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光系统II的光抑制。失活、蛋白质损伤与周转

Photoinhibition of Photosystem II. Inactivation, protein damage and turnover.

作者信息

Aro E M, Virgin I, Andersson B

机构信息

Department of Biology, University of Turku, Finland.

出版信息

Biochim Biophys Acta. 1993 Jul 5;1143(2):113-34. doi: 10.1016/0005-2728(93)90134-2.

Abstract

Even though light is the source of energy for photosynthesis, it can also be harmful to plants. Light-induced damage is targetted mainly to Photosystem II and leads to inactivation of electron transport and subsequent oxidative damage of the reaction centre, in particular to the D1 protein. Inactivation and protein damage can be induced by two different mechanisms, either from the acceptor side or from donor side of P680. The damaged D1 protein is triggered for degradation and digested by at least one serine-type proteinase that is tightly associated with the Photosystem II complex itself. The damaged Photosystem II complex dissociates from the light-harvesting antenna and migrates from appressed to non-appressed thylakoid regions where a new D1 protein is co-translationally inserted into the partially disassembled Photosystem II complex. D1 protein phosphorylation probably allows for coordinated biodegradation and biosynthesis of the D1 protein. After religation of cofactors and assembly of subunits, the repaired Photosystem II complex can again be found in the appressed membrane regions. Various protective mechanisms and an efficient repair cycle of Photosystem II allow plants to survive light stress.

摘要

尽管光是光合作用的能量来源,但它也可能对植物有害。光诱导的损伤主要针对光系统II,导致电子传递失活以及反应中心随后的氧化损伤,特别是对D1蛋白的损伤。失活和蛋白质损伤可由两种不同机制诱导,要么来自P680的受体侧,要么来自供体侧。受损的D1蛋白被触发降解,并被至少一种与光系统II复合物本身紧密相关的丝氨酸型蛋白酶消化。受损的光系统II复合物与捕光天线解离,并从紧密堆积的类囊体区域迁移到非紧密堆积的类囊体区域,在那里一种新的D1蛋白被共翻译插入到部分拆解的光系统II复合物中。D1蛋白磷酸化可能允许D1蛋白进行协调的生物降解和生物合成。在辅因子重新连接和亚基组装后,修复后的光系统II复合物可以再次出现在紧密堆积的膜区域。光系统II的各种保护机制和高效修复循环使植物能够在光胁迫下存活。

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