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Effects of leaf ascorbate content on defense and photosynthesis gene expression in Arabidopsis thaliana

Lookup NU author(s): Professor Christine Foyer


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Ascorbate deficiency in the Arabidopsis thaliana vtc1 mutant had no effect on photosynthesis, but modified defense pathways. The ascorbate content of vtc1 leaves was increased 14-fold after 10 mM ascorbate was supplied, without a concomitant change in redox state. High ascorbate modified the abundance of 495 transcripts. Transcripts encoding dehydroascorbate reductase, pathogenesis-related protein 1, and a peroxiredoxin were decreased, whereas those encoding salicylate induction-deficient protein 1, Cu,Zn superoxide dismutase, iron superoxide dismutase, metallothionein, and glutathione transferases were increased. Catalase transcripts were unaffected, but ascorbate peroxidase isoforms APX1 and tAPX were slightly decreased and sAPX transcripts increased. A number of nuclear encoded transcripts for photosynthetic electron transport components were repressed as a result of ascorbate accumulation, whereas those that were chloroplast-encoded were increased. High ascorbate caused decreases in mRNAs encoding chloroplast enzymes such as fructose-1,6-bisphosphatase and sedoheptulose-1,7-bisphosphatase that are activated by reduced thioredoxin. In contrast, others, such as glucose 6-phosphate dehydrogenase, whose activity is inactivated by reduced thioredoxin, were repressed. Together, these results show that ascorbate is involved in metabolic cross-talk between redox-regulated pathways. The abundance of this antioxidant provides information on redox buffering capacity that coordinates redox processes associated with the regulation of photosynthesis and plant defense.

Publication metadata

Author(s): Kiddle G, Pastori GM, Bernard B, Pignocchi C, Antoniw J, Verrier PJ, Foyer CH

Publication type: Article

Publication status: Published

Journal: Antioxidants and Redox Signalling

Year: 2003

Volume: 5

Issue: 1

Pages: 23-32

ISSN (print): 1523-0864

ISSN (electronic): 1557-7716

Publisher: Mary Ann Liebert, Inc. Publishers


DOI: 10.1089/152308603321223513


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