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光系统II亚基PsbS参与莱茵衣藻中依赖LHCSR蛋白的能量耗散诱导过程。

Photosystem II Subunit PsbS Is Involved in the Induction of LHCSR Protein-dependent Energy Dissipation in Chlamydomonas reinhardtii.

作者信息

Correa-Galvis Viviana, Redekop Petra, Guan Katharine, Griess Annika, Truong Thuy B, Wakao Setsuko, Niyogi Krishna K, Jahns Peter

机构信息

From the Plant Biochemistry, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany.

Howard Hughes Medical Institute, Department of Plant and Microbial Biology, University of California, Berkeley, California 94720-3102, and.

出版信息

J Biol Chem. 2016 Aug 12;291(33):17478-87. doi: 10.1074/jbc.M116.737312. Epub 2016 Jun 29.

Abstract

Non-photochemical quenching of excess excitation energy is an important photoprotective mechanism in photosynthetic organisms. In Arabidopsis thaliana, a high quenching capacity is constitutively present and depends on the PsbS protein. In the green alga Chlamydomonas reinhardtii, non-photochemical quenching becomes activated upon high light acclimation and requires the accumulation of light harvesting complex stress-related (LHCSR) proteins. Expression of the PsbS protein in C. reinhardtii has not been reported yet. Here, we show that PsbS is a light-induced protein in C. reinhardtii, whose accumulation under high light is further controlled by CO2 availability. PsbS accumulated after several hours of high light illumination at low CO2 At high CO2, however, PsbS was only transiently expressed under high light and was degraded after 1 h of high light exposure. PsbS accumulation correlated with an enhanced non-photochemical quenching capacity in high light-acclimated cells grown at low CO2 However, PsbS could not compensate for the function of LHCSR in an LHCSR-deficient mutant. Knockdown of PsbS accumulation led to reduction of both non-photochemical quenching capacity and LHCSR3 accumulation. Our data suggest that PsbS is essential for the activation of non-photochemical quenching in C. reinhardtii, possibly by promoting conformational changes required for activation of LHCSR3-dependent quenching in the antenna of photosystem II.

摘要

过量激发能的非光化学猝灭是光合生物中一种重要的光保护机制。在拟南芥中,高猝灭能力是组成型存在的,并且依赖于PsbS蛋白。在绿藻莱茵衣藻中,非光化学猝灭在高光适应时被激活,并且需要光捕获复合体应激相关(LHCSR)蛋白的积累。莱茵衣藻中PsbS蛋白的表达尚未见报道。在此,我们表明PsbS是莱茵衣藻中的一种光诱导蛋白,其在高光下的积累进一步受二氧化碳可用性的控制。在低二氧化碳条件下高光照射数小时后,PsbS积累。然而,在高二氧化碳条件下,PsbS在高光下仅短暂表达,并在高光暴露1小时后降解。在低二氧化碳条件下生长的高光适应细胞中,PsbS的积累与增强的非光化学猝灭能力相关。然而,在LHCSR缺陷型突变体中,PsbS不能补偿LHCSR的功能。PsbS积累的敲低导致非光化学猝灭能力和LHCSR3积累的降低。我们的数据表明,PsbS对于莱茵衣藻中非光化学猝灭的激活至关重要,可能是通过促进光系统II天线中LHCSR3依赖性猝灭激活所需的构象变化来实现的。

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