Towards a critical understanding of the photosystem II repair mechanism and its regulation during stress conditions

Abstract

Photosystem II (PSII) is vulnerable to high light (HL) illumination resulting in photoinhibition. In addition to photoprotection mechanisms, plants have developed an efficient PSII repair mechanism to save themselves from irreversible damage to PSII under abiotic stresses including HL illumination. The phosphorylation/dephosphorylation cycle along with subsequent degradation of photodamaged D1 protein to be replaced by the insertion of a newly synthesized copy of D1 into the PSII complex, is the core function of the PSII repair cycle. The exact mechanism of this process is still under discussion. We describe the recent progress in identifying the kinases, phosphatases and proteases, and in understanding their involvement in the maintenance of thylakoid structure and the quality control of proteins by PSII repair cycle during photoinhibition.

Keywords: Cyt b6f; D1; HL; LHCII; NADPH; NPQ; OEC; PSI; PSII; Photodamage and PSII repair cycle; Proteases and D1 protein degradation; RC; ROS; Reactive oxygen species (ROS); STN8 kinase and PSII core proteins phosphorylation; TEM; UV-B; Ultra-violet radiation; a 32kDa PSII reaction center protein which involves in PSII repair; cytochrome b6f complex; energy depending quenching; high light; light harvesting complex II; nicotinamide adenine dinucleotide phosphate; non-photochemical quenching; oxygen evolving complex; photoinhibitory quenching; photosystem I; photosystem II; qE; qI; qT; quenching related to state transitions; reaction center; reactive oxygen species; transmission electron microscope; ultra-violet radiation B.