Testing the Role of the N-Terminal Tail of D1 in the Maintenance of Photosystem II in Tobacco Chloroplasts.

Testing the Role of the N-Terminal Tail of D1 in the Maintenance of Photosystem II in Tobacco Chloroplasts.
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DOI:
10.3389/fpls.2016.00844
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发表时间:
2016
影响因子:
5.6
通讯作者:
Nixon PJ
Nixon PJ
中科院分区:
生物学2区
文献类型:
--
作者:
Michoux F;Ahmad N;Wei ZY;Belgio E;Ruban AV;Nixon PJ

文献摘要

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光失活的放氧光系统II(PSII)复合物修复的关键步骤是选择性识别和降解受损的PSII亚基,通常是D1反应中心亚基。FtsH蛋白酶在蓝藻和叶绿体中D1降解中起主要作用。在蓝细菌集胞藻属PCC 6803的情况下,D1缺乏20个氨基酸残基的N-末端截短突变体的分析提供了证据表明,FtsH复合物可以在暴露的N-末端尾部开始的进行性反应中去除受损的D1。为了验证N端D1尾在高等植物中的重要性,我们利用叶绿体转化技术在烟草中构建了等效截短突变体。由此产生的突变体生长不良,仅积累了约25%的野生型水平的PSII在幼叶下降,随着叶片的生长,使有很少的PSII活性在成熟叶片。截断D1导致损失的PSII超复合物和二聚体复合物的膜。广泛和快速的非光化学淬灭(NPQ)仍然诱导突变体,支持PSII复合物不需要NPQ的结论。叶片暴露于强光下的分析表明,在截断突变体的PSII修复受损的PSII的合成和/或组装的水平,但D1仍然可以被降解。这些数据支持这样的想法,即烟草植物具有一些备份和补偿途径,以消除严重的光胁迫下受损的D1。
A key step in the repair of photoinactivated oxygen-evolving photosystem II (PSII) complexes is the selective recognition and degradation of the damaged PSII subunit, usually the D1 reaction center subunit. FtsH proteases play a major role in D1 degradation in both cyanobacteria and chloroplasts. In the case of the cyanobacterium Synechocystis sp. PCC 6803, analysis of an N-terminal truncation mutant of D1 lacking 20 amino-acid residues has provided evidence that FtsH complexes can remove damaged D1 in a processive reaction initiated at the exposed N-terminal tail. To test the importance of the N-terminal D1 tail in higher plants, we have constructed the equivalent truncation mutant in tobacco using chloroplast transformation techniques. The resulting mutant grew poorly and only accumulated about 25% of wild-type levels of PSII in young leaves which declined as the leaves grew so that there was little PSII activity in mature leaves. Truncating D1 led to the loss of PSII supercomplexes and dimeric complexes in the membrane. Extensive and rapid non-photochemical quenching (NPQ) was still induced in the mutant, supporting the conclusion that PSII complexes are not required for NPQ. Analysis of leaves exposed to high light indicated that PSII repair in the truncation mutant was impaired at the level of synthesis and/or assembly of PSII but that D1 could still be degraded. These data support the idea that tobacco plants possess a number of back-up and compensatory pathways for removal of damaged D1 upon severe light stress.