First published online April 2, 2004; 10.1104/pp.103.032185
Plant Physiology 134:1784-1792 (2004)
© 2004 American Society of Plant Biologists
PLANTS INTERACTING WITH OTHER ORGANISMS
The Timing of Senescence and Response to Pathogens Is Altered in the Ascorbate-Deficient Arabidopsis Mutant vitamin c-11
Carina Barth,
Wolfgang Moeder,
Daniel F. Klessig and
Patricia L. Conklin*
Boyce Thompson Institute for Plant Research, Ithaca, New York 14853 (C.B., W.M., D.F.K.); and Department of Biological Sciences, State University of New York College at Cortland, Cortland, New York 13045 (P.L.C.)
The ozone-sensitive Arabidopsis mutant vitamin c-1 (vtc1) is deficient in L-ascorbic acid (AsA) due to a mutation in GDP-Man pyrophosphorylase (Conklin et al., 1999), an enzyme involved in the AsA biosynthetic pathway (Smirnoff et al., 2001). In this study, the physiology of this AsA deficiency was initially investigated in response to biotic (virulent pathogens) stress and subsequently with regards to the onset of senescence. Infection with either virulent Pseudomonas syringae or Peronospora parasitica resulted in largely reduced bacterial and hyphal growth in the vtc1 mutant in comparison to the wild type. When vitamin c-2 (vtc2), another AsA-deficient mutant, was challenged with P. parasitica, growth of the fungus was also reduced, indicating that the two AsA-deficient mutants are more resistant to these pathogens. Induction of pathogenesis-related proteins PR-1 and PR-5 is significantly higher in vtc1 than in the wild type when challenged with virulent P. syringae. In addition, the vtc1 mutant exhibits elevated levels of some senescence-associated gene (SAG) transcripts as well as heightened salicylic acid levels. Presumably, therefore, low AsA is causing vtc1 to enter at least some stage(s) of senescence prematurely with an accompanying increase in salicylic acid levels that results in a faster induction of defense responses.
1 This work was supported by the German Academic Exchange Service (postdoctoral fellowship D/00/22216 to C.B.), the National Science Foundation (grant no. MCB–0110404 to D.F.K.), and the U.S. Department of Agriculture National Research Initiative Competitive Grants Program (grant no. 96–35100–3212 to P.L.C.).
Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.103.032185.
* Corresponding author; e-mail conklinp{at}cortland.edu; fax 607–753–2927.
Received August 22, 2003;
returned for revision November 25, 2003;
accepted November 25, 2003.
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