The eggplant AG91-25 recognizes the Type III-secreted effector RipAX2 to trigger resistance to bacterial wilt (Ralstonia solanacearum species complex).

To deploy durable plant resistance, we must understand its underlying molecular mechanisms. Type III effectors (T3Es) and their recognition play a central role in the interaction between bacterial pathogens and crops. We demonstrate that the Ralstonia solanacearum species complex (RSSC) T3E ripAX2 triggers specific resistance in eggplant AG91-25, which carries the major resistance locus EBWR9.

Plant Pathogenicity Phenotyping of Ralstonia solanacearum Strains.

In this chapter, we describe different methods for phenotyping strains or mutants of the bacterial wilt agent, Ralstonia solanacearum, on four different host plants: Arabidopsis thaliana, tomato (Solanum lycopersicum), tobacco (Nicotiana benthamiana), or Medicago truncatula. Methods for preparation of high volume or low volume inocula are first described. Then, we describe the procedures for inoculation of plants by soil drenching, stem injection or leaf infiltration, and scoring of the wilting symptoms development.

Introduction of Genetic Material in Ralstonia solanacearum Through Natural Transformation and Conjugation.

Ralstonia solanacearum is a soil-borne plant pathogen, responsible of the bacterial wilt disease. Its unusual wide host range (more than 250 plant species), aggressiveness, and broad geographic distribution have made of this bacterium the main plant pathogenic model in the beta-Proteobacteria class. Many R.

Multihost experimental evolution of the pathogen Ralstonia solanacearum unveils genes involved in adaptation to plants.

Ralstonia solanacearum, the causal agent of a lethal bacterial wilt plant disease, infects an unusually wide range of hosts. These hosts can further be split into plants where R. solanacearum is known to cause disease (original hosts) and those where this bacterium can grow asymptomatically (distant hosts).

A competitive index assay identifies several Ralstonia solanacearum type III effector mutant strains with reduced fitness in host plants.

Ralstonia solanacearum, the causal agent of bacterial wilt, is a soil bacterium which can naturally infect a wide range of host plants through the root system. Pathogenicity relies on a type III secretion system which delivers a large set of approximately 75 type III effectors (T3E) into plant cells. On several plants, pathogenicity assays based on quantification of wilting symptoms failed to detect a significant contribution of R.

Two type III secretion system effectors from Ralstonia solanacearum GMI1000 determine host-range specificity on tobacco.

The model pathogen Ralstonia solanacearum GMI1000 is the causal agent of the bacterial wilt disease that attacks many solanaceous plants and other hosts but not tobacco (Nicotiana spp.). We found that two type III secretion system effector genes, avrA and popP1, are limiting the host range of strain GMI1000 on at least three tobacco species (N.

Inventory and functional analysis of the large Hrp regulon in Ralstonia solanacearum: identification of novel effector proteins translocated to plant host cells through the type III secretion system.

The ability of Ralstonia solanacearum strain GMI1000 to cause disease on a wide range of host plants (including most Solanaceae and Arabidopsis thaliana) depends on genes activated by the regulatory gene hrpB. HrpB controls the expression of the type III secretion system (TTSS) and pathogenicity effectors transiting through this pathway. In order to establish the complete repertoire of TTSS-dependent effectors belonging to the Hrp regulon and to start their functional analysis, we developed a rapid method for insertional mutagenesis, which was used to monitor the expression of 71 candidate genes and disrupt 56 of them.

A signal transfer system through three compartments transduces the plant cell contact-dependent signal controlling Ralstonia solanacearum hrp genes.

Ralstonia solanacearum hrp genes encode a type III secretion system required for disease development in host plants and for hypersensitive response elicitation on non-hosts. hrp genes are expressed in the presence of plant cells through the HrpB regulator. This activation, which requires physical interaction between the bacteria and the plant cell, is sensed by the outer membrane receptor PrhA.