This Article Full Text Full Text (PDF) Supplemental material Other Versions of this Article: JB.01757-07v1 190/8/2858    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Copyright Information Books from ASM Press MicrobeWorld Google Scholar Articles by Mohr, T. J. Articles by Vinatzer, B. A. PubMed PubMed Citation Articles by Mohr, T. J. Articles by Vinatzer, B. A.

Naturally Occurring Nonpathogenic Isolates of the Plant Pathogen Pseudomonas syringae Lack a Type III Secretion System and Effector Gene Orthologues ^,

Department of Plant Pathology, Physiology, and Weed Science, Virginia Tech, Latham Hall, Ag Quad Lane, Blacksburg, Virginia 24061,¹ INRA, Unité de Pathologie Végétale, BP 94, 84140 Montfavet, France,² Department of Molecular Genetics and Cell Biology, University of Chicago, 1103 East 57th Street, Chicago, Illinois 60637³

Received 2 November 2007/ Accepted 28 January 2008

Pseudomonas syringae causes plant diseases, and the main virulence mechanism is a type III secretion system (T3SS) that translocates dozens of effector proteins into plant cells. Here we report the existence of a subgroup of P. syringae isolates that do not cause disease on any plant species tested. This group is monophyletic and most likely evolved from a pathogenic P. syringae ancestor through loss of the T3SS. In the nonpathogenic isolate P. syringae 508 the genomic region that in pathogenic P. syringae strains contains the hrp-hrc cluster coding for the T3SS and flanking effector genes is absent. P. syringae 508 was also surveyed for the presence of effector orthologues from the closely related pathogenic strain P. syringae pv. syringae B728a, but none were detected. The absence of the hrp-hrc cluster and effector orthologues was confirmed for other nonpathogenic isolates. Using the AvrRpt2 effector as reporter revealed the inability of P. syringae 508 to translocate effectors into plant cells. Adding a plasmid-encoded T3SS and the P. syringae pv. syringae 61 effector gene hopA1 increased in planta growth almost 10-fold. This suggests that P. syringae 508 supplemented with a T3SS could be used to determine functions of individual effectors in the context of a plant infection, avoiding the confounding effect of other effectors with similar functions present in effector mutants of pathogenic isolates.

Published ahead of print on 8 February 2008.

Supplemental material for this article may be found at http://jb.asm.org/.