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Evolution of plant resistance to virus infection

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How plants resist infection

Researchers are investigating ways in which plants evolve resistance to pathogens, to better manage plant diseases.

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Plant diseases have as much of an impact on human welfare as those of humans or animals. Despite this, less is known about plant diseases than their human counterparts and there are fewer control options, particularly for plant viruses. Plant pathologists have two main theories about how pathogens evolve to infect plants and how their hosts co-evolve to resist infection. The EU-funded ERVIR (Evolution of plant resistance to virus infection) project wanted to determine how these theoretical mechanisms influence evolution of plant resistance to viral pathogens. In the gene-for-gene (GFG) model, pathogens produce proteins that allow them to infect a wide range of hosts. Correspondingly, recognition of these proteins by the hosts' defence systems allows plants to resist the attack. In the matching allele (MA) model, an exact genetic match between pathogen and host is required for pathogen infection and for host resistance. This limits the number of hosts that the pathogen can infect, and the number of pathogens that the host can defend against. To determine which model operates for different viruses, ERVIR infected Capsicum annuum, a wild relative of pepper, with two different viruses called tobamavirus and potyvirus. Researchers found that pepper could prevent tobamavirus infection via a resistance gene called the L gene, which they detected in the majority of pepper plants. Conversely, the potyvirus contained a vpg gene that allowed it to infect pepper if the plants had a corresponding pvr2 gene. The potyvirus could not infect plants that contained mutations in the pvr2 gene, which made the plants resistant by preventing interaction with the virus vpg. However, very few plants contained these resistant pvr2 genes. Supporting these results, researchers detected fewer tobamavirus infections than potyvirus infections and found that the pepper could not defend against two different potyvirus species. This indicates that potyvirus resistance occurs via the MA model, while tobamavirus resistance occurs via the GFG model. The findings of ERVIR will contribute to a better understanding of host-pathogen co-evolution, which is crucial for managing plant diseases.

Keywords

Plant resistance, virus infection, gene-for-gene, matching-allele, tobamavirus, potyvirus

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