Reduced susceptibility to B. cinerea is associated specifically
with anthocyanin accumulation. Anthocyanin levels have been
associated with reduced susceptibility to Botrytis in grapes
[25] and may reduce postharvest spoilage of fruits in general
by Botrytis. When we grew B. cinerea on agar plates supplemented with red and purple fruit
juice, neither extract inhibited the growth
of the fungus (Figure 4C). This indicates
that anthocyanins do not suppress the
growth of B. cinerea directly and that
the resistance requires living host cells.
Between 24 and 48 hr after infection
withB. cinerea, lesions on red fruit spread
quickly, while on purple fruit their size remained
small (Figure 1E). 3,30
-diaminobenzidine
(DAB) staining of H2O2 in infected
red and purple fruits during this
period showed that a ROS burst was
generated at the infection site. However,
the ROS burst on red fruit spread widely,
whereas on purple fruit strong ROS
induction was restricted to the inoculation
site (Figure 4D). The oxidative burst
is thought to potentiate infection by necrotrophic
pathogens that feed on dead
tissue, facilitating the expansion of
disease lesions [26–28]. Vacuum infiltration of diphenyleneiodonium
chloride (DPI), an NADPH oxidase inhibitor, into red fruit
prior to B. cinerea inoculation restricted the spread of lesions,
whereas infiltration of purple tomatoes with glucose and glucose
oxidase (which induce ROS, through the generation of H2O2)
increased lesion growth in purple fruit (Figure 4E). These data
suggest that in purple tomatoes, anthocyanins alter the dynamics of the ROS burst generated byB. cinereainfection and
limit the induction of cell death necessary for growth of the
necrotroph.