Agriculture Reference
In-Depth Information
Fusarium head blight
Resistance to Fusarium head blight has been dif-
fi cult to characterize and incorporate into adapted
cultivars because of the need to have both resis-
tance to infection and resistance to deoxynivale-
nol accumulation (Gartner et al., 2008). There are
also differences in genetic control of resistance to
fl oret infection (Type I), resistance to spread in
the spike (Type II), and resistance to deoxyniva-
lenol accumulation (Schroeder and Christensen
1963; Mesterhazy 1995; Somers et al., 2003;
Bai and Shaner 2004). Quantitative trait loci
(QTLs) for resistance have also been identifi ed
(Chen et al., 2006; Yu et al., 2008). Molecular
markers for resistance have accelerated the
incorporation of effective resistance into wheat
germplasm (Anderson 2007). The Chinese
cultivar Sumai 3 has a high level of Type II resis-
tance with good combining ability, and it has
been used throughout the world to improve
Fusarium head blight resistance (Bai and Shaner
2004).
Scharen 1988; Somasco et al., 1996; Simon and
Cordo 1997; Arraiano et al., 2001; Brading et al.,
2002; McCartney et al., 2003). Chartrain et al.
(2004b) found that disease severity was not
correlated between the seedling and adult
stages. Sources of resistance to septoria tritici
blotch have been found in primary, secondary,
and tertiary gene pools of wheat (Mergoum et al.,
2007; Simon et al., 2007; Singh et al., 2006).
Twelve genes for resistance to septoria tritici
blotch have been named and mapped (Goodwin
2007).
Tan spot
A major component in the management of tan
spot is host-plant resistance, which is the
most effective, economical, and environmentally
friendly way to control tan spot. Race-specifi c
resistance to tan spot is the result of insensitivity
to one or more of the host-selective toxins, plus
other factors that slow or inhibit pathogen growth
and development (Friesen et al., 2001b, 2003).
However, in the presence of toxin sensitivity,
quantitative resistance has also been identifi ed
(Faris and Friesen 2005). Resistance to races 1
and 5 of
Pyrenophora tritici-repentis
was identifi ed
in spring wheat seedlings under greenhouse con-
ditions (Ali et al., 2008). Resistance to race 1 was
found in a large array of wheat-alien species
derivatives and synthetic wheat lines (Xu et al.,
2004; Oliver et al., 2008).
In a fi eld evaluation of adult-plant resistance to
race 1, Duveiller et al. (2007) showed that resis-
tance in spring wheat was controlled by two gene
pairs. Evans et al. (1999) found a signifi cant cor-
relation between lesion length as determined
under greenhouse conditions and area under the
disease progress curve as determined in the fi eld,
thereby indicating that progress in breeding for
resistance could be made with either or both
techniques. Although some research has been
conducted to use Ptr toxins to screen wheat for
differences in susceptibility, and conditions for
in vitro
toxin production have been studied,
the correlation between toxin production and
pathogenicity has been poor (Brown and Hunger
1999).
FUTURE PERSPECTIVES
A common thread to each of these diseases is the
ability of the causal fungi to survive and undergo
sexual recombination on wheat residue. When
infested residue is not brought into contact with
soil, it can serve as a safe harbor for the pathogen
to survive between crops. Moreover, it allows the
pathogen to complete its life cycle, thus increas-
ing genetic variability and potentially new viru-
lence combinations. Increased amounts of wheat
residue on the soil surface increases the likelihood
of pathogens surviving on the residue, thereby
providing a source of inoculum that otherwise
may have been eliminated or minimized by tillage
(Bailey and Duczek 1996).
This does not mean that increased residue will
inevitably lead to greater disease. Disease inci-
dence and severity depend on many factors,
including a virulent pathogen, a susceptible host,
and environmental conditions conducive for
infection, growth, reproduction, and spread of
the pathogen. In addition, the level of disease on
