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 abscisic acid-deficient sitiens tomato ( Solanum lycopersicum ) mutant, which is highly resistant to B. cinerea , accumulation of hydrogen peroxide (H 2 O 2 ) was earlier and stronger than in the susceptible wild type at the site of infection. In sitiens , H 2 O 2 accumulation was observed from 4 h postinoculation (hpi), 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, H 2 O 2 started to accumulate 24 hpi 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 hpi 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 timely hyperinduction of H 2 O 2 -dependent defenses in the epidermal cell wall can effectively block early development of B. cinerea .
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