Abstract
Photodamage to Photosystem II (PSII) has been attributed either to excessive excitation of photosynthetic pigments or by direct of light absorption by Mn4CaO5 cluster. Here we investigated the time course of PSII photodamage and release of Mn in PSII-enriched membranes under high light illumination at 460 nm and 660 nm. We found that the loss of PSII activity, assayed by chlorophyll fluorescence, is faster than release of Mn from the Mn4CaO5 cluster, assayed by EPR. Loss of PSII activity and Mn release was slower during illumination in the presence of exogenous electron acceptors. Recovery of PSII activity was observed, after 30 min of addition of electron donor post illumination. The same behavior was observed under 460 and 660 nm illumination, suggesting stronger correlation between excessive excitation and photodamage compared to direct light absorption by the cluster. A unified model of PSII photodamage that takes into account present and previous literature reports is presented.
Highlights
There has been a great effort to solve the causes and mechanism of Photosystem II (PSII) photodamage in the last 30 years, attempts to explain PSII photodamage have been controversial
The data presented here shows that the other PSII components (Yz, P680, Pheo and the QA) retain high level of functionality as recovery of FV/FM is observed after incubation with exogenous electron donor following light exposure at 460 nm and 660 nm
In the two step mechanism[15], it has been proposed that light induces the release of one Mn2+ ion from the Mn4CaO5 cluster, impairing O2 evolving activity and PSII is inactivated
Summary
There has been a great effort to solve the causes and mechanism of PSII photodamage in the last 30 years, attempts to explain PSII photodamage have been controversial. Previous reports suggested[3, 6,7,8,9]: (1) The rate constant of photoinactivation (kPI) of PSII is directly proportional to the irradiance in the absence of repair; (2) The time course of photoinactivation of PSII in the absence of repair is a non-reversible process that follows a first order kinetic; (3) Higher photoinactivation effect derives from shorter wavelength; (4) Photoinactivation by UV light affects two targets, the Mn4CaO5 cluster and alterations at the acceptor side of PSII Based on these observations, three hypotheses have been proposed. The two-step hypothesis proposes that the direct light absorption by the Mn4CaO5 cluster causes photodamage by inducing modifications of the Mn-oxo coordination bonds in the cluster[15, 16] This leads to the release of a Mn ion and consequent inactivation of the PSII the reaction centre[15, 16]. A ‘Unified Model’ of photodamage which provides satisfactory rationalisation of previous inconsistencies in literature is presented and discussed
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