Comparative Large-Scale Analysis of Interactions between Several Crop Species and the Effector Repertoires from Multiple Pathovars of Pseudomonas and Ralstonia      

Abstract

Bacterial plant pathogens manipulate their hosts by injection of numerous effector proteins into host cells via type III secretion systems. Recognition of these effectors by the host plant leads to the induction of a defense reaction that often culminates in a hypersensitive response manifested as cell death. Genes encoding effector proteins can be exchanged between different strains of bacteria via horizontal transfer, and often individual strains are capable of infecting multiple hosts. Host plant species express diverse repertoires of resistance proteins that mediate direct or indirect recognition of bacterial effectors. As a result, plants and their bacterial pathogens should be considered as two extensive coevolving groups rather than as individual host species coevolving with single pathovars. To dissect the complexity of this coevolution, we cloned 171 effector-encoding genes from several pathovars of Pseudomonas and Ralstonia. We used Agrobacterium tumefaciens-mediated transient assays to test the ability of each effector to induce a necrotic phenotype on 59 plant genotypes belonging to four plant families, including numerous diverse accessions of lettuce (Lactuca sativa) and tomato (Solanum lycopersicum). Known defense-inducing effectors (avirulence factors) and their homologs commonly induced extensive necrosis in many different plant species. Nonhost species reacted to multiple effector proteins from an individual pathovar more frequently and more intensely than host species. Both homologous and sequence-unrelated effectors could elicit necrosis in a similar spectrum of plants, suggesting common effector targets or targeting of the same pathways in the plant cell.Plants and potential pathogens are locked in continual antagonism involving alternating cycles of selection to increase resistance and virulence, respectively. There are many biochemical exchanges between plants and pathogens, and selection can act at multiple points in the host-pathogen interaction. Several overlapping mechanisms of resistance in plants and strategies of pathogens to interdict these resistance responses are being elucidated (Jones and Dangl, 2006). The combined abilities of a pathogen to overcome host resistance mechanisms are major determinants of its host range and success as a pathogen.

In Planta Expression Screens ofPhytophthora infestansRXLR Effectors Reveal Diverse Phenotypes, Including Activation of theSolanum bulbocastanumDisease Resistance Protein Rpi-blb2

“…Here, we further validate the approach of screening effectors by expressing them directly inside plant cells Vleeshouwers et al, 2008;Guo et al, 2009;Wroblewski et al, 2009). The diverse activities ascribed here to several RXLR effectors support the view that these proteins form a critical class of host translocated effectors in oomycetes.…”

Phosphorylation of HopQ1, a Type III Effector from Pseudomonas syringae, Creates a Binding Site for Host 14-3-3 Proteins

“…8A), in contrast to the severe chloroses triggered by the effector in N. benthamiana leaves (Wroblewski et al, 2009). To determine whether modification of the 14-3-3 binding site is critical for HopQ1 recognition by the plant immune system, tobacco leaves were infiltrated with Agrobacterium tumefaciens Table IV.…”

The awr Gene Family Encodes a Novel Class of Ralstonia solanacearum Type III Effectors Displaying Virulence and Avirulence Activities

“…Similar results using other bacterial effectors have been described, further supporting the diverse host responses to AWR. A recent report where effector candidates from X. campestris, P. syringae, and R. solanacearum were transiently overexpressed in various plant species demonstrated that, although one-third produced visible phenotypes in at least one accession, none of them caused a reaction in all plants tested (Wroblewski et al 2009). HR-like phenotypes have been interpreted as a programmed cell death elicited by avirulence factors, although recent publications discuss whether this HR might be a cause or a consequence of cascade signaling downstream of effector recognition (Coll et al 2011).…”