Previous Article | Next Article ![]()
Applied and Environmental Microbiology, December 1999, p. 5564-5573, Vol. 65, No. 12
Department of Botany, National Taiwan
University, and Institute of Molecular Biology, Academia Sinica,
Taipei, Taiwan, Republic of China
Received 7 June 1999/Accepted 1 October 1999
A mutant (XT906) of Xanthomonas campestris pv. citri,
the causal agent of citrus canker, was induced by insertion of the
transposon Tn5tac1 and isolated. This mutant did not grow
or elicit canker disease in citrus leaves but was still able to induce
a hypersensitive response in a nonhost plant (the common bean). The
mutant was also unable to grow on minimal medium containing fructose or
glycerol as the sole carbon source. A 2.5-kb fragment of wild-type DNA that complemented the mutant phenotype of XT906 was isolated. Sequence
analysis revealed that this DNA fragment encoded a protein of 562 amino
acids that shows homology to phosphoglucose isomerase (PGI). Enzyme
activity assay confirmed that the encoded protein possesses PGI
activity. Analysis of the activity of the promoter of the
pgi gene revealed that it was inhibited by growth in
complex medium but induced by culture in plant extract. These results demonstrate that PGI is required for pathogenicity of X. campestris pv. citri.
0099-2240/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Requirement for Phosphoglucose Isomerase of
Xanthomonas campestris in Pathogenesis of Citrus
Canker
*
Corresponding author. Mailing address: Institute of
Molecular Biology, Academia Sinica, Nankang, Taipei 11529, Taiwan,
Republic of China. Phone: 886-2-27899213. Fax: 886-2-27826085. E-mail: tehkuo{at}ccvax.sinica.edu.tw.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»