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Published on July 18, 2008; 10.1104/pp.108.123372

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Received May 23, 2008
Accepted July 14, 2008

Monogalactosyldiacylglycerol deficiency in Arabidopsis thaliana affects pigment composition in the prolamellar body and impairs thylakoid membrane energization and photoprotection in leaves

Henrik Aronsson *, Mark A Schottler , Amelie A Kelly , Christer Sundqvist , Peter Dormann , Sazzad Karim , and Paul Jarvis

Department of Plant and Environmental Sciences, University of Gothenburg, Box 461, SE-405 30 Gothenburg, Sweden; Max-Planck-Institute of Molecular Plant Physiology, Am Muhlenberg 1, 14476 Golm, Germany; Department of Biochemistry and Biophysics, The Arrhenius Laboratories for Natural Sciences, Stockholm University, SE-106 91 Stockholm, Sweden; Department of Biology, University of Leicester, University Road, Leicester LE1 7RH, United Kingdom

* Corresponding author; email: henrik.aronsson{at}dpes.gu.se.

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 synthase 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) versus 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 (qE), 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 PSII 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.






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