Both type III effector proteins and nonribosomal peptide toxins play important roles for Pseudomonas syringae pathogenicity in host plants, but whether and how these pathways interact to promote infection remains unclear. Genomic evidence from one clade of P. syringae suggests a tradeoff between the total number of type III effector proteins and presence of syringomycin, syringopeptin, and syringolin A toxins. Here, we report the complete genome sequence from P. syringae CC1557, which contains the lowest number of known type III effectors to date and has also acquired genes similar to sequences encoding syringomycin pathways from other strains. We demonstrate that this strain is pathogenic on Nicotiana benthamiana and that both the type III secretion system and a new type III effector, hopBJ1, contribute to pathogenicity. We further demonstrate that activity of HopBJ1 is dependent on residues structurally similar to the catalytic site of Escherichia coli CNF1 toxin. Taken together, our results provide additional support for a negative correlation between type III effector repertoires and the potential to produce syringomycin-like toxins while also highlighting how genomic synteny and bioinformatics can be used to identify and characterize novel virulence proteins.
34Both type III effector proteins and non-ribosomal peptide toxins play important 35 roles for Pseudomonas syringae pathogenicity in host plants, but whether and how 36 these virulence pathways interact to promote infection remains unclear. Genomic 37 evidence from one clade of P. syringae suggests a tradeoff between the total number of 38 type III effector proteins and presence of syringomycin, syringopeptin, and syringolin A 39 toxins. Here we report the complete genome sequence from P. syringae CC1557, 40 which contains the lowest number of known type III effectors to date and has also 41 acquired genes similar to sequences encoding syringomycin pathways from other 42 strains. We demonstrate that this strain is pathogenic on Nicotiana benthamiana and 43 that both the type III secretion system and a new type III effector family, hopBJ1, 44 contribute to virulence. We further demonstrate that virulence activity of HopBJ1 is 45 dependent on similar catalytic sites as the E. coli CNF1 toxin. Taken together, our 46 results provide additional support for a negative correlation between type III effector 47 repertoires and the potential to produce syringomycin-like toxins while also highlighting 48 how genomic synteny and bioinformatics can be used to identify and characterize novel 49 virulence proteins. 50 51 Introduction 52
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