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variation in virulence frequencies over the three dates on which samples were
collected in the mobile sample than in the stationary sample. This was probably
because the latter was strongly influenced by the wind direction at the time of
sampling, and therefore consisted of isolates from different, nearby fields on the
three occasions, whereas the mobile sample included isolates from many fields, so
differences due to wind direction were smoothed out.
If it is not possible to sample airborne spores, a sample from a variety which is
susceptible to all pathotypes may be considered to be a random sample from the
local population. Replicate fields should be sampled to ensure that the sample is
indeed representative. Samples from varieties with resistance genes that differentiate
the current pathogen population are clearly not random. This point needs to be
emphasised, because statistical analyses of such samples are sometimes presented as
if they were actually random, as discussed by Barrett (1987).
3.4 MOLECULAR DETECTION OF VIRULENCE AND FUNGICIDE
RESISTANCE
Cloned genes now offer alternatives to pathology testing to detect virulence and
fungicide resistance. At present, the number of avirulence genes and fungicide
resistance genes in important pathogens that can be screened in this way is limited
but this is sure to be a growth area in plant pathology in the next decade or so. For
tests based on molecular information to be effective, the relevance of sequence
variation to pathogen phenotypes must be considered carefully. In addition,
molecular markers other than cloned genes may provide useful information about
the evolution of virulence and fungicide resistance.
3.4.1 Avirulence genes
Avirulence genes have been isolated from bacteria, fungi and oomycetes, including
several economically important pathogens (Skamnioti and Ridout, 2005). DNA
sequence information offers the opportunity not only to estimate frequencies of
avirulence and virulence phenotypes but also to investigate their distribution,
dispersal and evolution by examining variation between functional (avirulence) and
non-functional (virulence) alleles. The only example of this to date (Schürch et al. ,
2004) illustrates both the potential of this approach and also indicates some potential
pitfalls which may need to be considered.
(a) Alleles of avirulence genes
In Rhynchosporium secalis , (cause of barley leaf blotch or scald), an avirulence
gene, NIP1 or AvrRrs1 , produces a necrosis-inducing peptide, NIP1. The NIP1 gene
is involved in a gene-for-gene interaction because R. secalis isolates with a
functional NIP1 allele are unable to overcome resistance encoded by the Rrs1 gene
in barley. Eighteen NIP1 alleles of full or nearly full length have been detected
(Rohe et al. , 1995; Schürch et al. , 2004). Of these, five were isolated from virulent
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