Spectroscopic studies of photodamage and photoprotection of photosystem II

Abstract

Light is required for photosynthesis to occur, but it also has a deleterious effect by damaging the photosynthetic machinery, in particular Photosystem II (PSII). Photoinhibition of PSII is a complex process, balancing between photoinactivation, protective and repair mechanisms. Current understanding of photodamage is limited to competing hypotheses where the photosensitizer is either photosynthetic pigments or the Mn4CaO5 cluster itself, with little consensus on the mechanisms and consequences of PSII photoinactivation. Using different spectroscopic techniques, the author evaluated the mechanisms of photodamage and photoprotection of PSII under visible light. In the first Chapter a critical examination is presented of current evidence about the photodamage mechanisms, in particular that related to the action spectra of photodamage. The second Chapter examines if the damage to the Mn4CaO5 cluster is applicable to PSII under visible light as manganese absorbs visible light only weakly. The third Chapter was intended to determine which of the three main events of PSII photodamage occurs first: (1) Inactivation of the oxygen evolution; (2) inactivation of the PSII RC; (3) and release of Mn ions. The fourth Chapter evaluates whether quenching of excessive excitation does protect PSII from photodamage, as the recent rise of paradigms that advocate that photodamage is independent of excessive excitation has questioned the relevance of quenching mechanisms. Finally, the fifth Chapter discusses and integrates the result of the present thesis in the context of the current hypothesis to explain PSII photodamage. The main results of this work are: (1) visible light damages Mn4CaO5 cluster prior to photodamage to the PSII reaction center; (2) the two step model under visible light is explained mostly by limitations on the acceptor side; (3) release of Mn ions is not the cause of PSII inactivation but a later consequence; and (4) the discovery of a long-lived fluorescence quencher that accumulates faster than the light-induced loss of PSII efficiency shows that the induction of this quencher is a preventive mechanism to reduce the excitation pressure and not the consequence of photodamage. Upon critical examination of the previously reported evidence and the new discoveries in the present work, the hybrid mechanism of photoinactivation, sensitized mostly by photosynthetic pigments and in minor way the Mn4CaO5, is the most plausible explanation to PSII photodamage under visible light. Show more