Agriculture Reference
In-Depth Information
there is a cost in maintaining complex virulence mechanisms (Vanderplank, 1968).
Despite this, on exposure to multiple host resistance genotypes, though not necessarily in
mixtures, virulence patterns increase in complexity as each season progresses (Newton
et al
., 1998). Thus, exposure to multiple host genotypes is the basis on which mixtures
both inhibit epidemics of pathogens with simple virulence characteristics and select for
races with complex virulence thereby avoiding triggering resistance mechanisms. This
suggests there is a trade-off in the extent to which the pathogens are exposed to multiple
host genotypes with an optimum level of exposure to maximise epidemic control but
minimise selection for complex virulence.
Pathologists have often proposed multilines rather than variety mixtures to control
disease. These are isogenic or near-isogenic lines differing only in specifi c resistance
genes (Browning & Fey, 1969; Wolfe, 1985; Mundt, 2002a). Whilst potentially useful
for optimising control of pathogens with specifi c gene-for-gene interactions, they target
only such specifi c pathogens and will not capitalise on other heterogeneous interactions.
Furthermore, considerable investment is made in developing such lines in a variety which
may be superseded and for which therefore there is no market demand.
Even for disease control, the effi cacy of mixtures is not just dependent on specifi c
interactions between host and pathogen populations. The canopy structure can be crucial
in a number of ways, which can be well illustrated by the pathogen
Rhynchosporium
secalis
, causal agent of 'rhynchosporium', 'scald' or 'leaf blotch' on barley and common
in many regions of the world. It is splash-dispersed, such as from the soil, where spore
inoculum may survive on crop debris, then from leaf to leaf as it forms necrotic lesions or
asymptomatic infections and sporulates (Zhan
et al
., 2008). An open canopy will enable
rapid transmission by rain splash up the plant. Epidemic progress can be reduced by
molecular and morphological mechanisms. Genetic resistance results when specifi c geno-
types (races) of the pathogen are recognised by plant defence genes causing induction of
resistance expression mechanisms. If the host plant has only a single recognition gene then
the pathogen will mutate to produce new races not recognised by the pathogen, and multi-
ple host plant genotypes with many different recognition genes could be deployed, which
may lead to stability as discussed above. However, morphological differences between
component varieties in the mixture can be manipulated to reduce the epidemic progress
too. Plants with different height and leaf angle can be deployed together, providing a
complex canopy structure and disrupting vertical splash pathways for pathogen dispersal.
Multiple contrasting morphological types are particularly effective in this, particularly
those with contrasting dwarfi ng gene (Newton
et al
., 2004). Mixtures are effective against
other splash-dispersed pathogens which have even less host specifi city expressed, such as
Septoria Leaf Blotch (
Mycosphaerella graminicola
) on wheat (Cowger & Mundt, 2002)
and glume blotch (
Phaeosphaera nodorum
) on wheat (Jeger
et al
., 1981a) and again in
R. secalis
on barley (Jeger
et al
., 1981b).
Mixtures have been reported to have effi cacy against pathogens in the root environ-
ment. For example, eyespot was reduced in one study on wheat (Mundt
et al
., 1995), but
not on barley (Gieffers & Hesselbach, 1988). Perhaps more importantly when considering
the crop system rather than just disease control, yield benefi ts have been reported even
when disease is not always reduced for several soil pathogens such as
Phytophthora sojae
in soyabean (Wilcox & St. Martin, 1988) and
Cephalosporium graminearum
in wheat
(Mundt, 2002b).
Rhizoctonia solani
was reduced in sugar beet (Halloin & Johnson, 2000)
