Disease relevance of virC2

• Host recognition and macromolecular transfer of virulence-mediating effectors represent critical steps in the successful transformation of plant cells by Agrobacterium tumefaciens [1].
• Probing the surface of bvrR and bvrS transposon mutants with monoclonal antibodies showed all described major outer membrane proteins (Omps) but Omp25, a protein known to be involved in Brucella virulence [2].
• We describe a conserved family of bacterial gene products that includes the VirB1 virulence factor encoded by tumor-inducing plasmids of Agrobacterium spp., proteins involved in conjugative DNA transfer of broad-host-range bacterial plasmids, and gene products that may be involved in invasion by Shigella spp. and Salmonella enterica [3].
• The two-component system BvrR/BvrS essential for Brucella abortus virulence regulates the expression of outer membrane proteins with counterparts in members of the Rhizobiaceae [2].
• Type IV secretion systems mediate the translocation of virulence factors (proteins and/or DNA) from Gram-negative bacteria into eukaryotic cells [4].

High impact information on virC2

• The virulence determinants of A. tumefaciens reside on a large tumour-inducing (Ti) plasmid [5].
• We discuss genome architecture and evolution and additional genes potentially involved in virulence and metabolic parasitism of host plants [6].
• Seven phenolic compounds that are widely distributed among the angiosperm plants--catechol, gallic acid, pyrogallic acid, p-hydroxybenzoic acid, protocatechuic acid, beta-resorcylic acid, and vanillin--are able to induce the expression of the virulence loci [7].
• The Agrobacterium tumefaciens virulence D2 protein is responsible for precise integration of T-DNA into the plant genome [8].
• The virA gene of Agrobacterium tumefaciens encodes an inner membrane that mediates the transcriptional activation of virulence genes in response to plant signal molecules [9].

Chemical compound and disease context of virC2

• The T-DNA transfer process of Agrobacterium tumefaciens is activated by the induction of the Ti plasmid virulence (vir) loci by plant signal molecules such as acetosyringone [10].
• Crude protein extracts of induced and uninduced octopine wild-type strain of Agrobacterium tumefaciens, as well as several mutants of the virulence loci virA, -B, -G, -C, -D, and -E, were probed with single- and double-stranded synthetic oligodeoxynucleotides of different sequence and length in an electrophoretic retardation assay [11].
• Mechanism of activation of Agrobacterium virulence genes: identification of phenol-binding proteins [12].
• A nontransformable Triticum monococcum monocotyledonous culture produces the potent Agrobacterium vir-inducing compound ethyl ferulate [13].
• Virulence of Agrobacterium tumefaciens requires phosphatidylcholine in the bacterial membrane [14].

Biological context of virC2

• Based on its role in vir gene induction, homology to transcriptional regulators and membrane localization, we propose that VirA acts as an environmental sensor of plant-derived inducer molecules and transmits this information to the level of vir gene expression [15].
• These regions code for octopine catabolism, virulence and plant tumor phenotype [16].
• One hundred and twenty-four vir::Tn3-lac insertions were analyzed for their mutagenic effect on Agrobacterium virulence, and for their expression of beta-galactosidase activity, the lacZ gene product, in vegetative bacteria and in bacteria cocultivated with plant cells [17].
• To identify genes involved in T-strand production, pTiA6 virulence (vir) and chromosomal virulence (chv) mutant strains were analyzed [18].
• These studies suggest that the hdv locus is comprised of at least four genes arranged in an operon in the vir region [19].

Anatomical context of virC2

• Incubation of the membranes with increasing concentrations of the detergent differentially extracted virulence proteins [20].
• VirB8-like proteins are essential components of type IV secretion systems, bacterial virulence factors that mediate the translocation of effector molecules from many bacterial pathogens into eukaryotic cells [21].
• Exudates of dicotyledonous plants contain specific phenolic signal molecules, such as acetosyringone, which serve as potent inducers for the expression of the virulence (vir) regulon of the phytopathogen Agrobacterium tumefaciens [13].
• Thus, at least for the wheat cell line used in this study, monocotyledonous resistance to Agrobacterium transformation must result from a block to a step of the T-DNA transfer process subsequent to vir induction [13].
• A single-stranded DNA substrate is transported across the two cell walls along with the bacterial virulence proteins VirD2 and VirE2 [22].

Associations of virC2 with chemical compounds

• As virC mutants in the octopine-type plasmid pTiB6 are invariably avirulent in tests on various plant species, this gene seems to be essential for virulence and we are studying it in detail [23].
• Although many hydroxyphenylpropanoid and phenolic compounds can activate the virulence cascade, the only native inducers that have been identified to date are acetosyringone and hydroxyacetosyringone [24].
• We show here that a group of aldoses (L-arabinose, D-xylose, D-lyxose, D-glucose, D-mannose, D-idose, D-galactose, and D-talose) can markedly enhance acetosyringone-dependent expression of vir genes when the concentration of acetosyringone is limited (10 microM) but does not enhance the expression of noninducible genes [25].
• These findings indicate that plant GABA may modulate quorum sensing in A. tumefaciens, thereby affecting its virulence on plants [26].
• This molecule is shown to correspond to ethyl ferulate [C12H14O4; 3-(4-hydroxy-3-methoxyphenyl)-2-propenoic acid ethyl ester], to be more active for vir induction at low concentrations than acetosyringone, and to be produced in quantities giving significant levels of induction [13].

Physical interactions of virC2

• An octopine-type Ti plasmid, resident in different Agrobacterium tumefaciens chvB mutants, transferred at normal frequencies, demonstrating that this virulence locus affecting plant cell binding is not required for Ti plasmid conjugation [27].

Regulatory relationships of virC2

• However, an enriched subpopulation of motile tatC mutants exhibited enhanced virulence compared to the nonmotile variants [28].

Other interactions of virC2

• The virulence genes virD1 and virD2 from Agrobacterium tumefaciens that are required in bacteria for excision of T-strands from the tumor-inducing plasmid were placed under the control of the CaMV35S promoter and codelivered with a target plasmid containing border sequences flanking the gene of interest [29].
• Generally, the mutants of the apple isolate D10B/87 were altered in the tumor-inducing plasmid, harboring either deletions in this plasmid or point mutations in the regulatory virulence gene virG [30].
• The virD operon of the resident Ti plasmid of Agrobacterium tumefaciens contains loci involved in T-DNA processing and undefined virulence functions [31].
• A plasmid containing the virD region from octopine Ti plasmid could restore both virulence and processing to a nopaline virD2 mutant [32].
• We show here that the absence of pAtC58 in pTiC58-containing strains results in reduced virulence but that disruption of the attR gene does not result in avirulence or a reduction in virulence [33].

Analytical, diagnostic and therapeutic context of virC2

• We characterized this signal in the virulence protein VirF by alanine scanning and further site-directed mutagenesis [34].
• Molecular cloning and characterization of cgt, the Brucella abortus cyclic beta-1,2-glucan transporter gene, and its role in virulence [35].
• In this report, we show that the level of expression of one of these genes was increased dramatically by culture conditions that increased the expression of Ti plasmid virulence genes, including coculture with plant cells or treatment with acetosyringone, a plant phenolic compound [36].
• Western blot (immunoblot) analysis indicated that the observed loss of virulence could not be attributed to a decrease in the steady-state levels of the mutant VirB10 protein [37].
• A semiquantitative bioassay for relative virulence of Agrobacterium tumefaciens strains on Bryophyllum daigremontiana [38].

References