Agriculture Reference
In-Depth Information
The reliability of conclusions about pathogen virulences therefore depends on
the extent of knowledge about the genetics of resistance in the differential set. One
cannot assume that simply because two host lines are known to share one or more
genes, they can be treated as alternative differentials; they may in fact differ in some
other gene. This must be borne in mind when comparing results of experiments in
which different differential sets have been used.
Finally, a good differential variety should discriminate virulent and avirulent
isolates clearly, but the expression of a resistance gene's incompatible IT may vary
between varieties. This implies that that gene interacts with other, unknown genes.
For example, the international wheat yellow rust differential for
Yr6
, Heines Kolben,
also has
Yr2
, but the latter gene is expressed more weakly in that variety than in
Heines VII or Heines Peko, which also has
Yr2
+
Yr6
(Calonnec
et al.
, 1997b).
(c) Genetics of avirulence
The classic model of gene-for-gene interactions in which, as the name implies, one
pathogen avirulence gene matches one plant resistance gene does indeed apply quite
widely. As with most rules, however, there are exceptions - see reviews of plant
pathogenic fungi in general by Christ
et al.
(1987) and of powdery mildews in
particular by Brown (2002). In a common type of exception, two genes confer
avirulence to one resistance gene. For example, avirulence of
B. graminis
f.sp.
hordei
to
Mla13
resistance was shown by genetic analysis to be controlled by two
genes (Caffier
et al.
, 1996). Without comprehensive molecular genetic evidence,
however, one cannot determine if the two avirulence genes do indeed match a single
resistance gene, as has been demonstrated for
Pseudomonas syringae
infecting
Arabidopsis thaliana
(Bisgrove
et al.
, 1994), or actually match two closely linked
resistance genes with different specificities.
Mla13
has now been shown to be an
allele of the
Mla
gene (Halterman
et al.
, 2003) but there remains the possibility that
one of the avirulence genes discovered by Caffier
et al.
(1996) matches a different
gene, closely linked to the
Mla
locus. The complexity of avirulence genetics may be
still deeper; to continue with the example of
Mla13
, not only do two avirulence
genes match this resistance, but there may be other genes which inhibit these
avirulences (unpublished data). Genes that inhibit or suppress avirulence have been
identified in
Melampsora lini
, the flax rust fungus (Lawrence
et al.
, 1981; Ellis
et al.
, 1997).
At one level, these complexities do not matter: if one is simply interested in the
frequency of a virulence phenotype in the pathogen population, perhaps to predict
the level of risk to current cultivars, one does not need to know whether the genetics
of avirulence are simple or complex. Knowledge about the genetics of avirulence
may be desirable, however, if one wishes to use survey data to make quantitative
predictions about pathogen evolution (Hovmøller
et al.
, 1993), which is likely to be
affected by the details of the genetic control of avirulence.
A common misconception is that resistances which are expressed in a
quantitative manner are under polygenic control and are not race-specific. There are
very many exceptions to this supposed rule. One such is
Ml(Ab)
mildew resistance
