A congestion downstream of PSI causes the over-reduction of the electron transport chain inpgr5independent of membrane energization

Abstract

AbstractThe thylakoid protein Proton Gradient Regulation5 (PGR5) is thought to be a key component of cyclic electron flux around photosystem I. Thepgr5mutant is characterized by impaired proton motive force (pmf) formation across the thylakoid membrane, decreased photoprotective non-photochemical quenching (NPQ), and an over-reduction of the PSI acceptor side. This over-reduction has been attributed to impaired photosynthetic control, which down-regulates plastoquinol re-oxidation at the cytochrome b6f complex when the lumen is strongly acidified. Here, using thecgl160ATP synthase assembly mutant, we show that incgl160 pgr5double mutants, both the pmf across the thylakoid membrane and NPQ are fully restored to wild-type levels. However, the acceptor-side limitation of PSI in the double mutants stays comparable to the singlepgr5mutant. This demonstrates that impaired photosynthetic control is not causal for the over-reduction of the PSI acceptor side inpgr5. Instead, we show that both inpgr5and theclg160 pgr5mutants, the entire high-potential chain from cytochrome f to PSI remains strongly reduced in high light. This leads to insufficient oxidizing power for plastoquinol re-oxidation by the cytochrome b6f complex, thus impairing pmf formation. We conclude that PGR5 plays a critical role in electron partitioning downstream of PSI.