Service Communautaire d'Information sur la Recherche et le Développement - CORDIS

Final Activity and Management Report Summary - XAGENOMICS (Unravelling pathogenicity of Xanthomonas albilineans, the pathogen causing leaf scald disease of sugarcane)

Diseases caused by plant pathogens are major threats for crop productivity. Understanding the mechanisms used by these plant pathogens to infect their host and to cause disease symptoms, including the death of the plant, is therefore essential to develop new control methods.

Leaf scald is a lethal disease of sugarcane caused by a bacterial pathogen named xanthomonas albilineans that occurs worldwide in more than 60 sugarcane producing countries. The pathogen is spread by infected planting material and by aerial means. The disease is mainly controlled by screening and planting of resistant sugarcane cultivars, which is a long and fastidious process. Furthermore, the means used by x. albilineans to infect sugarcane and the mechanisms set up by the host plant to resist to the attacks by the pathogen are poorly understood. Bacterial pathogens generally possess numerous weapons to cause disease in plants, including a syringe like device that they use to inject molecules, called effectors, into the plant cell.

In contrast to most of these bacteria, xanthomonas albilineans does not possess this weapon. The objective of this project was therefore to identify the other strategies that have been put in place by this pathogen to attack sugarcane.

Two approaches were used to unravel the pathogenicity of the pathogen causing sugarcane leaf scald. The first approach was based on genomic comparisons and the genome sequence of x. albilineans was compared to all available genome sequences of other bacteria. Several candidate pathogenicity genes were identified; in particular a cluster of genes involved in bacterial cell to cell signalling and coordinated group behaviour. This gene cluster, called 'rpf' for regulation of pathogenicity factors, controlled various cellular and biological processes in several plant pathogenic bacteria. When these genes were mutated and no longer functional, the pathogen generally became much less virulent toward its host plant. However, when this gene cluster was inactivated in x. albilineans, the bacteria remained highly pathogenic. These results suggested that the 'rpf' gene cluster was not essential for the spreading of this pathogen in the sugarcane stalk and that other genes, which remained to be identified, were involved in cell to cell signalling in x. albilineans.

The second approach consisted of the production of numerous mutants of x. albilineans in which single genes were randomly inactivated. Sugarcane was inoculated with more than 1 200 mutants and those that did not induce symptoms or did not multiply in the sugarcane stalk were selected for further analysis. Using this method, we identified several genes that were excellent candidates for further investigation of the mechanisms used by x. albilineans to attack sugarcane. These genes were expected, for example, to encode transport proteins, outer membrane proteins and proteins involved in the biosynthesis of polysaccharides found on the surface of the bacterial cell. Several of these genes also encoded proteins for which no function had so far been found in any bacterial species.

This project was successful in identifying new candidate pathogenicity factors in the sugarcane invading pathogen x. albilineans. These findings would be useful not only to decipher the pathogenicity mechanisms of this bacterial species, but also of other bacterial species attacking plants. In the long run, our results should benefit the identification of new targets in the pathogen for the development of innovative control methods.

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