Abstract
The current hypotheses for the mechanisms of photosystem II (PSII) photodamage in vivo remain split on the primary damage site. However, most researchers have considered that PSII is inhibited by a sole mechanism and that the photoinhibited PSII consists of one population. In this perspective, we propose 'the mixed population hypothesis', in which there are four PSII populations: PSII with active/inactive Mn4 CaO5 oxygen-evolving complex respectively with functional/damaged primary quinone (QA ) reduction activity. This hypothesis provides a new insight into not only the PSII photoinhibition/photoprotection studies but also the repair process. We discuss our new data implying that the repair rate differs in the respective PSII populations.
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