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First published online October 31, 2008; 10.1105/tpc.107.056341

The Plant Cell 20:2909-2925 (2008)
© 2008 American Society of Plant Biologists

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The Arabidopsis onset of leaf death5 Mutation of Quinolinate Synthase Affects Nicotinamide Adenine Dinucleotide Biosynthesis and Causes Early Ageing[W]

Jos H.M. Schippersa, Adriano Nunes-Nesib, Roxana Apetreia, Jacques Hillea, Alisdair R. Fernieb and Paul P. Dijkwela,c,1

a Molecular Biology of Plants, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, 9751 NN Haren, The Netherlands
b Max Planck Institute for Molecular Plant Physiology, Potsdam-Golm 14476, Germany
c Institute of Molecular BioSciences, Massey University, Palmerston North 4442, New Zealand

1 Address correspondence to p.dijkwel{at}massey.ac.nz.

Leaf senescence in Arabidopsis thaliana is a strict, genetically controlled nutrient recovery program, which typically progresses in an age-dependent manner. Leaves of the Arabidopsis onset of leaf death5 (old5) mutant exhibit early developmental senescence. Here, we show that OLD5 encodes quinolinate synthase (QS), a key enzyme in the de novo synthesis of NAD. The Arabidopsis QS was previously shown to carry a Cys desulfurase domain that stimulates reconstitution of the oxygen-sensitive Fe-S cluster that is required for QS activity. The old5 lesion in this enzyme does not affect QS activity but it decreases its Cys desulfurase activity and thereby the long-term catalytic competence of the enzyme. The old5 mutation causes increased NAD steady state levels that coincide with increased activity of enzymes in the NAD salvage pathway. NAD plays a key role in cellular redox reactions, including those of the tricarboxylic acid cycle. Broad-range metabolite profiling of the old5 mutant revealed that it contains higher levels of tricarboxylic acid cycle intermediates and nitrogen-containing amino acids. The mutant displays a higher respiration rate concomitant with increased expression of oxidative stress markers. We postulate that the alteration in the oxidative state is integrated into the plant developmental program, causing early ageing of the mutant.




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