Plant basal resistance - Universiteit Utrecht

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General discussion
(Gianoli et al., 1996). Similarly, time ingesting from diets containing different quantities of
BXs (DIMBOA and DIMBOA-glc) was negatively correlated with BX concentration for five
cereal aphid species: M.dirhodum, R.padi, R.maidis, S.avenea and S.gramnium suggesting a
role of BXs as feeding deterrent (Givovich and Niemeyer, 1994). Performance of the Russian
wheat aphid (Diuraphis noxia) was lower on wheat cultivars with augmented levels of BXs
than those having lower quantities. In this study, aphid performance was measured by the
time aphids took to reach their feeding site and the number of aphids ultimately reaching
phloem. Aphids took more time to reach the phloem and a lower proportion of them were
able to reach the phloem of the cultivar with higher BXs contents and vice versa (Givovich
and Niemeyer, 1996).
The second objective of the work outlined in Chapter 3 was to examine the role
of BXs in maize defence against the necrotrophic fungal pathogen S. turcica. Pathogen
colonization was scored by measuring fungal hyphael lengths and the relative amount of
arrested fungal spores. As expected, Bx1 igl lines from both crosses were more resistant
to S. turcica than the corresponding bx1 igl lines (Chapter 3; Figure 3), demonstrating
that BXs play a role in basal resistance against microbial pathogens. In wheat and maize,
different studies have provided correlative evidence for the role of BXs in basal defense
against different pathogens, such as Helminthosporium turticum, Ceplphalosporium maydis,
and Puccinia graminis (Niemeyer, 2009). Our study has provided genetic and physiological
evidence for a significant contribution of maize BXs to basal resistance against pathogenic
fungi.
DIMBOA: A NOVEL APOPLASTIC REGULATOR OF POST-INVASIVE DEFENCE IN MAIZE
BXs are induced upon pathogen/insect attack (Leszczynski and Dixon, 1990; Weibull and
Niemeyer, 1995; Gianoli and Niemeyer, 1997) and our data from Chapter 3 are in agreement
with these findings. Interestingly, we found that most of these inductions took taking place in
the extracellular spaces (apoplast) of the leaf tissue. We chose to quantify BX concentrations
in the apoplast because the aphid stylet has to pass through this compartment to reach it
feeding site, the phloem, and fungal hyphae colonize the apoplast. As we hypothesised,
the most prominent increases in BXs upon aphid feeding, fungal infection and chitosan
treatment were found in the apoplastic fluid. These findings provide novel insight into the
role of BXs in fungal and aphid resistance. It was previously postulated that the release
of toxic BXs are dependent on tissue disruption/damage. Our study reveals for the first
time that BX dependent resistance in maize does not depend entirely on tissue disruption.
Although chewing insects inflict major tissue disruption, thereby causing cellular release of
vacuolar metabolites, the early stages of infestation by aphids and fungi are not associated
with major tissue damage. Nevertheless, induction of BX accumulation by these pests