The Receiver of the Agrobacterium tumefaciens VirA Histidine Kinase Forms a Stable Interaction with VirG to Activate Virulence Gene Expression.

Arlene A Wise,Andrew N Binns

doi:10.3389/fmicb.2015.01546

Abstract

The plant pathogen Agrobacterium tumefaciens carries a virulence gene system that is required for the initiation of crown gall tumors on susceptible plants. Expression of the vir genes is activated by the VirA/VirG two component regulatory system. VirA is a histidine kinase which signals the presence of certain chemicals found at the site of a plant wound. The receiver domain located at its carboxyl terminus defines VirA as a hybrid histidine kinase. Here, we show that the VirA receiver interacts with the DNA-binding domain of VirG. This finding supports the hypothesis that the receiver acts as a recruiting factor for VirG. In addition, we show that removal of the VirA receiver allowed vir gene expression in response to glucose in a dose dependent manner, indicating that the receiver controls VirG activation and suggesting that the supplementary ChvE-sugar signal increases this activity.

Highlights

Agrobacterium tumefaciens is the causative agent of crown gall tumors on dicotyledonous plants
In medium containing glucose and AS, vir gene expression was similar whether the cells constitutively expressed virG or virA R, with the aforementioned exception of constitutively expressed virG bypassing the requirement for AS
VirA and VirG are both essential for virulence, but their interdependent and self-regulated expression (Winans et al, 1988) means that these proteins are present in miniscule amounts in the early stages of induction (Lee et al, 1992; Wise et al, 2010)

Summary

Introduction

Agrobacterium tumefaciens is the causative agent of crown gall tumors on dicotyledonous plants. The virulence system that drives tumor formation depends on the ability of the VirA histidine kinase to signal the presence of certain chemical components found at the site of a plant wound. When the inducing signals (phenolics, monosaccharides, and low pH) are present, a phosphate group is transferred from the conserved histidine (H474) in VirA’s kinase region to a conserved aspartate (D52) in the receiver domain of the response regulator, VirG (see Figure 1). Certain monosaccharides (arabinose, glucose, galactose, glucuronic acid, and others), are not, by themselves, inducing agents. Their presence greatly enhances vir gene expression when the concentration of phenolic inducer is low (Ankenbauer and Nester, 1990; Cangelosi et al, 1990).

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Conclusion