Concepts actuels sur la pathogénie chez les bactéries phytopathogènes

What are the molecular determinants that make a bacterium a plant pathogen? In the last 10–20 years, important progress has been made in answering this question. In the early 20th century soon after the discovery of infectious diseases, the first studies of pathogenicity were undertaken. These early studies relied mostly on biochemistry and led to the discovery of several major pathogenicity determinants, such as toxins and hydrolytic enzymes which govern the production of major disease symptoms. From these pioneering studies, a simplistic view of pathogenicity arose. It was thought that only a few functions were sufficient to transform a bacterium into a pathogen. This view rapidly changed when modern techniques of molecular genetics were applied to analyse pathogenicity. Modern analyses of pathogenicity determinants took advantage of the relatively simple organization of the haploid genome of pathogenic bacteria. By creating non-pathogenic mutants, a large number of genes governing bacterium–host interactions were identified. These genes are required either for host colonization or for the production of symptoms. Even though the role of motility and chemotaxis in these processes is still unclear, it is clear that a strong attachment of Agrobacterium to plant cells is a prerequisite for efficient plant transformation and disease. Other important pathogenicity factors identified with a molecular genetic approach include hydrolytic enzymes such as pectinases and cellulases which not only provide nutrients to the bacteria but also facilitate pathogen invasion into host tissues. The precise role of exopolysaccharide in pathogenicity is still under discussion, however it is has been established that it is crucial for the induction of wilt symptoms caused by Ralstonia solanacearum. Trafficking of effector proteins from the invading bacterium into the host cell emerged recently as a new central concept. In plant pathogenic bacteria, protein translocation takes place through the so-called ‘type III secretion machinery’ encoded by hrp genes in the bacterium. These genes are present in representatives of all the major groups of Gram negative plant pathogenic bacteria except Agrobacterium. Most of these genes have counterparts in pathogens of mammals (including those of human) and they also play a central role in pathogenicity. Additionally, recent evidence suggests that a ‘type IV secretion machinery’ injects bacterial proteins into host cells. This machinery, originally found to be involved in the transfer of t-DNA from Agrobacterium into plant cells, was recently shown to translocate pathogenicity proteins in pathogens of mammals such as Helicobacter pylori and Brucella. Discovery of the trafficking of proteins from the pathogen into host cells revolutionized our conception of pathogenicity. First, it rather unexpectedly established the conservation of basic pathogenicity strategies in plant and animal pathogens. Second, this discovery changes our ideas about the overall strategy (or mechanism) of pathogenicity, although we still think the end result is exploitation of host cell nutritive components. Rather than killing the host cell from outside, we envision a more subtle approach in which pathogens inject effector proteins into the host cell to effect a change in host cell biology advantageous to the pathogen. Identification of the effector proteins, of their function and of the corresponding molecular targets in the host is a new challenge which will contribute to the conception of new strategies to control diseases.