Protein synthesis is the primary target of reactive oxygen species in the photoinhibition of photosystem II
Protein synthesis is the primary target of reactive oxygen species in the photoinhibition of photosystem II
复制标题
DOI：
10.1111/j.1399-3054.2011.01457.x
复制
发表时间：
2011-05-01
影响因子：
6.4
通讯作者：
Murata, Norio
中科院分区：
文献类型：
--
作者：
Nishiyama, Yoshitaka;Allakhverdiev, Suleyman I.;Murata, Norio
光系统II（PSII）的光抑制发生时，光损伤的PSII的速度超过光损伤的PSII的修复速度。最近的光抑制的光损伤和修复的单独测定的检查已经显示，光损伤的PSII的速率是成正比的入射光的强度和PSII的修复是特别敏感的活性氧（ROS）的失活。ROS诱导的修复失活是由于抑制了蛋白质的从头合成，如D1蛋白，这是在翻译延伸水平上修复PSII所必需的。此外，分子分析表明，ROS诱导的蛋白质合成的抑制与通过形成分子内二硫键的延伸因子G的特异性失活有关。各种保护PSII免受光抑制的机制，包括光呼吸、激发能的热耗散和电子的循环运输的损害，通过抑制蛋白质合成来降低PSII的修复速率。本文综述了新近建立的PSII光抑制修复调控模型及其生理意义。
Photoinhibition of photosystem II (PSII) occurs when the rate of photodamage to PSII exceeds the rate of the repair of photodamaged PSII. Recent examination of photoinhibition by separate determinations of photodamage and repair has revealed that the rate of photodamage to PSII is directly proportional to the intensity of incident light and that the repair of PSII is particularly sensitive to the inactivation by reactive oxygen species (ROS). The ROS-induced inactivation of repair is attributable to the suppression of the synthesis de novo of proteins, such as the D1 protein, that are required for the repair of PSII at the level of translational elongation. Furthermore, molecular analysis has revealed that the ROS-induced suppression of protein synthesis is associated with the specific inactivation of elongation factor G via the formation of an intramolecular disulfide bond. Impairment of various mechanisms that protect PSII against photoinhibition, including photorespiration, thermal dissipation of excitation energy, and the cyclic transport of electrons, decreases the rate of repair of PSII via the suppression of protein synthesis. In this review, we present a newly established model of the mechanism and the physiological significance of repair in the regulation of the photoinhibition of PSII.