“…Histochemical staining in Botrytis ‐infected Arabidopsis leaves revealed that the oxidative burst in a compatible interaction comprises the simultaneous production of hydrogen peroxide and nitric oxide, as well as the formation of proteolytic, autophagosome‐like vesicles at the host–pathogen interface (van Baarlen et al ., 2007). B. cinerea infection leads to the accumulation of free radicals, both at the host–pathogen interface and at some distance from the invading hyphae (Muckenschnabel et al ., 2001a, 2003) culminating in lipid peroxidation (Deighton et al ., 1999; Muckenschnabel et al ., 2001b, 2002) and depletion of antioxidants (Muckenschnabel et al ., 2002). Altogether, these oxidative processes cause massive perturbation of the redox status in and around the infected tissue, thereby promoting disease progress (Lyon et al ., 2004).…”