Agriculture Reference
In-Depth Information
and Hovmoller 2002; Hsam and Zeller 2002).
Breeding for powdery mildew resistance in wheat
began in the early 1930s with the pioneering host-
pathogen interaction work of Mains (Mains 1934).
Many of the initial powdery mildew resistance
(
Pm
) genes identifi ed were major or seedling
genes, which conferred a hypersensitive resis-
tance reaction (Briggle 1966). Later studies, par-
ticularly in Europe, showed that widespread
deployment of single, major genes typically
resulted in the selection of races capable of over-
coming the resistance (Svec and Miklovicova
1998).
Researchers have identifi ed about 50
Pm
genes
or alleles, occurring at 33 loci, with 5 of the
loci (
Pm1
,
Pm3
,
Pm4
,
Pm5
, and
Pm8
) having
multiple alleles (Hsam and Zeller 2002; Miranda
et al., 2006). A number of the genes and alleles
for powdery mildew resistance probably have
not been deployed. As a result, germplasm devel-
oped with these
Pm
genes and combinations
of these
Pm
genes could have a high level of
resistance to populations of
B. g. tritici
(Engle
et al., 2006).
In the absence of genetic analyses or reliable
molecular markers, it is still possible to postulate
the presence of specifi c
Pm
genes using pathogen
isolates with particular virulence-avirulence
profi les, because the wheat-powdery mildew
pathosystem typically follows a gene-for-gene
relationship. By comparing the reactions of
well-characterized
B. g. tritici
isolates on a
differential host series with their reactions on
unknown wheat genotypes, the identity of
Pm
genes in the unknown lines can be deduced. Leath
and Heun (1990) used gene postulation to identify
known
Pm
genes in 22 soft red winter wheat
cultivars.
In addition to major-gene resistance, wheat
also has partial, adult-plant, or minor-gene resis-
tance to powdery mildew. This partial resistance
may take the form of defeated yet not completely
susceptible major genes such as
Pm3c
(Nass
et al., 1981),
Pm4b
(Mingeot et al., 2002), and
Pm5
(Keller et al., 1999). In addition, adult-plant
resistance has been identifi ed in the cultivars
Knox (Shaner 1973), Knox 62, and Massey
(Griffey and Das 1994). This resistance delays
infection and reduces growth and reproduction
of
B. g. tritici
in adult plants (Gustafson and
Shaner 1982). Because this adult-plant (slow
mildewing) resistance is thought to be race-
nonspecifi c (Elen and Skinnes 1988), the proba-
bility of
B. g. tritici
developing races highly
adapted to adult-plant resistance is much less
than that for seedling, hypersensitive resistance
(Hautea et al., 1987). Molecular markers would
be useful for quantitative mildew resistance,
which is diffi cult to assess phenotypically. Two
major quantitative trait loci (QTLs) and about 18
minor QTLs have been identifi ed in different
environments and at different developmental
stages (Keller et al., 1999; Mingeot et al., 2002;
Bougot et al., 2006; Jakobson et al., 2006; Tucker
et al., 2007).
Stagonospora nodorum blotch
Much of the early work on stagonospora nodorum
blotch indicated that resistance was under poly-
genic control (Nelson and Marshall 1990). Major
gene resistance has also been found, with some
reported differences in the numbers of genes con-
trolling resistance to leaf symptoms (Wilkinson et
al., 1990; Ma and Hughes 1995; Kim et al., 2004).
Two QTLs have been identifi ed (Liu et al., 2004).
Ali et al. (2008) were able to identify wheat geno-
types having multiple resistance to
Stagonospora
nodorum
,
S. tritici
, and
Pyrenophora tritici-repentis
(Ali et al., 2008). With the recent fi nding of host-
selective toxins involved in the
S. nodorum
×
wheat interaction, greater precision and insight
may be available on methods to breed for resis-
tance to stagonospora nodorum blotch (Friesen
et al., 2008).
Septoria tritici blotch
Even though there are isolate × cultivar interac-
tions, resistance to septoria tritici blotch is assessed
quantitatively, typically by determining the
percentage of leaf area covered by lesions
(Chartrain et al., 2004a). Resistance in wheat to
S. tritici
has been shown to be both monogenically
and polygenically controlled (van Ginkel and
