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JB Accepts, published online ahead of print on 8 February 2008
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J. Bacteriol. doi:10.1128/JB.01757-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Naturally Occurring Non-pathogenic Isolates of the Plant Pathogen Species Pseudomonas syringae Lack a Type III Secretion System and Effector Gene Orthologues

Toni J Mohr, Haijie Liu, Shuangchun Yan, Cindy E. Morris, José A. Castillo, Joanna Jelenska, and Boris A Vinatzer*

Department of Plant Pathology, Physiology, and Weed Science, Virginia Tech, Latham Hall, Ag Quad Lane, Blacksburg, VA-24061, USA; INRA, Unité de Pathologie Végétale, BP 94, 84140 Montfavet, France; Department of Molecular Genetics and Cell Biology, The University of Chicago, 1103 East 57th Street, Chicago, IL-60637, USA

* To whom correspondence should be addressed. Email: vinatzer{at}vt.edu.


   Abstract

Pseudomonas syringae causes plant diseases using as main virulence mechanism a type III secretion system (T3SS) to translocate dozens of effector proteins into plant cells. Here we report the existence of a sub-group of P. syringae isolates that do not cause disease on any tested plant species. This group is monophyletic and most likely evolved from a pathogenic P. syringae ancestor through loss of the T3SS. In the non-pathogenic isolate P. syringae 508 (Psy508) the genomic region that in pathogenic P. syringae contains the hrp/hrc cluster coding for the T3SS and flanking effector genes is absent. Psy508 was also surveyed for the presence of effector orthologues from the closely related pathogenic PsyB728a strain but none were detected. Absence of hrp/hrc and effector orthologues was confirmed for other non-pathogenic isolates. Using the AvrRpt2 effector as reporter revealed the inability of Psy508 to translocate effectors into plant cells. Adding a plasmid-encoded T3SS and the effector hopA1Psy61 increased in planta growth almost 10 fold. This suggests that Psy508 supplemented with a T3SS could be used to unravel functions of individual effectors in the context of a plant infection, avoiding the confounding effect of other effectors with similar function present in effector mutants of pathogenic isolates.







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