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首页> 外文期刊>Biochimica et biophysica acta. Bioenergetics >Disturbed excitation energy transfer in Arabidopsis thaliana mutants lacking minor antenna complexes of photosystem II
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Disturbed excitation energy transfer in Arabidopsis thaliana mutants lacking minor antenna complexes of photosystem II

机译:缺乏光系统II较小天线复合物的拟南芥突变体中扰动的激发能转移

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摘要

Minor light-harvesting complexes (Lhcs) CP24, CP26 and CP29 occupy a position in photosystem II (PSII) of plants between the major light-harvesting complexes LHCII and the PSII core subunits. Lack of minor Lhcs in vivo causes impairment of PSII organization, and negatively affects electron transport rates and photoprotection capacity. Here we used picosecond-fluorescence spectroscopy to study excitation-energy transfer (EET) in thylakoid membranes isolated from Arabidopsis thaliana wild-type plants and knockout lines depleted of either two (koCP26/24 and koCP29/24) or all minor Lhcs (NoM). In the absence of all minor Lhcs, the functional connection of LHCII to the PSII cores appears to be seriously impaired whereas the "disconnected" LHCII is substantially quenched. For both double knock-out mutants, excitation trapping in PSII is faster than in NoM thylakoids but slower than in WT thylakoids. In NoM thylakoids, the loss of all minor Lhcs is accompanied by an over-accumulation of LHCII, suggesting a compensating response to the reduced trapping efficiency in limiting light, which leads to a photosynthetic phenotype resembling that of low-light-acclimated plants. Finally, fluorescence kinetics and biochemical results show that the missing minor complexes are not replaced by other Lhcs, implying that they are unique among the antenna subunits and crucial for the functioning and macro-organization of PSII. (C) 2014 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license
机译:次要光采光复合物(Lhcs)CP24,CP26和CP29在主要光采光复合物LHCII和PSII核心亚基之间的植物光系统II(PSII)中占据位置。体内缺乏少量Lhcs会导致PSII组织受损,并对电子传输速率和光保护能力产生负面影响。在这里,我们使用皮秒荧光光谱法研究了拟南芥野生型植物和敲除品系中的两种(koCP26 / 24和koCP29 / 24)或所有次要Lhcs(NoM)都耗尽的类囊体膜中的激发能转移(EET)。 。在没有所有次要Lhcs的情况下,LHCII与PSII核心的功能连接似乎受到严重损害,而“断开连接”的LHCII则被彻底淬灭。对于两个双敲除突变体,PSII中的诱捕诱捕都比NoM类囊体快,但比WT类囊体慢。在NoM类囊体中,所有次要Lhcs的丧失都伴随着LHCII的过度积累,这表明在有限的光照条件下,对捕集效率降低的补偿性反应导致了光合表现型,类似于低光照条件下的植物。最后,荧光动力学和生化结果表明,缺失的次要复合物不能被其他Lhcs取代,这表明它们在触角亚基中是独特的,对于PSII的功能和宏观组织至关重要。 (C)2014作者。由Elsevier B.V.发布。这是CC BY-NC-ND许可下的开放获取文章

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