Contribution of NDH-dependent cyclic electron transport around photosystem I to the generation of proton motive force in the weak mutant allele of pgr5

• Published in: Biochimica et biophysica acta. Bioenergetics 2019-05, Vol.1860 (5), p.369-374
• Main Authors: Nakano, Hiroshi, Yamamoto, Hiroshi, Shikanai, Toshiharu
• Format: Article
• Language: English
• Subjects: Cyclic electron transport; NDH; PGR5; pH; Photosynthesis
• ISSN: 0005-2728; 1879-2650
• DOI: 10.1016/j.bbabio.2019.03.003

In angiosperms, cyclic electron transport (CET) around photosystem I (PSI) consists of two pathways, depending on PGR5/PGRL1 proteins and the chloroplast NDH complex. In single mutants defective in chloroplast NDH, photosynthetic electron transport is only slightly affected at low light intensity, but in double mutants impaired in both CET pathways photosynthesis and plant growth are severely affected. The question is whether this strong mutant phenotype observed in double mutants can be simply explained by the additive effect of defects in both CET pathways. In this study, we used the weak mutant allele of pgr5-2 for the background of double mutants to avoid possible problems caused by the secondary effects due to the strong mutant phenotype. In two double mutants, crr2-2 pgr5-2 and ndhs-1 pgr5-2, the plant growth was unaffected and linear electron transport was only slightly affected. However, NPQ induction was more severely impaired in the double mutants than in the pgr5-2 single mutant. A similar trend was observed in the size of the proton motive force. Despite the slight reduction in photosystem II parameters, PSI parameters were severely affected in the pgr5-2 single mutant, the phenotype that was further enhanced by adding the NDH defects. Despite the lack of ∆pH-dependent regulation at the cytochrome b6f complex (donor-side regulation of PSI), the plastoquinone pool was more reduced in the double mutants than in the pgr5-2 single mutants. This phenotype suggests that both PGR5/PGRL1- and NDH-dependent CET contribute to supply sufficient acceptors from PSI by balancing the ATP/NADPH production ratio. •In the background of the weak allele of pgr5-2, the NDH defects reduced the size of NPQ and proton motive force in the absence of the growth defect•Despite the slight effect on PSII, PSI yield was dramatically reduced in pgr5-2 and the phenotype was enhanced by adding the NDH defects•The induction of ∆pH-dependent control of the cytochrome b6f complex was severely impaired in the double mutants•Despite the lack of donor-side regulation, the plastoquinone pool was reduced in the double mutants, suggesting the acceptor-limitation from PSI