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Applied and Environmental Microbiology, April 2009, p. 2275-2283, Vol. 75, No. 8
0099-2240/09/$08.00+0 doi:10.1128/AEM.01964-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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Department of Plant Pathology and Microbiology, University of California, Riverside, California 92521,1 Institute of Agricultural and Environmental Research, Tennessee State University, Nashville, Tennessee 37209,2 Department of Microbiology, Center for Scientific Research and Higher Education of Ensenada, Km. 107 Ctra. Tijuana-Ensenada, 22860 Ensenada, Baja California, Mexico3
Received 23 August 2008/ Accepted 3 February 2009
The xylem-limited, insect-transmitted bacterium Xylella fastidiosa causes Pierce's disease in grapes through cell aggregation and vascular clogging. GacA controls various physiological processes and pathogenicity factors in many gram-negative bacteria, including biofilm formation in Pseudomonas syringae pv. tomato DC3000. Cloned gacA of X. fastidiosa was found to restore the hypersensitive response and pathogenicity in gacA mutants of P. syringae pv. tomato DC3000 and Erwinia amylovora. A gacA mutant of X. fastidiosa (DAC1984) had significantly reduced abilities to adhere to a glass surface, form biofilm, and incite disease symptoms on grapevines, compared with the parent (A05). cDNA microarray analysis identified 7 genes that were positively regulated by GacA, including xadA and hsf, predicted to encode outer membrane adhesion proteins, and 20 negatively regulated genes, including gumC and an antibacterial polypeptide toxin gene, cvaC. These results suggest that GacA of X. fastidiosa regulates many factors, which contribute to attachment and biofilm formation, as well as some physiological processes that may enhance the adaptation and tolerance of X. fastidiosa to environmental stresses and the competition within the host xylem.
Published ahead of print on 13 February 2009.
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