in which changes in q(E) sensitivity result from variable partitioning of proton motive force into the electric field and pH gradient components. The implications of this mechanism for the storage of proton motive force and the regulation of the light reactions are discussed.
能量依赖型激子猝灭，即q(E)，可保护高等植物光合机构免受光损伤。q(E)的启动涉及紫黄质脱环氧化酶和光系统II天线复合体的一个组分PsbS的质子化，这是光合电子传递驱动的类囊体腔酸化的结果。现已明确，q(E)对线性电子流的响应，即“q(E)敏感性”，必须根据环境条件的波动进行调节。此前，已提出三种机制来解释q(E)的调节：(i) q(E)对类囊体腔pH的敏感性发生改变；(ii) 围绕光系统I的循环电子流增加会使质子向类囊体腔的转运增加；(iii) 降低类囊体ATP合酶对质子的传导性（g(H+)）会形成更大的稳态质子动力势（pmf）。对类囊体固有色素的电致变色位移进行动力学分析，这是类囊体跨膜电场成分的线性指标，结果表明，当仅将CO₂从350 ppm降至50 ppm时，q(E)敏感性的调节仅可由传导性的变化来解释。同时降低CO₂（至50 ppm）和O₂（至1%）会导致q(E)敏感性进一步增加，这无法通过传导性变化或与光系统I相关的循环电子流来解释。本文提出了第四种机制的证据，即q(E)敏感性的变化源于质子动力势在电场和pH梯度成分之间的可变分配。讨论了该机制对质子动力势储存和光反应调节的影响。
