Effector gene persistence in bacterial plant pathogens

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The co-evolution of plant pathogens and their hosts is a complex and dynamic process. Pathogens can rapidly evolve to overcome host resistance to become virulent pathogens. This is a major cause for concern because of the threat it poses to UK and global food security. It is therefore important that we understand the causes and consequences of pathogen evolution to deliver better strategies for plant protection. In this project we aim to study the ability of plant pathogenic bacteria to overcome plant disease resistance. One of the ways that bacterial plant pathogens cause disease is to inject proteins into plant cells that inactivate plant defence mechanisms and allow them to grow inside plant tissues. These proteins are known as effector proteins. One way in which plants can protect themselves against infection is to recognise the effector proteins as they are being injected into the plant cells. If the protein is recognised the plants cells deliberately die, releasing anti-microbial chemicals, thus cutting off the source of nutrients for the bacteria and making the plant resistant to attack. However bacteria can evolve to overcome host plant resistance by losing or changing their effector genes so that the proteins they produce are not recognised by the plant. We have worked with a model bacteria-plant system that has allowed us to study in more detail how the bacteria can evolve to overcome host 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 has allowed us to study both microbial evolution and the factors that increase or decrease the durability of plant disease resistance.In the case of the Pph-bean system we have so far concentrated on the fate of one particular effector gene called avrPphB. This effector gene is interesting because it is carried on a mobile piece of DNA known as a genomic island, which can be acquired and lost by the bacteria. When the bacteria carrying this island infect a plant that is resistant, because the plant recognises avrPphB, the bacteria loses the island and can therefore go onto infect the plant without being recognised. This is an excellent example of the evolution of a pathogen to overcome host resistance. However, surprisingly, we have observed the complete loss of this effector over many experiments. Recently, using a combination of mathematical modelling and laboratory experiments, we have shown that over the course of many weeks in the resistant plant, the bacterial population will still maintain a low level of the effector gene, below the level that can be recognised by the plant, and if conditions change so the effector gene is no longer recognized, its frequency can increase. In this proposal we now aim to look in more detail at why this 'effector persistence' occurs. We will specifically study whether island and effector persistence confer any additional benefits to the bacteria. We will develop our mathematical model to provide additional insight into the basis of pathogen evolution and effector retention, and investigate whether this phenomenon is widespread. 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.