Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 103, Issue 12, Pages 4658-4662Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0600366103
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- NIGMS NIH HHS [R01 GM032618, GM 32618] Funding Source: Medline
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Agrobacterium tumefaciens induces crown gall tumors by transferring a piece of its tumor-inducing plasmid into plant cells. This transferred DNA encodes the synthesis of indole acetic acid (IAA) and cytokinin, and their overproduction results in tumor formation. The transfer is initiated by a two-component regulatory system, VirA/G recognizing plant signal molecules in the plant rhizosphere and activating a regulon on the tumor-inducing plasmid, which is required for the processing and transfer of DNA and protein. Although a great deal is known about vir gene activation, nothing is known about whether or how the vir gene regulon is inactivated after plant cell transformation. Presumably, just as a mechanism exists for activating the vir gene regulon only when a plant is in the immediate environment, a mechanism should exist for inactivating the same regulon once it has fulfilled its mission to transferred DNA into plant cells. We now show that IAA inactivates vir gene expression by competing with the inducing phenolic compound acetosyringone for interaction with VirA. IAA does not inhibit the vir genes in cells containing a constitutive sensor virA locus, which does not require any signal molecules to become phosphorylated. At higher concentrations, IAA inhibits the growth of Agrobacterium and many other plant-associated bacteria but not the growth of bacteria that occupy other ecological niches. These observations provide the missing link in the cycle of vir gene activation and inactivation.
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