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Final Report Summary - AVRBLB2-CPT (Manipulation of host target by the AvrBlb2 effector of the late blight pathogen Phytophthora infestans)

The oomycete Phytophthora infestans causes late blight, a re-emerging and ravaging disease of potato and tomato. It is renowned for its "high evolutionary potential" that allows to rapidly overcoming sources of resistance introduced in crop varieties. In recent years, the regular emergence of new P. infestans genotypes caused destructive epidemics in Europe and North America. Pathogens in Phytophthora infestans lineage, like many plant pathogens, evolve by host jumps followed by specialization, processes that play a critical role in the emergence of new P. infestans epidemics. However, how host jumps impact genome evolution remains largely unknown. An improved understanding of the genomic basis of adaptation to host plants will lead to conceptual advances in plant pathology and renewed opportunities for durable management of disease resistance in crop plants. The long-term objective of our work is to understand the mechanisms underlying the emergence of pathogenicity and virulence in filamentous plant pathogens. We revised the initial proposal focused on the detailed characterization of one effector protein to adopt a large scale approach based on next generation sequencing. The overall objective of this project was to characterize genome evolution in P. infestans lineage in order to understand how this pathogen adapted to new hosts. Questions we expected to address, include how polymorphisms distribute across P. infestans genome, how do effector genes evolve, can we use P. infestans genomic data to propose new strategies for the management of resistance in crops?

To determine the patterns of sequence variation and selective forces that shape sequence variation in the P. infestans lineage, we resequenced eight representative genomes of covering four sister species and four P. infestans strains using Illumina technology (Figure 1). We aligned re-sequenced genomes to P. infestans reference genome (Haas et al., Nature 2009) to identify presence/absence polymorphisms, estimate copy number variation and identify single nucleotide polymorphisms. Haas et al. reported that the P. infestans genome experienced a repeat-driven expansion relative to distantly related Phytophthora spp. (74% repeats versus <40%) and shows an unusual discontinuous distribution of gene density. Disease effector genes, such as members of the RXLR and CRN families, localize to expanded, repeat-rich and gene-sparse regions of the genome, in sharp contrast to core ortholog genes, which occupy repeat-poor and gene-dense regions. We demonstrated that highly dynamic genome compartments enriched in non-coding sequences underpin accelerated gene evolution following host jumps (Figure 2). Gene-sparse regions that drive the extremely uneven architecture of the P. infestans genome are highly enriched in plantinduced genes, particularly effectors, therefore implicating host adaptation as a driving force of genome evolution in this lineage. In addition, we unexpectedly identified several genes involved in epigenetic processes, notably histone methyltransferases, as rapidly evolving residents of the gene-sparse regions (Raffaele et al. Science 2010).

Next, we combined genome architecture analysis, transcriptomics and prediction of secreted proteins to identify novel proteins potentially involved in pathogenicity in P. infestans (Raffaele et al. BMC Genomics 2010). We have also exploited our expertise in genomics and in silico analysis to develop a new methodology for the classification of effector gene candidates and to identify promising candidates in the genome of rust fungi (Saunders et al., Plos One 2012).

Our data, and other recent reports, point to an unexpected role of repeat-driven genome expansion in the adaptability of several lineages of filamentous plant pathogens. This trend is opposite to the well documented view that specialized parasites and symbionts evolve by genome reduction. This suggests that the cost of maintaining large genomes is counterbalanced by the benefits of adaptability conferred by repeat-rich genome regions in these lineages. In a recent review (Raffaele and Kamoun, Nat Rev Microbiol. 2012) we propose a model in which large adaptable genomes confer a macro-evolutionary advantage by reducing the likelihood of pathogen lineage extinction due to the depletion of host plants in the biota.

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THE SAINSBURY LABORATORY
United Kingdom
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