Maintaining the Chloroplast Redox Balance through the PGR5-Dependent Pathway and the Trx System Is Required for Light-Dependent Activation of Photosynthetic Reactions
Maintaining the Chloroplast Redox Balance through the PGR5-Dependent Pathway and the Trx System Is Required for Light-Dependent Activation of Photosynthetic Reactions
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DOI：
10.1093/pcp/pcab148
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发表时间：
2022-01-01
影响因子：
4.9
通讯作者：
Motohashi, Ken
中科院分区：
文献类型：
--
作者：
Okegawa, Yuki;Tsuda, Natsuki;Motohashi, Ken
从黑暗到光明的转变后，光合作用的快速诱导需要叶绿体酶的光依赖性激活。硫氧还蛋白（Trx）系统在此过程中发挥着核心作用。在叶绿体中，Trx 系统由两条途径组成：铁氧还蛋白 (Fd)/Trx 途径和烟酰胺腺嘌呤二核苷酸磷酸 (NADPH)-Trx 还原酶 C (NTRC) 途径。在任一途径有缺陷的拟南芥（Arabidopsis thaliana）突变体中，硫醇酶的光还原受到损害，导致碳固定减少。最近阐明了 Fd/Trx 途径与质子梯度调节 5 (PGR5) 依赖性光系统 I 循环电子传递 (PSI CET) 在光合作用诱导中的密切关系。然而，PGR5 依赖性途径如何参与 NTRC 途径尚不清楚，尽管 NTRC 已被认为与 PGR5 发生物理相互作用。在本研究中，我们分析了 ntrc 突变体背景中缺乏 PGR5 或叶绿体 NADH 脱氢酶样复合物 (NDH) 依赖的 PSI CET 途径的拟南芥突变体。当在长日照条件下生长时，ntrc pgr5双突变体抑制了ntrc突变体的生长缺陷和高非光化学猝灭表型。相比之下，用氯呼吸还原2-2突变体灭活NDH活性未能抑制任一表型。我们发现 pgr5 对 ntrc 的表型拯救是由 Trx 依赖性硫醇酶还原的部分恢复引起的。这些结果表明，在光合作用诱导过程中，需要适当调节 PGR5 依赖性途径和 Trx 系统的电子分配，以激活 Calvin-Benson-Bassham 循环酶。
Light-dependent activation of chloroplast enzymes is required for the rapid induction of photosynthesis after a shift from dark to light. The thioredoxin (Trx) system plays a central role in this process. In chloroplasts, the Trx system consists of two pathways: the ferredoxin (Fd)/Trx pathway and the nicotinamide adenine dinucleotide phosphate (NADPH)-Trx reductase C (NTRC) pathway. In Arabidopsis (Arabidopsis thaliana) mutants defective in either pathway, the photoreduction of thiol enzymes was impaired, resulting in decreased carbon fixation. The close relationship between the Fd/Trx pathway and proton gradient regulation 5 (PGR5)-dependent photosystem I cyclic electron transport (PSI CET) in the induction of photosynthesis was recently elucidated. However, how the PGR5-dependent pathway is involved in the NTRC pathway is unclear, although NTRC has been suggested to physically interact with PGR5. In this study, we analyzed Arabidopsis mutants lacking either the PGR5 or the chloroplast NADH dehydrogenase-like complex (NDH)-dependent PSI CET pathway in the ntrc mutant background. The ntrc pgr5 double mutant suppressed both the growth defects and the high non-photochemical quenching phenotype of the ntrc mutant when grown under long-day conditions. By contrast, the inactivation of NDH activity with the chlororespiratory reduction 2-2 mutant failed to suppress either phenotype. We discovered that the phenotypic rescue of ntrc by pgr5 is caused by the partial restoration of Trx-dependent reduction of thiol enzymes. These results suggest that electron partitioning to the PGR5-dependent pathway and the Trx system needs to be properly regulated for the activation of the Calvin-Benson-Bassham cycle enzymes during the induction of photosynthesis.