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Applied and Environmental Microbiology, March 2007, p. 1612-1621, Vol. 73, No. 5
0099-2240/07/$08.00+0 doi:10.1128/AEM.00261-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Plant Molecular and Cell Biology Program and Department of Plant Pathology, University of Florida, Gainesville, Florida 32611-0680,1 The Institute for Genomic Research, 9712 Medical Center Dr., Rockville, Maryland 20650,2 ICBR Biotechnology Program, Box 110695, University of Florida, Gainesville, Florida 326113
Received 1 February 2006/ Accepted 1 November 2006
Xanthomonas citri pv. citri is a clonal group of strains that causes citrus canker disease and appears to have originated in Asia. A phylogenetically distinct clonal group that causes identical disease symptoms on susceptible citrus, X. citri pv. aurantifolii, arose more recently in South America. Genomes of X. citri pv. aurantifolii strains carry two DNA fragments that hybridize to pthA, an X. citri pv. citri gene which encodes a major type III pathogenicity effector protein that is absolutely required to cause citrus canker. Marker interruption mutagenesis and complementation revealed that X. citri pv. aurantifolii strain B69 carried one functional pthA homolog, designated pthB, that was required to cause cankers on citrus. Gene pthB was found among 38 open reading frames on a 37,106-bp plasmid, designated pXcB, which was sequenced and annotated. No additional pathogenicity effectors were found on pXcB, but 11 out of 38 open reading frames appeared to encode a type IV transfer system. pXcB transferred horizontally in planta, without added selection, from B69 to a nonpathogenic X. citri pv. citri (pthA::Tn5) mutant strain, fully restoring canker. In planta transfer efficiencies were very high (>0.1%/recipient) and equivalent to those observed for agar medium with antibiotic selection, indicating that pthB conferred a strong selective advantage to the recipient strain. A single pathogenicity effector that can confer a distinct selective advantage in planta may both facilitate plasmid survival following horizontal gene transfer and account for the origination of phylogenetically distinct groups of strains causing identical disease symptoms.
Published ahead of print on 12 January 2007.
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