PT  - JOURNAL ARTICLE
AU  - Kevin L. Hockett
AU  - Marc T. Nishimura
AU  - Erik Karlsrud
AU  - Kevin Dougherty
AU  - David A. Baltrus
TI  - Interactions Between Genome Architecture and Virulence Genes in <em>Pseudomonas syringae</em>, strain CC1557 as a model
AID  - 10.1101/000869
DP  - 2013 Jan 01
TA  - bioRxiv
PG  - 000869
4099  - http://biorxiv.org/content/early/2013/11/23/000869.short
4100  - http://biorxiv.org/content/early/2013/11/23/000869.full
AB  - Both type III effector proteins and non-ribosomal peptide toxins play important roles for Pseudomonas syringae pathogenicity in host plants, but if and how these virulence 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 a highly similar toxin to syringomycin through horizontal transfer. We demonstrate that this strain is pathogenic on Nicotiana benthamiana and that both the type III secretion system and a new type III effector family, hopBJ1, contribute to virulence. Taken together, our results provide independent evolutionary confirmation of a negative correlation between type III effector repertoires and some non-ribosomal peptide toxins while also highlighting how genomic synteny can be used to identify novel virulence proteins.