Natural selection: how to get from population genetics to population
J.K.M. Brown, L.S. Arraiano, J.C. Makepeace, R.A. Wyand and H.N. Slatter
Department of Disease and Stress Biology, John Innes Centre, Colney, NORWICH,
NR4 7UH, England
Over the last two decades, the use of molecular markers has become central
to research on the population genetics of plant pathogens. In appropriately
designed surveys and experiments, DNA markers provide valuable information
about the structure of pathogen populations, particularly rates and directions
of migration but also recombination, genetic drift and mutation. However,
while these processes alter the structure of a pathogen population and
reassort genes between places (migration) or between genomes (recombination),
they do not change frequencies of genes or genotypes in the population
as a whole. They are therefore merely the background to the principal
driving force of evolution, natural selection.
Yet while studies of DNA marker variation have flourished, research on
natural selection in pathogen populations has been comparatively neglected.
This has limited our understanding of populations of plant pathogens because,
to estimate the rate of evolution of a trait, it is necessary to understand
its costs as well as its benefits. Although it is obvious that the use
of a resistant crop variety will select for the corresponding pathogen
virulence, or that the use of a pesticide will select for resistance to
that chemical, an understanding of the dynamics of these pathogen traits,
especially their long-term persistence, requires knowledge of their costs.
Equally, while plant disease resistance is obviously desirable in order
to control disease, its value for plant breeders and farmers may be limited
if it is costly.
We will present recent research in our lab in which we have investigated
costs of pathogen traits (virulence and fungicide resistance) and of plant
disease resistance. Examples will be drawn from fungal diseases of cereals:
yellow rust (Puccinia striiformis), powdery mildew (Blumeria graminis)
and septoria tritici blotch (Mycosphaerella graminicola). Three general
themes emerge from this research: a full understanding of pathogen population
biology requires knowledge of processes that determine pathogen population
structure to be integrated with knowledge of natural selection; knowledge
about natural selection of host and pathogen traits can be applied to
improve methods of crop protection; and rates and the direction of natural
selection are strongly dependent on the environment. We suggest that the
last point is one reason why recent research on pathogen population biology
has largely neglected natural selection, because it is often difficult
to design laboratory experiments that produce results which have a simple
interpretation in field conditions.