Understanding how plant antimicrobial 'hot zones' can accelerate pathogen evolution

UWE Bristol (Professor Dawn Arnold) has teamed up with the Universities of Oxford (Dr Gail Preston) and Reading (Dr Robert Jackson) to win a £500,000 grant to study ways of increasing crop yields by reducing disease. The award from the Biotechnologies and Biological Sciences Research Council (BBSRC) enables researchers to build on recent discoveries about how disease spreads in bean plants. The three year project could result in developing new ways to prevent diseases in this valuable food crop.

Most of the microorganisms that cause plant disease are engaged in a constant arms race with plants such that microorganisms are rapidly evolving to infect disease resistant plants while plants are evolving to resist pathogen attack. In an agricultural setting, plant breeders face the increasingly difficult challenge of developing new disease-resistant varieties to replace those rendered ineffective due to microbial evolution. To prolong the usefulness of disease resistant plant varieties, and to reduce the rate at which microorganisms overcome disease resistance, it is imperative that we fully understand how microorganisms evolve and the drivers of this evolution. We have developed a model system for understanding microbial evolution to overcome plant disease resistance. This system uses a bacterium called Pseudomonas syringae pv. phaseolicola (Pph), which causes an important disease of bean plants known as halo blight, and represents an excellent system for studying both microbial evolution and the factors that increase or decrease the durability of plant disease resistance.

In the case of Pph and bean, the plant has developed mechanisms to recognise specific strains of Pph, and so resist invasion. In this dynamic system the bacterium has a number of ways of changing its genome, and therefore the proteins it expresses, in order to evade plant recognition. Alterations in the structure or production of bacterial proteins may prevent their detection by potential host plants and allow the bacteria to grow within the plant. We have shown that changes in the genome of Pph allow this bacterium to overcome plant disease resistance. Certain strains of Pph carry a gene that produces a protein the plant can detect as belonging to Pph, alerting it to trigger its defence systems and prevent Pph growth. The gene for this protein lies within a discrete region of the Pph genome known as a genomic island. To counter plant recognition, Pph removes the genomic island from its chromosome such that daughter cells no longer have the island. Interestingly, we observed that this dramatic change in Pph occurs most frequently in infection site 'hot zones' in resistant varieties of bean. These hot zones generate highly antimicrobial conditions following bacterial invasion. Therefore the chemical changes that occur in resistant plants actually accelerate the evolution of a more virulent form of the pathogen.

In this proposal we aim to study the chemical composition of the 'hot zone' to understand which factors are responsible for inducing gene loss and gene gain in Pph. This research will help to elucidate the fundamental mechanisms underpinning the evolution of bacterial pathogenicity and the breakdown of disease resistance in crop plants, providing knowledge that, in the future, may be used to improve the disease management strategies used against disease-causing microorganisms.

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