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Journal of Bacteriology, January 2005, p. 213-223, Vol. 187, No. 1
0021-9193/05/$08.00+0 doi:10.1128/JB.187.1.213-223.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
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Andrew N. Binns
Plant Science Institute, Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania
Received 16 July 2004/ Accepted 17 September 2004
The VirA/VirG two-component regulatory system of Agrobacterium tumefaciens regulates expression of the virulence (vir) genes that control the infection process leading to crown gall tumor disease on susceptible plants. VirA, a membrane-bound homodimer, initiates vir gene induction by communicating the presence of molecular signals found at the site of a plant wound through phosphorylation of VirG. Inducing signals include phenols, monosaccharides, and acidic pH. While sugars are not essential for gene induction, their presence greatly increases vir gene expression when levels of the essential phenolic signal are low. Reception of the sugar signal depends on a direct interaction between ChvE, a sugar-binding protein, and VirA. Here we show that the sugar signal received in the periplasmic region of one subunit within a VirA heterodimer can enhance the kinase function of the second subunit. However, sugar enhancement of vir gene expression was vector dependent. virA alleles expressed from pSa-derived vectors inhibited signal transduction by endogenous VirA. Inhibition was conditional, depending on the induction medium and the virA allele tested. Moreover, constitutive expression of virG overcame the inhibitory effect of some but not all virA alleles, suggesting that there may be more than one inhibitory mechanism.
Present address: Robert Wood Johnson Medical School, Piscataway, N.J.
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