Higher order photoprotection mutants reveal the importance of ΔpH-dependent photosynthesis-control in preventing light induced damage to both photosystem II and photosystem I

Abstract

Although light is essential for photosynthesis, when in excess, it may damage the photosynthetic apparatus, leading to a phenomenon known as photoinhibition. photoinhibition was thought as a light-induced damage to photosystem ii; however, it is now clear that even photosystem i may become very vulnerable to light. one main characteristic of light induced damage to photosystem ii (pSii) is the increased turnover of the reaction center protein, D1: when rate of degradation exceeds the rate of synthesis, loss of pSii activity is observed. With respect to photosystem i (pSi), an excess of electrons, instead of an excess of light, may be very dangerous. plants possess a number of mechanisms able to prevent, or limit, such damages by safe thermal dissipation of light energy (non-photochemical quenching, npQ), slowing-down of electron transfer through the intersystem transport chain (photosynthesis-control, pSc) in cooperation with the proton Gradient Regulation (pGR) proteins, PGR5 and PGRL1, collectively called as short-term photoprotection mechanisms, and the redistribution of light between photosystems, called state transitions (responsible of fluorescence quenching at PSII, qt), is superimposed to these short term photoprotective mechanisms. in this manuscript we have generated a number of higher order mutants by crossing genotypes carrying defects in each of the short-term photoprotection mechanisms, with the final aim to obtain a direct comparison of their role and efficiency in photoprotection. We found that mutants carrying a defect in the ΔpH-dependent photosynthesis-control are characterized by photoinhibition of both photosystems, irrespectively of whether pSBS-dependent npQ or state transitions defects were present or not in the same individual, demonstrating the primary role of pSc in photoprotection. Moreover, mutants with a limited capability to develop a strong PSBS-dependent NPQ, were characterized by a high turnover of the D1 protein and high values of Y(NO), which might reflect energy quenching processes occurring within the PSII reaction center. Photoinhibition of photosynthesis is a long-known phenomenon 1. Due to the discovery of the high turnover D1-protein 2 and its subsequent recognition as a main component of PSII reaction center harboring most of PSII redox cofactors 3,4 , photoinhibition was thought as the increase of degradation rate for the D1 over its synthesis or, more in general, as an unbalance between damage and repair of PSII 5,6. The repair cycle of PSII is now a

Dynamic thylakoid stacking and state transitions work synergistically to avoid acceptor-side limitation of photosystem I

“…In contrast the WT Y(NA) remains comparatively low under all conditions (Fig. 5A) 40,58,59 . We investigated whether HL treatment resulted in detectable damage to PSI by assessing the ECS a-phase amplitude in leaves infiltrated with DCMU.…”

Cytochrome b6f – Orchestrator of photosynthetic electron transfer

“…Over-reduction of PSI promotes the reduction of oxygen to superoxide, which in turn can cause photo-oxidative damage, leading to PSI photoinhibition [109,110]. Since PSI does not possess a rapid repair cycle (unlike PSII), photoinhibition of PSI can have a significant impact on an organism's growth and fitness [111][112][113]. In phototrophic organisms, these detrimental effects are largely mitigated through photosynthetic control, which serves to limit the build-up of excess electrons on the PSI acceptor-side by controlling the rate of electron donation to the primary PSI electron donor P700 + .…”

Resistance of Antarctic moss Sanionia uncinata to photoinhibition: chlorophyll fluorescence analysis of samples from the western and eastern coasts of the Antarctic Peninsula

“…In laboratory‐based studies, photoinhibition is typically measured as a decrease in F V /F M or Φ PSII from control values (before PIT), and the value reached immediately after treatment (typically 30 min, 60 min; Barbato et al . 2020; Barták et al . 2012).…”