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PLANT PHYSIOLOGY , Vol 115, Issue 3 1277-1285, Copyright © 1997 by American Society of Plant Biologists

BIOCHEMISTRY AND ENZYMOLOGY

L-Ascorbic Acid Metabolism in the Ascorbate-Deficient Arabidopsis Mutant vtc1

P. L. Conklin, J. E. Pallanca, R. L. Last and N. Smirnoff
Boyce Thompson Institute for Plant Research and Section of Genetics and Development, Cornell University, Ithaca, New York 14853-1801 (P.L.C., R.L.L.)

The biosynthesis of L-ascorbic acid (vitamin C) is not well understood in plants. The ozone-sensitive Arabidopsis thaliana mutant vitamin c-1 (vtc1; formerly known as soz1) is deficient in ascorbic acid, accumulating approximately 30% of wild-type levels. This deficiency could result from elevated catabolism or decreased biosynthesis. No differences that could account for the deficiency were found in the activities of enzymes that catalyze the oxidation or reduction of ascorbic acid. The absolute rate of ascorbic acid turnover is actually less in vtc1 than in wild type; however, the turnover rate relative to the pool of ascorbic acid is not significantly different. The results from [U-14C]Glc labeling experiments suggest that the deficiency is the result of a biosynthetic defect: less L-[14C]ascorbic acid as a percentage of total soluble 14C accumulates in vtc1 than in wild type. The feeding of two putative biosynthetic intermediates, D-glucosone and L-sorbosone, had no positive effect on ascorbic acid levels in either genotype. The vtc1 defect does not appear to be the result of a deficiency in L-galactono-1,4-lactone dehydrogenase, an enzyme able to convert L-galactono-1,4-lactone to ascorbic acid.


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