Genetic study offers hope on crop disease

Groundbreaking research by British scientists has uncovered the molecular mechanism that allows crops such as tomatoes, cucumbers and beans to become infected with the bacterium Pseudomonas syringae.

Researchers from the Department of Life Sciences at Imperial College London - funded by the Biotechnology & Biological Sciences Research Council - found that two genes in the bacterium work together to launch the infection process that kills the plant's cells, causes disease and reduces crop quality and yield.

P. syringae is responsible for major disease outbreaks in an enormous range of economically important food plants - for example, one P. syringae variety recently infected half of all chestnut trees in the UK.

Researchers hope that by understanding how the bacteria attack plant cells at a molecular level they will be able to find new targets for pesticides and devise better strategies for disease management.

Dr Jorg Schumacher, the study's senior author, said: "These bacteria have quite a sophisticated system for infecting plants. They use remarkable needle-like structures called pili to penetrate and inject a range of proteins into a plant's cells that then work to suppress its immune response and kill infected cells.

"P. syringae are very versatile bacteria and their pili help them to infect a very large range of plants causing numerous symptoms in different plants - for example, the black/brown specks on tomato fruits.

"From what we know, these bacteria only produce their pili and launch infection when they have already invaded the plant tissue. It is unclear how they sense the plant tissue environment that triggers infection, but we do know that the regulatory mechanism that controls pili formation is essential in this process.

"What distinguishes P. syringae from other related pathogens that also use pili to infect plants is that it has duplicated a gene during evolution that is involved in producing the pili. Indeed, the researchers have found the duplicated gene in all the strains of P. syringae they have studied, which makes them think that it is very likely to provide some selective advantage in the infection process."


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