Chlororespiration as a Protective Stress-inducible Electron Transport Pathway in Chloroplasts

Abstract

Chlororespiration is the uptake of oxygen into the respiratory electron transport chain (ETC) localized in the thylakoid membranes of chloroplasts. The chlororespiratory ETC interacts with photosynthetic electron transport and participates in the non-photochemical reduction/oxidation of the plastoquinone pool (PQP) accompanied by O₂ consumption. The two key thylakoid enzymes in chlororespiration are the plastid-encoded NAD(P)H dehydrogenase complex (NDH) and the nucleus-encoded terminal plastoquinol oxidase (PTOX). The contribution of chlororespiratory electron flux to the total electron flow in non-stressed plants is considered insignificant. In contrast, under abiotic stresses, chlororespiration appears to be triggered, at least in some photosynthetic organisms, acting as a protective alternative electron transport pathway. There is evidence of NDH complex and PTOX increasing their activity and/or abundance when plants experience high light, drought, heat, or low-temperature stresses. Alternative electron transfer to oxygen via PTOX protects PQP from over-reduction under stress conditions. For instance, it was shown that PTOX-dependent electron drainage accounted for up to 30% of total PSII electron flow in salt-stressed plants. PTOX is not bound to the thylakoid membrane in dark-adapted leaves but is associated with it at intense illumination and high transmembrane proton gradient (ΔpH) or membrane potential (Δψ). It was also shown that PTOX is capable of lateral translocation from stromal lamellae to granal thylakoid stacks under salt stress. Such changes in PTOX localization increase the accessibility of the substrate (plastoquinol) and the turnover rate of the enzyme. The available data allow considering PTOX as a possible target for manipulation to increase stress tolerance in sensitive plants.