Abstract
The quenching of chlorophyll fluorescence caused by photodamage of Photosystem II (qI) is a well recognized phenomenon, where the nature and physiological role of which are still debatable. Paradoxically, photodamage to the reaction centre of Photosystem II is supposed to be alleviated by excitation quenching mechanisms which manifest as fluorescence quenchers. Here we investigated the time course of PSII photodamage in vivo and in vitro and that of picosecond time-resolved chlorophyll fluorescence (quencher formation). Two long-lived fluorescence quenching processes during photodamage were observed and were formed at different speeds. The slow-developing quenching process exhibited a time course similar to that of the accumulation of photodamaged PSII, while the fast-developing process took place faster than the light-induced PSII damage. We attribute the slow process to the accumulation of photodamaged PSII and the fast process to an independent quenching mechanism that precedes PSII photodamage and that alleviates the inactivation of the PSII reaction centre.
Highlights
PSII and PSII reaction centre (RC) photoinactivation
Since the decrease in τAV might be related to damage of the Mn4CaO5 cluster or induced by photosynthetic pigments, we compared the effect of blue light versus red light where photodamage is mostly driven by photosynthetic pigments
We have shown that quenchers can be formed before Total PSII inactivation takes place, so it is within reason to hypothesize that the observed quenchers photoprotect the RC to some extent
Summary
The Mn photoinactivation model suggests that photodamage of PSII is caused by direct absorption of light by the Mn4CaO5 cluster[3,12] within PSII and is independent of excessive excitation of chlorophyll. For supporters of the Mn photoinactivation model, the physiological role of NPQ is not to avoid Total PSII damage but to protect RC and the PSII repair mechanisms[15]. Even though most reports about NPQ acknowledge its role as a mechanism of Total PSII photoprotection[13,14,16,17,18], experimental evidence suggests that quenching of excitation has low efficiency in protecting against the light-induced loss of the Total PSII activity[15,19,20,21]. The time-dependent PSII activity decrease and quenching fluorescence lifetime are compared to the time course of PSII photoinactivation
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