Principles of Plant Genetics and Breeding

372 CHAPTER 20
Genetics of host–pathogen reactions
Genetics of resistance
R. H. Biffen is credited with providing the first report
on the genetics of resistance. Working on stripe rust
(Puccinia striiformis), he reported that resistance to disease
was controlled by a single Mendelian gene. Since
then many reports have supported this finding that
much host resistance to pathogens is simply inherited.
Dominance gene action is very common for resistance
to pests and pathogens (especially hypersensitive resistance).
Monogenic recessive resistance is less common.
However, it is known that resistance may be controlled
by any number of genes whose effects may be large or
small. Further, the genes may interact epistatically or
additively. Commonly, resistance and virulence genes
usually operate on a gene-for-gene basis as discussed
next. Also, genes for resistance are often reported to be
clustered in linkage groups. Vertical resistance or racespecific
resistance is oligogenic. Other examples are the
Sr (for stem rust), Lr (for leaf rust), and Pr (for powdery
mildew) genes of wheat (cause hypersensitive reaction
for resistance), and the Dm (for downy mildew) genes of
lettuce.
The inheritance of horizontal resistance is more complex
than for vertical resistance. Resistance is often
polygenic, such as the partial resistance in potato to
Phytophthora infestans and in maize to Puccinia sorghi.
Any number of genes could be involved in horizontal
resistance. It is a stable resistance because a pathogen
has to change for a number of genes to overcome the
defense mechanism in that one host (non-specific).
Horizontal resistance may arise when: (i) the host genes
do not operate in a gene-for-gene fashion with the
pathogen genes (no differential interactions are possible);
or (ii) when several to many host genes with small effects
operate on a gene-for-gene basis with an equivalent
number of genes in the pathogen population (differential
effects are too small to be detectable and appear to
be horizontal resistance).
Vertical resistance and horizontal resistance may be
viewed as extremes of a continuum, if one assumes that
gene-for-gene relationships are common in host-specific
pathogen systems. When few genes with large effects
occur, differential interactions are readily identified and
the result is vertical resistance. However, when more
genes with smaller effects are involved in the reaction,
differential interactions are less readily identified, resulting
in a mixture of vertical and horizontal resistance.
When numerous genes of small effect are involved,
differential reactions cannot be discerned, and the resistance
is primarily horizontal resistance.
Gene-for-gene reactions (genetics of specificity)
Working on flax rust (caused by Melamspora lini),
H. H. Flor discovered that the major genes for resistance
in the host interacted specifically with major genes
for avirulence in the fungus. He proposed the gene-forgene
concept that states that for each gene conditioning
resistance in the host, there is a specific gene conditioning
virulence in the parasite. In other words, a resistance
gene can act only if a locus in the pathogen carries a
matching allele for avirulence. By themselves, resistance
genes are ineffective if the pathogen caries the appropriate
allele for virulence (usually a recessive allele). Most
researchers agree that the specific interaction occurs
between dominant resistance alleles and the dominant
avirulence alleles (Figure 20.1).
The original concept proposed in 1950 by H. H. Flor
suggests that the virulence of a pathogen and the resistance
of a host have a genetic basis. For each gene that
confers resistance in the host, there is a corresponding
gene in the pathogen that confers virulence to the
pathogen, and vice versa. This host–pest interaction is
called the gene-for-gene hypothesis. J. A. Browning
simplified the hypothesis by comparing the interaction
between the genetic systems of the host and pathogen
to a set of locks and keys. The host has the locks – each
locus that conditions resistance to a pathogen is a potential
for a lock. The locks are equivalent to dominant
alleles that inhibit pathogen establishment in the host
(plant). To succeed, the pathogen must have the appropriate
key (a virulent allele) to open the lock, or the host
must have no lock for the key. For example, a genotype
AABBcc in a plant requires the pathogen to have the
genotype aabb– – to be susceptible. The third allele can
be C or c, since there is no lock in the host.
Host
rrss
RRss
rrSS
RRSS
AB
+
−
−
−
Pathogen
Figure 20.1 Demonstration of the concept of gene-forgene
interaction in disease resistance.
Ab
+
+
−
−
‘a,’ differential interaction
Ab
+
_ a
+
−
ab
+
+
+
+