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微小天线蛋白CP24和CP26影响拟南芥基粒膜中光系统II亚基之间的相互作用以及电子传递速率。

Minor antenna proteins CP24 and CP26 affect the interactions between photosystem II subunits and the electron transport rate in grana membranes of Arabidopsis.

作者信息

de Bianchi Silvia, Dall'Osto Luca, Tognon Giuseppe, Morosinotto Tomas, Bassi Roberto

机构信息

Dipartimento Scientifico e Tecnologico, Università di Verona, I-37134 Verona, Italy.

出版信息

Plant Cell. 2008 Apr;20(4):1012-28. doi: 10.1105/tpc.107.055749. Epub 2008 Apr 1.

Abstract

We investigated the function of chlorophyll a/b binding antenna proteins Chlorophyll Protein 26 (CP26) and CP24 in light harvesting and regulation of photosynthesis by isolating Arabidopsis thaliana knockout lines that completely lacked one or both of these proteins. All three mutant lines had a decreased efficiency of energy transfer from trimeric light-harvesting complex II (LHCII) to the reaction center of photosystem II (PSII) due to the physical disconnection of LHCII from PSII and formation of PSII reaction center depleted domains in grana partitions. Photosynthesis was affected in plants lacking CP24 but not in plants lacking CP26: the former mutant had decreased electron transport rates, a lower DeltapH gradient across the grana membranes, reduced capacity for nonphotochemical quenching, and limited growth. Furthermore, the PSII particles of these plants were organized in unusual two-dimensional arrays in the grana membranes. Surprisingly, overall electron transport, nonphotochemical quenching, and growth of the double mutant were restored to wild type. Fluorescence induction kinetics and electron transport measurements at selected steps of the photosynthetic chain suggested that limitation in electron transport was due to restricted electron transport between Q(A) and Q(B), which retards plastoquinone diffusion. We conclude that CP24 absence alters PSII organization and consequently limits plastoquinone diffusion.

摘要

我们通过分离完全缺失叶绿素 a/b 结合天线蛋白叶绿素蛋白 26(CP26)和 CP24 其中之一或两者的拟南芥敲除系,研究了 CP26 和 CP24 在光合作用的光能捕获及调节中的功能。由于 LHCII 与光系统 II(PSII)的物理分离以及在基粒分区中形成 PSII 反应中心耗尽域,所有三个突变系从三聚体捕光复合物 II(LHCII)到 PSII 反应中心的能量传递效率均降低。光合作用在缺乏 CP24 的植株中受到影响,但在缺乏 CP26 的植株中未受影响:前一种突变体的电子传递速率降低,跨基粒膜的 ΔpH 梯度较低,非光化学猝灭能力降低,生长受限。此外,这些植株的 PSII 颗粒在基粒膜中以异常的二维阵列形式排列。令人惊讶的是,双突变体的整体电子传递、非光化学猝灭和生长恢复到了野生型水平。光合链特定步骤的荧光诱导动力学和电子传递测量表明,电子传递受限是由于 Q(A) 和 Q(B) 之间的电子传递受限,这阻碍了质体醌的扩散。我们得出结论,缺失 CP24 会改变 PSII 的组织,从而限制质体醌的扩散。

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