Septoria and Stagonospora Diseases of Cereals - CIMMYT ...

Session 6A / Session 6B — C.C. Mundt, C. Cowger, and M.E. Hoffer
114
Greenhouse tests indicated that non-inoculated genotypes
host diversity had a substantial comprising 35-40% of the
impact on pathogenicity of M. population later in the season. In
graminicola (Table 1). All populations contrast, natural inoculum has been
derived from the mixtures produced estimated to result in hundreds of
less disease on its component unique genotypes per m
varieties in the greenhouse than the
mean of the populations derived
from the pure stand components in
the field.
Molecular analyses (Zhan et al.,
1998) have previously shown that the
artificial inoculation used in the
1994/95 season competitively
excluded 97% of potential ascospore
infections early in the season, though
immigration and sexual
recombination among inoculated
and/or naturally occurring
genotypes within plots resulted in
2
(McDonald et al., 1996). For the
artificially-inoculated plots,
epidemic progression for the
Madsen/Stephens mixture was
approximately midway between
the two pure stands throughout the
epidemic (Figure 2). By contrast, in
the naturally-inoculated plots,
epidemic progression in the
mixture began midway between
the pure stands, but became
suppressed to near that of the
moderately resistant variety as the
season progressed (Figure 2).
Table 1. Disease severity (percent of second leaf
area covered by septoria tritici blotch lesions)
caused by Mycosphaerella graminicola populations
derived from single wheat varieties and variety
mixtures in replicated field plots.
Source of population
Variety mixture Mixturea Pure standsb Madsen/Stephens 9.5 15.9
Madsen/W-301 9.3 11.6
Cashup/Stephens 10.8 13.4
Cashup/W-301 6.6 9.0
a Mean disease severity for populations derived from a
given mixture when tested separately on each of the
component varieties. For example, populations
collected from the Madsen/Stephens mixture in the
field were tested separately on Madsen and Stephens
in the greenhouse.
b Mean disease severity for populations derived from the
component pure stands and tested on the same variety.
For example, to compare with populations derived from
the Madsen/Stephens mixture, populations collected
from pure stands of Madsen in the field were tested on
Madsen in the greenhouse and populations derived
from pure stands of Stephens in the field were tested
on Stephens in the greenhouse.
percent disease
percent disease
100
90
80
70
60
50
40
30
20
10
0
25-Jan
100
90
80
70
60
50
40
Discussion
Our results indicate that some
variety mixtures suppress epidemic
progression of septoria tritici blotch
even in the absence of major genes for
resistance. There are at least two
plausible explanations for this result.
First, the models of Jeger et al. (1981a)
have shown that, in absence of host/
pathogen specificity, mixtures can
decrease, increase, or have no effect
on epidemic progression, depending
on the relative levels of sporulation
and infection frequency in the
component varieties. Thus,
differences between mixtures and
pure stands in our experiment might
be explained by differences in
resistance components between
cultivars, though we have not
measured these components.
Artificially inoculated plots
Madsen
Stephens
Stephens/Madsen mixture
15-Mar 4-May 23-Jun
Naturally inoculated plots
Madsen
Stephens
Stephens/Madsen mixture
30
20
10
0
25-Jan 15-Mar 4-May 23-Jun
Figure 2. Disease progress of septoria tritici blotch on a
moderately resistant variety (Madsen), a susceptible
variety (Stephens) and a 1:1 mixture of the two varieties
in epidemics initiated from artificial inoculation with 10
isolates or from naturally occurring inoculum.