PHOTOINHIBITION OF PHOTOSYSTEM-2 - INACTIVATION, PROTEIN DAMAGE AND TURNOVER

被引:1956
作者
ARO, EM
VIRGIN, I
ANDERSSON, B
机构
[1] UNIV STOCKHOLM, ARRHENIUS LABS NAT SCI, DEPT BIOCHEM, S-10691 STOCKHOLM, SWEDEN
[2] UNIV TURKU, DEPT BIOL, SF-20500 TURKU 50, FINLAND
基金
芬兰科学院; 瑞典研究理事会;
关键词
D1-PROTEIN; ELECTRON TRANSPORT; LIGHT STRESS; OXIDATIVE DAMAGE; PHOTOSYSTEM-II; REACTION CENTER; PROTEOLYSIS;
D O I
10.1016/0005-2728(93)90134-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:113 / 134
页数:22
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