AI Article Synopsis

  • The study investigates how certain effector proteins help the tobacco pathogen Pseudomonas syringae pv. tabaci adapt to its hosts, using a comparative analysis of seven strains through multilocus sequence typing (MLST).
  • It was found that these strains share many effector genes with the closely related bean pathogen P. syringae pv. phaseolicola 1448A, particularly noting that 10 effectors were common between them.
  • The specific effector hopQ1-1 enhances growth and disease severity in beans but reduces virulence in tobacco, indicating that changes in effector profiles during host adaptation can decrease a pathogen's effectiveness in non-host plants.

Article Abstract

To study the role of type III-secreted effectors in the host adaptation of the tobacco (Nicotiana sp.) pathogen Pseudomonas syringae pv. tabaci, a selection of seven strains was first characterized by multilocus sequence typing (MLST) to determine their phylogenetic affinity. MLST revealed that all strains represented a tight phylogenetic group and that the most closely related strain with a completely sequenced genome was the bean (Phaseolus vulgaris) pathogen P. syringae pv. phaseolicola 1448A. Using primers designed to 21 P. syringae pv. phaseolicola 1448A effector genes, it was determined that P. syringae pv. phaseolicola 1448A shared at least 10 effectors with all tested P. syringae pv. tabaci strains. Six of the 11 effectors that failed to amplify from P. syringae pv. tabaci strains were individually expressed in one P. syringae pv. tabaci strain. Although five effectors had no effect on phenotype, growth in planta and disease severity of the transgenic P. syringae pv. tabaci expressing hopQ1-1(Pph1448A) were significantly increased in bean, but reduced in tobacco. We conclude that hopQ1-1 has been retained in P. syringae pv. phaseolicola 1448A, as this effector suppresses immunity in bean, whereas hopQ1-1 is missing from P. syringae pv. tabaci strains because it triggers defences in Nicotiana spp. This provides evidence that fine-tuning effector repertoires during host adaptation lead to a concomitant reduction in virulence in non-host species.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6640246PMC
http://dx.doi.org/10.1111/j.1364-3703.2009.00577.xDOI Listing

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