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Journal of Bacteriology, April 2009, p. 2266-2275, Vol. 191, No. 7
0021-9193/09/$08.00+0 doi:10.1128/JB.01152-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung 404, Taiwan,1 Department of Biotechnology, Asia University, Wufeng, Taichung County 413, Taiwan2
Received 15 August 2008/ Accepted 29 December 2008
In prokaryotes, flagellar biogenesis is a complicated process involving over 40 genes. The phytopathogen Xanthomonas campestris pv. campestris possesses a single polar flagellum, which is essential for the swimming motility. A
54 activator, FleQ, has been shown to be required for the transcriptional activation of the flagellar type III secretion system (F-T3SS), rod, and hook proteins. One of the two rpoN genes, rpoN2, encoding
54, is essential for flagellation. RpoN2 and FleQ direct the expression of a second alternative sigma FliA (
28) that is essential for the expression of the flagellin FliC. FlgM interacts with FliA and represses the FliA regulons. An flgM mutant overexpressing FliC generates a deformed flagellum and displays an abnormal motility. Mutation in the two structural genes of F-T3SS, flhA and flhB, suppresses the production of FliC. Furthermore, FliA protein levels are decreased in an flhB mutant. A mutant defective in flhA, but not flhB, exhibits a decreased infection rate. In conclusion, the flagellar biogenesis of Xanthomonas campestris requires alternative sigma factors RpoN2 and FliA and is temporally regulated by FlhA, FlhB, and FlgM.
Published ahead of print on 9 January 2009.
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