Ralstonia Solanacearum - Virulence Mechanisms

Virulence Mechanisms

R. solanacearum possesses genes for all six protein secretion pathways that have been characterized in Gram-negative bacteria. Perhaps the best-studied of these is the Type III secretion system (T3SS or TTSS), which secretes infection-promoting effector proteins (T3Es) into host cells. Approximately 74 suspected or confirmed T3Es have been identified in R. solanacearum to date, although the functions of very few are currently known. Despite being just one of several protein secretion systems, the T3SS is necessary for R. solanacearum to cause disease. No single effector protein has been found to significantly alter pathogenicity of R. solanacearum, but simultaneous disruption of certain subsets of effectors (such as the set of seven GALA effectors in strain GMI1000) strongly affects virulence of the pathogen. GALA 7 is necessary for virulence on Medicago truncatula, hinting that T3E diversity may play a role in determining the broad host range of the R. solanacearum species complex.

The Type III secretion system is not unique to R. solanacearum and is, in fact, very ancient. The evolutionary history of the T3SS is contested; a high degree of similarity to the flagellum has sparked debate over the relationship between these two structures.

Approximately half of T3SS proteins are highly conserved in R. solanacearum and likely constitute a very old and stabilized effector core. Among the other half showing variation among different strains of R. solanacearum, only a third show evidence of lateral gene transfer. The origins of the remaining effectors are unknown, although some researchers hypothesize that gene-for-gene interactions may play a significant role in shaping virulence genes in R. solanacearum. Some of these effector proteins are homologous to Transcription Activator-like effectors (TAL effectors) from Xanthomonas and could possibly have a similar function of activating specific genes in the host plant cells during R. solanacearum pathogenesis.

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