Sugars induce the Agrobacterium virulence genes through a periplasmic binding protein and a transmembrane signal protein.

Cangelosi, Gerard A.; Ankenbauer, Robert G.; Nester, Eugene W.

doi:10.1073/pnas.87.17.6708

Cited by 301 publications

(281 citation statements)

References 29 publications

(36 reference statements)

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“…In addition, the araA homologue in A. tumefaciens (chvE) has been shown to be necessary for the induction of plant virulence factors by various sugars (Huang et al, 1990;Cangelosi et al, 1990). These reports led us to ask whether mutations in the ara operon would affect the symbiotic ability of S. meliloti.…”

Section: Plant Symbiosis and Competition For Nodule Occupancymentioning

confidence: 99%

“…The gene araA is a homologue of chvE in Agrobacterium tumefaciens, which has been shown to couple sugar binding with the induction of plant virulence genes (Huang et al, 1990;Cangelosi et al, 1990), and is thought to be the periplasmic sugar-binding protein of an ATP-binding cassette (ABC) transporter (Kemner et al, 1997). An InterProScan search showed that AraA is a member of the periplasmic binding protein family (InterPro accession number IPR001761).…”

Section: Analysis Of Arabinose Transcriptional Unitmentioning

confidence: 99%

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Sinorhizobium meliloti pSymB carries genes necessary for arabinose transport and catabolism

et al. 2007

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Arabinose is a known component of plant cell walls and is found in the rhizosphere. In this work, a previously undeleted region of the megaplasmid pSymB was identified as encoding genes necessary for arabinose catabolism, by Tn5-B20 random mutagenesis and subsequent complementation. Transcription of this region was measured by b-galactosidase assays of Tn5-B20 fusions, and shown to be strongly inducible by arabinose, and moderately so by galactose and seed exudate. Accumulation of [ 3 H]arabinose in mutants and wild-type was measured, and the results suggested that this operon is necessary for arabinose transport. Although catabolite repression of the arabinose genes by succinate or glucose was not detected at the level of transcription, both glucose and galactose were found to inhibit accumulation of arabinose when present in excess. To determine if glucose was also taken up by the arabinose transport proteins, [ 14 C]glucose uptake rates were measured in wild-type and arabinose mutant strains. No differences in glucose uptake rates were detected between wild-type and arabinose catabolism mutant strains, indicating that excess glucose did not compete with arabinose for transport by the same system. Arabinose mutants were tested for the ability to form nitrogen-fixing nodules on alfalfa, and to compete with the wild-type for nodule occupancy. Strains unable to utilize arabinose did not display any symbiotic defects, and were not found to be less competitive than wild-type for nodule occupancy in co-inoculation experiments. Moreover, the results suggest that other loci are required for arabinose catabolism, including a gene encoding arabinose dehydrogenase.

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Section: Plant Symbiosis and Competition For Nodule Occupancymentioning

confidence: 99%

Section: Analysis Of Arabinose Transcriptional Unitmentioning

confidence: 99%

Sinorhizobium meliloti pSymB carries genes necessary for arabinose transport and catabolism

et al. 2007

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“…Table 1A, R -'^^1, R' -CH2Br), Unexpectedly, no evidence was found for incorporation of the radiolabel into VirA; rather, two low-molecular-weight proteins, piO and p21, reacted specifically with the labelled inhibitor under physiologic conditions and failed to react with other compounds designed to test non-specific reactivity. Like ChvE, the monosaccharide binding protein which modulates the activity of phenols in vir induction (Caneglosi et ai, 1990;Shimoda et ai, 1990), these potential phenol receptors appear to be encoded by the bacterial chromosome and to be constitutively expressed.…”

Section: The Complexity Of Phenol Recognition: Virulence and Chemotaxismentioning

confidence: 99%

Strategies in pathogenesis: mechanistic specificity in the detection of generic signals

Duban

Lee

Lynn

1993

Molecular Microbiology

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SummaryThe virulence genes of the plant pathogen Agrobacterium tumefaciens are induced by more than 40 lowmolecular-weight phenolic compounds. The prevailing opinion is that (i) wound-derived phenols produced on breach of the integrity of the cell wall act as the initiating signal in a series of events which results in host cell transformation, and (ii) a classical membrane receptor, putatively VirA, is responsible for the recognition of all such phenolic inducers. Here, we argue that the discovery of the subset of inducers that are relatives of the dehydrodiconiferyl alcohol glucoside (DCG) growth factors redirects our attention to work on the plant wound as a site of cell division, and suggests that we further explore the implications of early work on the relationship between transformation efficiency and the status of the cell cycle of the host. In addition, we argue that the significant structural diversity allowed in the para position of the phenol ring of inducers suggests that a receptor-ligand interaction based solely on structural recognition is insufficient, but that recognition followed by a specific proton transfer event may be sufficient to explain vir induction activity. Hence, the specificity of the response of A. tumefaciens may be a consequence of the features required for a chemical reaction to occur on the receptor surface. Finally, we review affinity labelling studies which exploit this phenol detection mechanism and which provide evidence that the phenol receptor may be other than VirA, the sensory kinase of the two component regulatory system implicated in Agrobacterium virulence. Taken together, these hypotheses form a model which has predictive and therefore experimental value, and which may be of broader interest in that it calls attention to the possibility of an intricate co-evolution of signalling pathways of host and pathogen.

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“…According to the accepted mechanism, A. tumefaciens is attracted to wound sites of the root surfaces by chemotaxis, and the presence of phenolic compounds, such as acetosyringone, in synergy with a certain class of monosaccharides (D-glucose, D-galactose, L-arabinose) triggers the activation of the virulence genes [2]. In order to transfer its T-DNA into the plant cell, the bacterium has to be adsorbed on the wounded area; this event is modulated by the components of the external membrane of the bacterium, both the proteins and the lipopolysaccharides (LPS) [3].…”

mentioning

confidence: 99%

Structural determination of the O‐chain polysaccharide from Agrobacterium tumefaciens, strain DSM 30205

Castro

Molinaro

et al. 2002

European Journal of Biochemistry

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Agrobacterium tumefaciens is a Gram-negative, phytopathogenic bacterium and is characterized by an unique mode of action on dicotyledonous plants: it is able to genetically modify the host, and because of this feature, it is used as a tool for transgenic plants. Many experiments have demonstrated that lipopolysaccharides (LPSs) play an important role for the disease development, as they are involved in the adhesion process of the bacterium on the plant cell wall. Despite the wealth of information on the role of LPS on phytopathogenesis, the present paper appears as the first report on the molecular primary structure of the O-chain produced from Agrobacterium. Its repeating unit was determined by means of chemical and spectroscopical analysis, and has the following structure:Keywords: lipopolysaccharides; Agrobacterium tumefaciens; structure; phytopathogenesis.Agrobacterium tumefaciens is a Gram-negative phytopathogenic bacterium [1], which induces the crown gall disease on a wide range of dicotyledonous (broad-leaved) plants, and especially to the members of the rose family such as apple, pear and cherry; some strains can attack also almond trees and grapevines. The disease gains its name from the large tumour-like swellings (galls) that typically occur at the crown of the plant, just above soil level. The growth of all these plants is compromised, leading damages to nursery stocks and to their marketability. This disease is one of the most widely studied because of its remarkable biology; basically, the bacterium transfers the T-DNA, a portion of its plasmidial DNA (called Ti, i.e. Tumor inducing), into the plant host genome, where it is integrated, causing the uncontrolled growth of the modified plant cells and then the formation of the tumour. The unique mode of action of A. tumefaciens has enabled this bacterium to be used as a tool for trans-genetic plants.The development of the pathogenesis is a complex process and it is conditioned by the recognition and absorption of the bacterium on the host. According to the accepted mechanism, A. tumefaciens is attracted to wound sites of the root surfaces by chemotaxis, and the presence of phenolic compounds, such as acetosyringone, in synergy with a certain class of monosaccharides (D-glucose, D-galactose, L-arabinose) triggers the activation of the virulence genes [2]. In order to transfer its T-DNA into the plant cell, the bacterium has to be adsorbed on the wounded area; this event is modulated by the components of the external membrane of the bacterium, both the proteins and the lipopolysaccharides (LPS) [3]. In the latter case, the interaction is based on the recognition of a portion of the lipopolysaccharide, defined with the term epitope, by particular receptor proteins [4] situated on the plant cell wall. In fact, it is possible to saturate these receptors with an LPS solution leading to the protection of the plant from the bacterial action. Further studies showed that the epitope recognized by the plant is located on the O-antigenic part of LPS, that is the...

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Sugars induce the Agrobacterium virulence genes through a periplasmic binding protein and a transmembrane signal protein.

Cited by 301 publications

References 29 publications

Sinorhizobium meliloti pSymB carries genes necessary for arabinose transport and catabolism

Sinorhizobium meliloti pSymB carries genes necessary for arabinose transport and catabolism

Strategies in pathogenesis: mechanistic specificity in the detection of generic signals

Structural determination of the O‐chain polysaccharide from Agrobacterium tumefaciens, strain DSM 30205

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