The Genetic Basis of Disease Resistance in Maize - Translational Genomics for Crop Breeding: Biotic Stress - page 33

The emergence of some diseases is related
to changes in farming practices and production.
For example, the increase in BLSB is correlated
with an increase in maize production near rice
paddies (Pingali 2001). R. solani , causal agent of
BLSB, has a broad host range, and isolates viru-
lent on rice can also infect maize (Pascual et al.
2000). Reduced tillage, which allows inoculum
to overwinter in stalk debris on the soil surface
and to reinfect maize the following season, has
increased the distribution and severity of diseases
such as GLS (Latterell and Rossi 1983; Ward
et al. 1999).
In some cases, agronomic techniques or bio-
cides are used to manage diseases. Diversity at
the population level can be used to suppress
disease progress (e.g., Mundt 2002), so syn-
thetic populations or other open-pollinated vari-
eties may present opportunities for deployment
of population-level genetic diversity for disease
management. Varietal resistance is, however, the
dominant and most convenient approach to dis-
ease management in crops in general, as well as
in maize. For purposes of this chapter, we con-
sider genetic resistance in the context of analyz-
ing or breeding individual genotypes. The overall
genetic diversity available within maize is high
compared to most crop species (Goodman 1983;
Tenaillon et al. 2001; Sachs et al. 2009), and the
primary gene pool is a rich source of disease
resistance alleles for crop improvement. While
the genetic diversity among elite hybrids is rel-
atively low (Smith et al. 1992), diverse exotic
germplasm can be utilized to identify and intro-
duce novel disease resistance genes and alleles
into maize varieties (Goodman 1999).

egories are often presented as quite distinct, there
is a gray area between these types of resis-
tance in practice (Poland et al. 2009; see dis-
cussion later in the chapter). A number of quali-
tative resistance genes (often referred to as major
genes) have been cloned in a number of different
plant systems (e.g. Ellis et al. 2000; Sanseverino
et al. 2010). Most major genes function by detect-
ing the presence or the activity of pathogen-
derived proteins and then inducing a rapid, local-
ized defense response (called a hypersensitive
response) at the point of infection, which lim-
its pathogen growth (Bent and Mackey 2007).
This type of defense is often referred to as
effector-triggered immunity or ETI (Jones and
Dangl 2006), and major genes of this type have
been referred to as R-genes. R-genes gener-
ally provide high levels of resistance and are
easy to manipulate in breeding programs. How-
ever, they generally provide only race-specific
resistance and are often easily overcome by
the pathogen, such that they are typically not
durable in an agricultural context (McDonald
and Linde 2002).
At least 17 qualitative resistance genes have
been identified and mapped for several diverse
maize diseases, including maize streak virus,
NLB, and southern and common rust (Wisser
et al. 2006). Four of these genes ( Rp1 , Rp3 ,
Rxo1 , and Hm1 ) have been cloned .Rp1 , Rp3 ,
and Rxo1 all carry the domain typical of R-
genes, the nucleotide binding site-leucine rich
repeat (NBS-LRR) (Collins et al. 1999; Webb
et al. 2002; Zhao et al. 2005). Rp1 and Rp3
confer resistance to specific races of common
rust while Rxo1 confers resistance to bacte-
rial stripe of maize. Hm1 , which confers resis-
tance to Cochliobolus carbonum race 1, encodes
an NADPH-dependent HC-toxin reductase that
detoxifies HC-toxin produced by the fungus
(Johal and Briggs 1992). Interestingly, the Hm1
gene is extremely widespread in maize and con-
sequently only a few lines that lack the Hm1
gene are susceptible to C. carbonum race 1. Fur-
thermore, genes with high homology to Hm1
are present in all grass genomes tested. Specific

Understanding theSystem:
GeneticArchitecture of Disease
Resistance in Maize and
BiologicalInsights

Plant disease resistance is often categorized as
qualitative (complete) or quantitative (partial)
based on the extent of disease in a “resistant”
interaction (Vanderplank 1968). While these cat-