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Enhanced function of non-photoinhibited photosystem II complexes upon PSII photoinhibition

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DOI: 10.1016/j.bbabio.2023.148978

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PSII photoinhibition; Lincomycin; Protein phosphorylation; Light reactions; Photosynthesis; Thylakoid membrane

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Light-induced photosystem II photoinhibition causes inactivation and irreversible damage to the reaction center protein(s), but the light harvesting complexes continue to collect light energy. This study investigates the consequences of such photoinhibition on thylakoid light harvesting and electron transfer reactions in Arabidopsis thaliana leaves. The results show that without blocking the repair of damaged photosystem II centers, photoinhibition increases the excitation of photosystem II relative to photosystem I, while blocking repair leads to increased excitation of photosystem I and strong oxidation of the electron transfer chain. It is hypothesized that dynamic regulation of the LHCII system plays a crucial role in controlling excitation energy transfer during photosystem II damage and repair to maintain efficient and safe photosynthesis.
Light induced photosystem (PS)II photoinhibition inactivates and irreversibly damages the reaction center protein(s) but the light harvesting complexes continue the collection of light energy. Here we addressed the consequences of such a situation on thylakoid light harvesting and electron transfer reactions. For this purpose, Arabidopsis thaliana leaves were subjected to investigation of the function and regulation of the photosynthetic machinery after a distinct portion of PSII centers had experienced photoinhibition in the presence and absence of Lincomycin (Lin), a commonly used agent to block the repair of damaged PSII centers. In the absence of Lin, photoinhibition increased the relative excitation of PSII and decreased NPQ, together enhancing the electron transfer from still functional PSII centers to PSI. In contrast, in the presence of Lin, PSII photoinhibition increased the relative excitation of PSI and led to strong oxidation of the electron transfer chain. We hypothesize that plants are able to minimize the detrimental effects of high-light illumination on PSII by modulating the energy and electron transfer, but lose such a capability if the repair cycle is arrested. It is further hypothesized that dynamic regulation of the LHCII system has a pivotal role in the control of excitation energy transfer upon PSII damage and repair cycle to maintain the photosynthesis safe and efficient.

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