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Published on June 15, 2007; 10.1104/pp.107.099226

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Received March 12, 2007
Accepted June 6, 2007

Resistance to Botrytis cinerea in sitiens, an Abscisic Acid-Deficient Tomato Mutant, Involves a Timely Production of Hydrogen Peroxide and Cell Wall Modifications in the Epidermis

Bob Asselbergh , Katrien Curvers , Soraya C. França , Kris Audenaert , Marnik Vuylsteke , Frank Van Breusegem , and Monica Höfte *

Department of Plant Systems Biology, Flanders Institute for Biotechnology, 9052 Gent, Belgium; Department of Molecular Genetics, Ghent University, 9052 Gent, Belgium; and Laboratory of Phytopathology, Ghent University, 9000 Gent, Belgium

* Corresponding author; email: monica.hofte{at}ugent.be.

Plant defense mechanisms against necrotrophic pathogens such as Botrytis cinerea are considered to be complex and to differ from those that are effective against biotrophs. In the ABA-deficient sitiens tomato (Solanum lycopersicum) mutant, which is highly resistant to B. cinerea, accumulation of hydrogen peroxide was earlier and stronger than in the susceptible wild type at the site of infection. In sitiens, hydrogen peroxide accumulation was observed from 4 h post inoculation, specifically in the leaf epidermal cell walls, where it caused modification by protein cross-linking and incorporation of phenolic compounds. In wild-type tomato plants, hydrogen peroxide started to accumulate 24 h post inoculation in the mesophyll layer and was associated with spreading cell death. Transcript profiling analysis using TOM1 microarrays revealed that defense-related transcript accumulation prior to infection was higher in sitiens than in wild type. Moreover, further elevation of sitiens defense gene expression was stronger than in wild type 8 h post inoculation, both in number of genes and in their expression levels and confirmed a role for cell wall modification in the resistant reaction. Although in general, plant defense-related reactive oxygen species formation facilitates necrotrophic colonization, these data indicate that a timely hyperinduction of hydrogen peroxide-dependent defenses in the epidermal cell wall can effectively block early development of B. cinerea.




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