In addition to linear electron transport, photosystem I cyclic electron transport (PSI-CET) contributes to photosynthesis and photoprotection. In Arabidopsis (Arabidopsis thaliana), PSI-CET consists of two partially redundant pathways, one of which is the PROTON GRADIENT REGULATION5 (PGR5)/PGR5-LIKE PHOTOSYNTHETIC PHENOTYPE1 (PGRL1)–dependent pathway. Although the physiological significance of PSI-CET is widely recognized, the regulatory mechanism behind these pathways remains largely unknown. Here, we report on the regulation of the PGR5/PGRL1-dependent pathway by the m-type thioredoxins (Trx m). Genetic and phenotypic characterizations of multiple mutants indicated the physiological interaction between Trx m and the PGR5/PGRL1-dependent pathway in vivo. Using purified Trx proteins and ruptured chloroplasts, in vitro, we showed that the reduced form of Trx m specifically decreased the PGR5/PGRL1-dependent plastoquinone reduction. In planta, Trx m4 directly interacted with PGRL1 via disulfide complex formation. Analysis of the transgenic plants expressing PGRL1 Cys variants demonstrated that Cys-123 of PGRL1 is required for Trx m4-PGRL1 complex formation. Furthermore, the Trx m4-PGRL1 complex was transiently dissociated during the induction of photosynthesis. We propose that Trx m directly regulates the PGR5/PGRL1-dependent pathway by complex formation with PGRL1.

除了线性电子传输外，光系统 I 循环电子传输 (PSI-CET) 还有助于光合作用和光保护。在拟南芥 ( Arabidopsis thaliana ) 中，PSI-CET 由两条部分冗余的通路组成，其中之一是质子梯度调节 5 (PGR5)/PGR5-LIKE PHOTOSYNTHETIC PHENOTYPE1 (PGRL1) 依赖通路。尽管 PSI-CET 的生理意义已得到广泛认可，但这些途径背后的调控机制在很大程度上仍是未知的。在这里，我们报告了m型硫氧还蛋白 (Trx m )对 PGR5/PGRL1 依赖性途径的调节。多个突变体的遗传和表型特征表明 Trx m之间的生理相互作用和体内 PGR5/PGRL1 依赖性途径。在体外使用纯化的 Trx 蛋白和破裂的叶绿体，我们发现 Trx m的还原形式特异性地降低了 PGR5/PGRL1 依赖性质体醌的减少。在植物中，Trx m 4 通过二硫化物复合物的形成直接与 PGRL1 相互作用。对表达 PGRL1 Cys 变体的转基因植物的分析表明，形成Trx m 4-PGRL1 复合物需要 PGRL1 的 Cys-123 。此外，Trx m 4-PGRL1 复合物在光合作用的诱导过程中被瞬时解离。我们建议 Trx m通过与 PGRL1 形成复合物直接调节 PGR5/PGRL1 依赖性途径。