Electron transfer via cytochrome b6f complex displays sensitivity to antimycin A upon STT7 kinase activation. Issue 1 (14th January 2022)

• Record Type: Journal Article
• Authors: Buchert, Felix; Scholz, Martin; Hippler, Michael
• Is Part Of: Biochemical journal. Volume 479:Issue 1(2022)
• Page Start: 111
• Page End: 127
• Publication Date: 2022-01-14
• Subjects: Chlamydomonas reinhardtii -- cyclic electron flow -- cytochrome b6f complex -- photosynthesis -- state transitions; Biochemistry -- Periodicals; 572
• DOI: 10.1042/BCJ20210802
• Languages: English
• ISSNs: 0264-6021

Abstract

Abstract : The cytochrome b 6 f complex ( b 6 f ) has been initially considered as the ferredoxin-plastoquinone reductase (FQR) during cyclic electron flow (CEF) with photosystem I that is inhibited by antimycin A (AA). The binding of AA to the b 6 f Qi-site is aggravated by heme- c i, which challenged the FQR function of b 6 f during CEF. Alternative models suggest that PROTON GRADIENT REGULATION5 (PGR5) is involved in a b 6 f -independent, AA-sensitive FQR. Here, we show in Chlamydomonas reinhardtii that the b 6 f is conditionally inhibited by AA in vivo and that the inhibition did not require PGR5. Instead, activation of the STT7 kinase upon anaerobic treatment induced the AA sensitivity of b 6 f which was absent from stt7-1 . However, a lock in State 2 due to persisting phosphorylation in the phosphatase double mutant pph1 ; pbcp did not increase AA sensitivity of electron transfer. The latter required a redox poise, supporting the view that state transitions and CEF are not coercively coupled. This suggests that the b 6 f -interacting kinase is required for structure-function modulation of the Qi-site under CEF favoring conditions. We propose that PGR5 and STT7 independently sustain AA-sensitive FQR activity of the b 6 f . Accordingly, PGR5-mediated electron injection into an STT7-modulated Qi-site drives a Mitchellian Q cycle in CEF conditions.