Life in a black hole — the micro-environment of the vascular pathogen

Pegg, G. F.

doi:10.1016/s0007-1536(85)80151-0

Cited by 43 publications

(34 citation statements)

References 80 publications

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“…This affirms that ammonium, an easily metabolized nitrogen source that represses uptake and metabolism of other nitrogen sources, is not present in this environment (4). Although this nitrogen scavenging behavior is consistent with the long-held idea that plant xylem is a relatively nutrient-poor environment, this description should be used carefully (44). The nitrogen-scavenging behavior revealed by gene expression analysis does not necessarily indicate that the organism is nitrogen starved.…”

Section: R Solanacearum Uses Nitrate Assimilation During Pathogenesissupporting

confidence: 76%

Nitrate Assimilation Contributes to Ralstonia solanacearum Root Attachment, Stem Colonization, and Virulence

Dalsing

Allen

2013

Journal of Bacteriology

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Ralstonia solanacearum, an economically important plant pathogen, must attach, grow, and produce virulence factors to colonize plant xylem vessels and cause disease. Little is known about the bacterial metabolism that drives these processes. Nitrate is present in both tomato xylem fluid and agricultural soils, and the bacterium's gene expression profile suggests that it assimilates nitrate during pathogenesis. A nasA mutant, which lacks the gene encoding the catalytic subunit of R. solanacearum's sole assimilatory nitrate reductase, did not grow on nitrate as a sole nitrogen source. This nasA mutant exhibited reduced virulence and delayed stem colonization after soil soak inoculation of tomato plants. The nasA virulence defect was more severe following a period of soil survival between hosts. Unexpectedly, once bacteria reached xylem tissue, nitrate assimilation was dispensable for growth, virulence, and competitive fitness. However, nasA-dependent nitrate assimilation was required for normal production of extracellular polysaccharide (EPS), a major virulence factor. Quantitative analyses revealed that EPS production was significantly influenced by nitrate assimilation when nitrate was not required for growth. The plant colonization delay of the nasA mutant was externally complemented by coinoculation with wild-type bacteria but not by coinoculation with an EPS-deficient epsB mutant. The nasA mutant and epsB mutant did not attach to tomato roots as well as wild-type strain UW551. However, adding either wild-type cells or cell-free EPS improved the root attachment of these mutants. These data collectively suggest that nitrate assimilation promotes R. solanacearum virulence by enhancing root attachment, the initial stage of infection, possibly by modulating EPS production.

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Section: R Solanacearum Uses Nitrate Assimilation During Pathogenesissupporting

confidence: 76%

Nitrate Assimilation Contributes to Ralstonia solanacearum Root Attachment, Stem Colonization, and Virulence

Dalsing

Allen

2013

Journal of Bacteriology

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“…During the initial bacterial colonization, nutrients in the plant are scarce, especially in the xylem (49). In E. coli, acrAB expression increases in carbon-starved cells, probably because starvation triggers a general bacterial stress response, resulting in increased MDR expression (53).…”

Section: Discussionmentioning

confidence: 99%

Two Host-Induced Ralstonia solanacearum Genes, acrA and dinF , Encode Multidrug Efflux Pumps and Contribute to Bacterial Wilt Virulence

Brown

Swanson

Allen

2007

Appl Environ Microbiol

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Multidrug efflux pumps (MDRs) are hypothesized to protect pathogenic bacteria from toxic host defense compounds. We created mutations in the Ralstonia solanacearum acrA and dinF genes, which encode putative MDRs in the broad-host-range plant pathogen. Both mutations reduced the ability of R. solanacearum to grow in the presence of various toxic compounds, including antibiotics, phytoalexins, and detergents. Both acrAB and dinF mutants were significantly less virulent on the tomato plant than the wild-type strain. Complementation restored near-wild-type levels of virulence to both mutants. Addition of either dinF or acrAB to Escherichia coli MDR mutants KAM3 and KAM32 restored the resistance of these strains to several toxins, demonstrating that the R. solanacearum genes can function heterologously to complement known MDR mutations. Toxic and DNA-damaging compounds induced expression of acrA and dinF, as did growth in both susceptible and resistant tomato plants. Carbon limitation also increased expression of acrA and dinF, while the stress-related sigma factor RpoS was required at a high cell density (>10 7 CFU/ml) to obtain wild-type levels of acrA expression both in minimal medium and in planta. The type III secretion system regulator HrpB negatively regulated dinF expression in culture at high cell densities. Together, these results show that acrAB and dinF encode MDRs in R. solanacearum and that they contribute to the overall aggressiveness of this phytopathogen, probably by protecting the bacterium from the toxic effects of host antimicrobial compounds.Many bacteria can survive and even grow in the presence of toxic compounds (48). One of the means by which bacteria survive in toxic environments is by extruding toxins through membrane-bound efflux pumps (7, 69). These efflux proteins, called multidrug resistance efflux pumps (MDRs), transport a broad range of structurally unrelated compounds out of the cell and can confer resistance to a wide variety of toxins, including antibiotics (7, 36).The following five MDR families have been characterized: (i) the ATP binding cassette (ABC) superfamily (13), (ii) the major facilitator superfamily (54,55,66), (iii) the resistance nodulation-cell division (RND) superfamily (66), (iv) the small multidrug resistance (SMR) superfamily (47), and (v) the multidrug and toxic compound extrusion (MATE) superfamily (10). These superfamilies vary in the mechanism of transport, the number of transmembrane domains, and substrate specificity. The SMR superfamily has been found only in prokaryotes, while members of the RND, major facilitator, ABC, and MATE superfamilies are present in all domains of life (48).The role of MDRs in human and animal pathogens in association with the emergence of antibiotic-resistant strains has been well studied (36). However, comparative genomic analyses have revealed that MDRs are widely distributed in both pathogenic and nonpathogenic bacteria (55). This ubiquity underscores the importance of MDRs in bacterial life cycles. Despite the genomic abundan...

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“…1). If siderophores are produced by pseudomonads in the rhizosphere indeed, germination and subsequent active penetration of the pathogen into the roots (Pegg, 1985) may be reduced. No reports on quantitative estimates of pseudobactin concentrations in the rhizosphere are available, although Reid et al (1984) extracted hydroxamate siderophores in concentrations of 10 tzM from rhizosphere soil.…”

Section: Discussionmentioning

confidence: 99%

Siderophore-mediated competition for iron and induced resistance in the suppression of fusarium wilt of carnation by fluorescent Pseudomonas spp

Duijff

Meijer

Bakker

et al. 1993

Netherlands Journal of Plant Pathology

109

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The mechanisms of suppression of fusarium wilt of carnation by two fluorescent Pseudomonas strains were studied.Treatments of carnation roots with Pseudomonas sp. WCS417r significantly reduced fusarium wilt caused by Fusarium oxysporum f. sp. dianthi (Fod). Mutants of WCS417r defective in siderophore biosynthesis (sid) were less effective in disease suppression compared with their wild-type. Treatments of carnation roots with Pseudomonas putida WCS358r tended to reduce fusarium wilt, whereas a sid-mutant of WCS358 did not.Inhibition of conidial germination of Fod in vitro by purified siderophores (pseudobactins) of both Pseudomonas strains was based on competition for iron. The ferrated pseudobactins inhibited germination significantly less than the unferrated pseudobactins. Inhibition of mycelial growth of Fod by both Pseudomonas strains on agar plates was also based on competition for iron: with increasing iron content of the medium, inhibition of Fod by the Pseudomonas strains decreased. The sid-mutant of WCS358 did not inhibit Fod on agar plates, whereas the sid-mutants of WCS417r still did. This suggests that inhibition of Fod by WCS358r in vitro was only based on siderophoremediated competition for iron, whereas also a non-siderophore antifungal factor was involved in the inhibition of Fod by strain WCS417r.The ability of the Pseudomonas strains to induce resistance against Fod in carnation grown in soil was studied by spatially separating the bacteria (on the roots) and the pathogen (in the stem). Both WCS417r and its sid-mutant reduced disease incidence significantly in the moderately resistant carnation cultivar Pallas, WCS358r did not.It is concluded that the effective and consistent suppression of fusarium wilt of carnation by strain WCS417r involves multiple mechanisms: induced resistance, siderophore-mediated competition for iron and possibly antibiosis. The less effective suppression of fusarium wilt by WCS358r only depends on siderophore-mediated competition for iron.

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Life in a black hole — the micro-environment of the vascular pathogen

Cited by 43 publications

References 80 publications

Nitrate Assimilation Contributes to Ralstonia solanacearum Root Attachment, Stem Colonization, and Virulence

Nitrate Assimilation Contributes to Ralstonia solanacearum Root Attachment, Stem Colonization, and Virulence

Two Host-Induced Ralstonia solanacearum Genes, acrA and dinF , Encode Multidrug Efflux Pumps and Contribute to Bacterial Wilt Virulence

Siderophore-mediated competition for iron and induced resistance in the suppression of fusarium wilt of carnation by fluorescent Pseudomonas spp

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