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First published online July 18, 2008; 10.1104/pp.108.123372

Plant Physiology 148:580-592 (2008)
© 2008 American Society of Plant Biologists

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BIOENERGETICS AND PHOTOSYNTHESIS

Monogalactosyldiacylglycerol Deficiency in Arabidopsis Affects Pigment Composition in the Prolamellar Body and Impairs Thylakoid Membrane Energization and Photoprotection in Leaves1,[W],[OA]

Henrik Aronsson*, Mark A. Schöttler2, Amélie A. Kelly2,3, Christer Sundqvist, Peter Dörmann4, Sazzad Karim5 and Paul Jarvis

Department of Plant and Environmental Sciences, University of Gothenburg, SE–405 30 Gothenburg, Sweden (H.A., C.S., S.K.); Max-Planck-Institute of Molecular Plant Physiology, 14476 Golm, Germany (M.A.S., P.D.); Department of Biochemistry and Biophysics, Arrhenius Laboratories for Natural Sciences, Stockholm University, SE–106 91 Stockholm, Sweden (A.A.K.); and Department of Biology, University of Leicester, Leicester LE1 7RH, United Kingdom (P.J.)

Monogalactosyldiacylglycerol (MGDG) is the major lipid constituent of chloroplast membranes and has been proposed to act directly in several important plastidic processes, particularly during photosynthesis. In this study, the effect of MGDG deficiency, as observed in the monogalactosyldiacylglycerol synthase1-1 (mgd1-1) mutant, on chloroplast protein targeting, phototransformation of pigments, and photosynthetic light reactions was analyzed. The targeting of plastid proteins into or across the envelope, or into the thylakoid membrane, was not different from wild-type in the mgd1 mutant, suggesting that the residual amount of MGDG in mgd1 was sufficient to maintain functional targeting mechanisms. In dark-grown plants, the ratio of bound protochlorophyllide (Pchlide, F656) to free Pchlide (F631) was increased in mgd1 compared to the wild type. Increased levels of the photoconvertible pigment-protein complex (F656), which is photoprotective and suppresses photooxidative damage caused by an excess of free Pchlide, may be an adaptive response to the mgd1 mutation. Leaves of mgd1 suffered from a massively impaired capacity for thermal dissipation of excess light due to an inefficient operation of the xanthophyll cycle; the mutant contained less zeaxanthin and more violaxanthin than wild type after 60 min of high-light exposure and suffered from increased photosystem II photoinhibition. This is attributable to an increased conductivity of the thylakoid membrane at high light intensities, so that the proton motive force is reduced and the thylakoid lumen is less acidic than in wild type. Thus, the pH-dependent activation of the violaxanthin de-epoxidase and of the PsbS protein is impaired.


1 This work was supported by the Swedish Research Council FORMAS (to H.A.) and VR (to C.S.), by the Wenner-Gren Foundation (to H.A. and A.A.K.), by the Royal Society of Arts and Sciences in Göteborg (to H.A.), by the Royal Swedish Academy of Sciences (to H.A.), by the Deutsche Forschungsgemeinschaft (grant no. SFB429, A12 to M.A.S.; and grant no. SFB429, B6 to P.D.), by the Royal Society Rosenheim Research Fellowship (to P.J.), and by the Biotechnology and Biological Sciences Research Council (to P.J.).

2 These authors contributed equally to the article.

3 Present address: HRI/University of Warwick, Wellesbourne, Warwick CV35 9EF, United Kingdom.

4 Present address: University of Bonn, Institute of Molecular Physiology and Biotechnology of Plants, Karlrobert-Kreiten-Strasse 13, 53115 Bonn, Germany.

5 Present address: Institute of Biology, University of Tromsø, NO–9037 Tromsø, Norway.

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Henrik Aronsson (henrik.aronsson{at}dpes.gu.se).

[W] The online version of this article contains Web-only data.

[OA] Open Access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.108.123372

* Corresponding author; e-mail henrik.aronsson{at}dpes.gu.se.

Received May 23, 2008; accepted July 14, 2008; published July 18, 2008.







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