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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

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Record number 33501
Title Mechanistic aspects of the inhibition of photosynthesis by light = [Mechanistische aspekten van de remming van de fotosynthese door licht]
Author(s) Schansker, G.
Source Agricultural University. Promotor(en): W.J. Vredenberg; J.J.S. van Rensen. - S.l. : Schansker - ISBN 9789054854661 - 116
Department(s) Laboratory of Plant Physiology
EPS
Publication type Dissertation, internally prepared
Publication year 1996
Keyword(s) fotosynthese - photosynthesis
Categories Plant Physiology / Photosynthesis
Abstract
The photosynthetic apparatus is sensitive to excess light. This phenomenon is called photoinhibition. It affects specifically photosystem II (PSII) and is related in some way to the turnover of the DI protein, a central component of PSII.

Measurements performed with plant systems that were photoinhibited under in vivo conditions give evidence for the conclusion that the photoinactivation site is localized on the acceptor side of PSII. Several mechanisms have been postulated to explain the inactivation process. In Chapter 3, one of these mechanisms is treated more extensively. The protonation of the secondary electron acceptor, Q B , is as yet badly understood. It is hypothesized (Chapter 3) that the acceptor side of (PSII) shows carbonic anhydrase activity. A C0 2 and a H 2 0 molecule can bind to the non-heme iron and can react with each other to form bicarbonate and to release a proton. The theory postulates that during a photoinhibitory treatment the probability that bicarbonate/C0 2 disappears from its binding site increases. It is further argued that this loss is irreversible.

Silicomolybdate is an electron acceptor that is able to accept electrons from the non-heme iron. Binding of SiMo to its acceptor site causes displacement of bicarbonate/CO 2 . In Chapter 4 the interaction between SiMo, bicarbonate/C0 2 and (PSII) was analyzed. Information was obtained on the binding site of SiMo, and the binding characteristics of both SiMo and bicarbonate/CO 2 . The characterization of SiMo binding was necessary to be able to use the compound for photoinhibition studies.

In Chapter 5 it was established that in pea thylakoids the inactivation site of photoinhibition is indeed located on the acceptor side of PSII. Further it was observed that the donor side is also inactivated though at a much slower rate. Photoinactivation of both donor and acceptor side are light dose dependent. Displacement studies of bicarbonate/CO 2 with nitric oxide (NO) and SiMo indicated that the displacement of bicarbonate is irreversible. As expected, the addition of bicarbonate does not give any lasting protection against photoinhibition. The pH- dependence of acceptor side inactivation corresponds with theoretical considerations of bicarbonate/CO 2 behavior: an increased sensitivity towards photoinhibition below pH 7 and a maximum difference between the rate of donor and acceptor side inactivation around pH 6.4. These observations support the theory that bicarbonate release is responsible for the photoinactivation of PSII.

In Chapter 6 a site-directed mutant of Synechocystis sp. PCC 6803 was used to find support for our hypothesis. This mutant is mutated in the binding environment of the non-heme iron. It is four times more sensitive to photoinhibition than a reference strain. One of the main effects of the mutation is a ten times higher sensitivity to formate (formate displaces bicarbonate). This indicates that bicarbonate is more loosely bound to PSII. in this mutant. This may explain the increased sensitivity to photoinhibition and in that case this result supports our hypothesis.

In Chapter 7 the effects of photoinhibition on the regulation of photosynthetic electron transport were studied. A combination of photoacoustic and fluorescence spectroscopy was used. A small population of (PSII) reaction centers was found that does not produce oxygen, but does fluoresce. The fluorescence data were corrected for these inactive centers. Initially, the fraction of reduced PSII reaction centers increases as a consequence of the photoinhibitory treatment (photochemical quenching, q P decreases). Possibly this change is brought about by dephosphorylation of the antenna complex. A more severe photoinhibitory treatment causes an oxidation of the (PSII) reaction centers (q P , increases). Other components of the electron transport chain, apart from (PSII) are hardly affected by a photoinhibitory treatment and therefore, the demand for electrons remains at the same level. As a consequence the still active PSII reaction centers can work progressively more efficient. The decline of energetic quenching, q E , during a photoinhibitory treatment could almost entirely be explained by a decline of the available number of (PSII) reaction centers. A small part of the decline of q E has other causes, possibly an increase of the lumen pH as a consequence of a lower proton excretion into the lumen or an increased proton permeability of the thylakoid membrane. The fluorescence data also indicated that the recovery rate of photoinhibition depends on the rate of ATP synthesized by linear electron transport. Cyclic electron transport is not able to compensate for the lost capacity of linear electron transport to induce ATP synthesis during a photoinhibitory treatment.

In conclusion, the effects of a moderate photoinhibitory treatment in pea leaves can be explained by dephosphorylation of the antenna system. The effects of a severe photoinhibitory treatment are caused by a progressive inactivation of PSII. Indications were collected supporting the hypothesis that bicarbonate/CO 2 release is the trigger leading to the inactivation of PSII.

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