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Blight epidemiology and population biology

Image of blight on a leafOur work on the epidemiology and population biology of P. infestans forms part of the larger late blight team at SCRI.

Phytophthora infestans, the oomycete pathogen that causes late blight, infects potato foliage and tubers, reducing yield and quality of ware and seed potato crops. Growers can limit the impact of blight in their crops by managing sources of primary inoculum but are nevertheless reliant on regular pesticide applications. A need for more sustainable solutions for disease control is increasing the relevance of new sources of effectively deployed cultivar resistance.

All of the above approaches to disease management are influenced by population genetic structure of P. infestans. At a practical level our work seeks to address both the role of various sources of inoculum and the impact of changing pathogen populations on the epidemiology and management of disease. We also consider the P. infestans/potato interaction to be an excellent model with which to study the processes involved in host-parasite co-evolution. We are examining the evolutionary forces that drive population change and, in collaboration with SCRI colleagues, the behaviour of pathogen effectors in populations. Our work has national and international dimensions.

Primary inoculum

Image of an oosporeCurrently, the main sources of P. infestans primary inoculum each season are considered to be tuber cull piles, seed tubers or infected volunteer potato plants. However, a change in the population of P. infestans (see below) has increased concerns about sexual oospores: a potentially serious source of long-lived soil-borne primary inoculum that can germinate to initiate early epidemics. Where both the A1 and A2 mating types of P. infestans exist together there is a risk of oospore formation.

Using a P. infestans diagnostic and SSR assays developed at SCRI that allow the detection, quantification and tracking of the pathogen we are examining the relative contribution of different sources of inoculum (tubers and oospores) in causing disease. The influence of host resistance, other pathogen interactions and climate on these processes are also considered.

Population change

Pathogen populations change over time; either in response to specific selection pressures or via chance events such as ‘founder effects’ (for example, migration of a single pathogen genotype to a new region). Several dramatic shifts in P. infestans populations on an international scale have been documented since its ‘escape’ from its centre of origin in Central or South America. Such a transition in Western Europe has been occurring in recent years with dramatic increases in the frequency of the A2 mating type being recorded. Understanding the mechanisms, processes and rates of P. infestans evolution is an important goal of our research since it influences the effectiveness and durability of new management practices.

Neutral markersExample image of heterozygous alleles at the Pi70 locus

At SCRI we are monitoring the population genetic dynamics of P. infestans using panels of multiplexed microsatellite (or Simple Sequence Repeat; SSR) markers (Lees et al., 2006). Such data is providing an objective measure of pathogen diversity and was critical to the SCRI-led EUCABLIGHT project in which a database of almost 17 thousand European P. infestans isolates has been assembled. David Cooke is responsible for the continued development of this resource that is currently being extended into Central and Southern America via links with CIP and Alison Lees continues to be involved in the management of an ongoing European network (EuroBlight)  working on the integrated control of late blight and how this is influenced by changes in the pathogen population.

Map of SSR-defined genotypes of P. infestans and their GB distribution in 2006We have established good national and international collaborations to examine populations at a range of scales. In particular, a British Potato Council  sponsored project (2006-8) is examining population change within GB potato crops in great detail. The primary objectives are to monitor the increase in the P. infestans A2 mating type, establish whether oospores are present in GB soils and evaluate whether the increase of a specific A2 lineages is due to an increase in it’s aggressiveness. Currently results suggest a single lineage of A2 accounts for much of the change in the population.

Effector genes

In addition to variation at ‘neutral’ microsatellite loci we are examining variation in pathogen effector genes (for example, virulence genes) in national and international P. infestans populations. Establishing the frequency of different effector alleles in natural populations allows inferences to be drawn on selection pressures (+ve or –ve) and thus the function of different alleles. In the longer term, understanding the natural variation and mutation rates in effector genes will inform decisions on deployment of any associated resistance.

Image showing SNP determining virulence in the P. infestans avr3a gene

Host Resistance

We work closely with colleagues in the genetics and breeding programme to screen germplasm and breeding material for durable resistance to foliage and tuber blight, taking into consideration changes in the P. infestans population. With colleagues at SASA and SAC we are also involved in the BPC funded Independent Variety Trials that provide an integrated GB potato variety testing system to deliver independent disease and pest resistance ratings for the potato industry.

References

Cooke, D.E.L., Lees, A.K. 2004. Markers, old and new, for examining Phytophthora infestans diversity. Plant Pathology 53, 692-704.

Lees A.K., Wattier R., Shaw D.S., Sullivan L., Williams N.A. and Cooke D.E.L. 2006. Novel microsatellite markers for the analysis of Phytophthora infestans populations. Plant Pathology 55, 311-319.