Department of Botany, Graduate School of Science, Kyoto University, Kyoto 606-8502, Japan.
Plant Physiol. 2022 Feb 4;188(2):1264-1276. doi: 10.1093/plphys/kiab541.
Plastid terminal oxidase (PTOX) accepts electrons from plastoquinol to reduce molecular oxygen to water. We introduced the gene encoding Chlamydomonas reinhardtii (Cr)PTOX2 into the Arabidopsis (Arabidopsis thaliana) wild-type (WT) and proton gradient regulation5 (pgr5) mutant defective in cyclic electron transport around photosystem I (PSI). The accumulation of CrPTOX2 only mildly affected photosynthetic electron transport in the WT background during steady-state photosynthesis but partly complemented the induction of nonphotochemical quenching (NPQ) in the pgr5 background. During the induction of photosynthesis by actinic light (AL) of 130 µmol photons m-2 s-1, the high level of PSII yield (Y(II)) was induced immediately after the onset of AL in WT plants accumulating CrPTOX2. NPQ was more rapidly induced in the transgenic plants than in WT plants. P700 was also oxidized immediately after the onset of AL. Although CrPTOX2 does not directly induce a proton concentration gradient (ΔpH) across the thylakoid membrane, the coupled reaction of PSII generated ΔpH to induce NPQ and the downregulation of the cytochrome b6f complex. Rapid induction of Y(II) and NPQ was also observed in the pgr5 plants accumulating CrPTOX2. In contrast to the WT background, P700 was not oxidized in the pgr5 background. Although the thylakoid lumen was acidified by CrPTOX2, PGR5 was essential for oxidizing P700. In addition to acidification of the thylakoid lumen to downregulate the cytochrome b6f complex (donor-side regulation), PGR5 may be required for draining electrons from PSI by transferring them to the plastoquinone pool. We propose a reevaluation of the contribution of this acceptor-side regulation by PGR5 in the photoprotection of PSI.
质体末端氧化酶（PTOX）从质醌接受电子，将分子氧还原为水。我们将编码莱茵衣藻（Chlamydomonas reinhardtii）（Cr）PTOX2 的基因导入拟南芥（Arabidopsis thaliana）野生型（WT）和质子梯度调节 5 突变体（pgr5），后者在 PSI 周围的环式电子传递中存在缺陷。在稳态光合作用中，CrPTOX2 的积累仅在 WT 背景下轻度影响光合作用电子传递，但部分弥补了 pgr5 背景中非光化学猝灭（NPQ）的诱导。在 130 μmol 光子 m-2 s-1 的光激活（AL）下诱导光合作用时，在积累 CrPTOX2 的 WT 植物中，在 AL 开始后立即诱导出高水平的 PSII 产量（Y（II））。在转基因植物中，NPQ 的诱导比在 WT 植物中更快。在 AL 开始后，P700 也立即被氧化。尽管 CrPTOX2 不会直接诱导类囊体膜的质子浓度梯度（ΔpH），但 PSII 的偶联反应会产生 ΔpH 以诱导 NPQ 和细胞色素 b6f 复合物的下调。在积累 CrPTOX2 的 pgr5 植物中也观察到 Y（II）和 NPQ 的快速诱导。与 WT 背景不同，在 pgr5 背景中 P700 未被氧化。尽管 CrPTOX2 酸化了类囊体腔，但 PGR5 对于氧化 P700 是必需的。除了通过将电子转移到质醌池中使细胞色素 b6f 复合物下调（供体侧调节）来酸化类囊体腔之外，PGR5 可能还需要将电子从 PSI 中排出。我们建议重新评估 PGR5 在 PSI 光保护中的这种受体侧调节的贡献。
