- Volume 153, Issue 7, 2007
Volume 153, Issue 7, 2007
- Genes And Genomes
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Secondary structures as predictors of mutation potential in the lacZ gene of Escherichia coli
More LessFour independent nonsense mutations were engineered into the Escherichia coli chromosomal lacZ gene, and reversion rates back to LacZ+ phenotypes were determined. The mutation potential of bases within putative DNA secondary structures formed during transcription was predicted by a sliding-window analysis that simulates successive folding of the ssDNA creating these structures. The relative base mutabilities predicted by the mfg computer program correlated with experimentally determined reversion rates in three of the four mutants analysed. The nucleotide changes in revertants at one nonsense codon site consisted of a triple mutation, presumed to occur by a templated repair mechanism. Additionally, the effect of supercoiling on mutation was investigated and, in general, reversion rates increased with higher levels of negative supercoiling. Evidence indicates that predicted secondary structures are in fact formed in vivo and that directed mutation in response to starvation stress is dependent upon the exposure of particular bases, the stability of the structures in which these bases are unpaired and the level of DNA supercoiling within the cell.
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Studies on Prevotella nuclease using a system for the controlled expression of cloned genes in P. bryantii TC1-1
More LessAvailable tools for genetic analysis in the anaerobic rumen bacterium Prevotella bryantii are limited to only two known systems for gene delivery, and no genes, with the exception of plasmid maintenance and selection genes, have been successfully expressed from plasmids in any species of the genus Prevotella until now. It is shown here that nucB, a newly cloned nuclease gene from P. bryantii, can be controllably expressed from shuttle vector pRH3 in P. bryantii strain TC1-1, depending on the tetracycline concentration in the growth medium. nucB expression is also growth-medium dependent and this regulation presumably takes place at the translational level. His-tagged NucB was purified from P. bryantii TC1-1 culture supernatant and was shown to degrade DNA as well as RNA; it is most likely a minor 36 kDa P. bryantii non-specific nuclease.
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Acid-shock responses in Staphylococcus aureus investigated by global gene expression analysis
More LessA general overview is presented of the changes in the genetic expression along a time curve through the first 20 min after acidification to pH 4.5 of exponentially growing cultures of the food pathogenic strain Staphylococcus aureus 50583. A newly developed method for statistical significance testing was used to detect significant gene expression responses. Most responses showed an increase or decrease from time zero to 10 min after acidification, and then generally a stabilization in expression level from 10 to 20 min. Increased urease activity appeared to be an important factor in the acid defence, along with proton excretion by NADH dehydrogenase and macromolecule repair mechanisms. Oxidative-stress responses, such as increased expression of thioredoxin genes and upregulation of pentose phosphate pathway genes to generate more reducing power, were also induced. A general reduction in the expression of genes encoding ribosomal proteins and genes involved in nucleotide synthesis, as well as fatty acid and lipoprotein metabolism, reflected the lowered growth rate after acidification. The pH shock did not appear to trigger major virulence responses or biofilm formation. Metal ion regulation and transport were affected by the acid shock, and production of several cofactors such as molybdopterin was increased. Many of the presented observations could be explained, while some represent still-unknown mechanisms. The patterns of regulation were confirmed by quantitive reverse transcriptase PCR (QRT-PCR). Together, these results showed the main responses of S. aureus and will be a good starting point for future, more specific, in-depth studies of specific gene responses that occur in conjunction with the acid-stress defence of S. aureus.
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Genetic and physiological characterization of the Borrelia burgdorferi ORF BB0374-pfs-metK-luxS operon
More LessThe Lyme disease spirochaete, Borrelia burgdorferi, produces the LuxS enzyme both in vivo and in vitro; this enzyme catalyses the synthesis of homocysteine and 4,5-dihydroxy-2,3-pentanedione (DPD) from a by-product of methylation reactions. Unlike most bacteria, B. burgdorferi is unable to utilize homocysteine. However, DPD levels alter expression levels of a subset of B. burgdorferi proteins. The present studies demonstrate that a single B. burgdorferi operon encodes both of the enzymes responsible for synthesis of DPD, as well as the enzyme for production of the Lyme spirochaete's only activated-methyl donor and a probable phosphohydrolase. Evidence was found for only a single transcriptional promoter, located 5′ of the first gene, which uses the housekeeping σ 70 subunit for RNA polymerase holoenzyme function. All four genes are co-expressed, and mRNA levels are growth-rate dependent, being produced during the exponential phase. Thus, high metabolic activity is accompanied by increased cellular levels of the only known borrelial methyl donor, enhanced detoxification of methylation by-products, and increased production of DPD. Therefore, production of DPD is directly correlated with cellular metabolism levels, and may thereby function as an extracellular and/or intracellular signal of bacterial health.
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- Pathogens And Pathogenicity
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Role of autolysin-mediated DNA release in biofilm formation of Staphylococcus epidermidis
More LessStaphylococcus epidermidis has become a serious nosocomial pathogen frequently causing infections associated with implanted foreign materials. Biofilm formation is considered a major factor determining S. epidermidis pathogenicity in such device-associated infections. Here, evidence is presented that extracellular DNA is important for the initial phase of biofilm development by S. epidermidis on polystyrene or glass surfaces under static or hydrodynamic conditions. Comparative PCR amplification from S. epidermidis chromosomal and extracellular DNA indicated that the extracellular DNA is similar to chromosomal DNA. Experiments involving the S. epidermidis wild-type and an isogenic atlE mutant indicated that most of the extracellular DNA in S. epidermidis cultures and biofilms is generated through activity of the autolysin AtlE. The presented results suggest that extracellular DNA is generated in S. epidermidis populations through AtlE-mediated lysis of a subpopulation of the bacteria, and that the extracellular DNA promotes biofilm formation of the remaining population.
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The β-lactam-resistance modifier (−)-epicatechin gallate alters the architecture of the cell wall of Staphylococcus aureus
More Less(−)-Epicatechin gallate (ECg), a component of green tea, sensitizes meticillin-resistant Staphylococcus aureus (MRSA) to β-lactam antibiotics, promotes staphylococcal cell aggregation and increases cell-wall thickness. The potentiation of β-lactam activity against MRSA by ECg was not due to decreased bacterial penicillin-binding protein (PBP) 2a expression or ECg binding to peptidoglycan. A 5–10 % reduction in peptidoglycan cross-linking was observed. Reduced cross-linking was insufficient to compromise the integrity of the cell wall and no evidence of PBP2a activity was detected in the muropeptide composition of ECg-grown cells. ECg increased the quantity of autolysins associated with the cell wall, even though the cells were less susceptible to Triton X-100-induced autolysis than cells grown in the absence of ECg. ECg promoted increased lysostaphin resistance that was not due to alteration of the pentaglycine cross-bridge configuration or inhibition of lysostaphin activity. Rather, decreased lysostaphin susceptibility was associated with structural changes to wall teichoic acid (WTA), an acid-labile component of peptidoglycan. ECg also promoted lipoteichoic acid (LTA) release from the cytoplasmic membrane. It is proposed that ECg reduces β-lactam resistance in MRSA either by binding to PBPs at sites distinct from the penicillin-binding site or by intercalation into the cytoplasmic membrane, displacing LTA from the phospholipid palisade. Thus, ECg-mediated alterations to the physical nature of the bilayer will elicit structural changes to WTA that result in modulation of the cell-surface properties necessary to maintain the β-lactam-resistant phenotype.
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Expression of phospholipase D, the major virulence factor of Corynebacterium pseudotuberculosis, is regulated by multiple environmental factors and plays a role in macrophage death
More LessCorynebacterium pseudotuberculosis is the aetiological agent of caseous lymphadenitis, a disease affecting sheep and goats. Phospholipase D (Pld), a major virulence determinant of C. pseudotuberculosis, is believed to play a critical role in dissemination of bacteria from the site of infection to the lymph nodes. Although the pld gene has been studied for some time, it is only recently that it has been identified as being down-regulated following heat shock from 37 to 43 °C. To gain insights into the mechanisms of Pld action, this study investigated how it was regulated under varying environmental conditions. Studies measuring pld mRNA levels or utilizing a reporter construct containing the pld promoter upstream of a gfp gene were performed. These showed that pld was upregulated in a cell-density-dependent manner, was regulated by heat shock at all cell-culture densities, and was highly expressed in a tissue-culture macrophage-infection model. Finally, the expression of Pld by intracellular C. pseudotuberculosis was shown to play a small but significant role in the reduction of macrophage viability following infection. This study demonstrates that the regulation of C. pseudotuberculosis pld is complex. This regulatory complexity may play an important role in allowing the pathogen to successfully adapt to the changing host environment during infection, migration, establishment and disease progression.
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Impact of Pseudomonas aeruginosa quorum sensing on biofilm persistence in an in vivo intraperitoneal foreign-body infection model
Pseudomonas aeruginosa is an opportunistic human pathogen that causes chronic biofilm-based infections in host organisms. P. aeruginosa employs quorum sensing (QS) to control expression of its virulence, and to establish and maintain chronic infections. Under such conditions, the biofilm mode of growth contributes significantly to P. aeruginosa tolerance to the action of the innate and adaptive defence system and numerous antibiotics. In the present study, an in vivo foreign-body infection model was established in the peritoneal cavity of mice. Experimental data showed that QS-deficient P. aeruginosa are cleared more rapidly from silicone implants as compared to their wild-type counterparts. Concurrently, treatment with the QS inhibitor furanone C-30 of mice harbouring implants colonized with the wild-type P. aeruginosa resulted in a significantly faster clearing of the implants as compared to the placebo-treated group. These results were obtained with both an inbred (BALB/c) and an outbred (NMRI) mouse strain. The present results support a model by which functional QS systems play a pivotal role in the ability of bacteria to resist clearing by the innate immune system and strongly suggest that the efficiency of the mouse innate defence against biofilm-forming P. aeruginosa is improved when the bacteria are treated with QS drugs that induce QS deficiency.
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The role of F9 fimbriae of uropathogenic Escherichia coli in biofilm formation
More LessUropathogenic Escherichia coli (UPEC) is the primary cause of urinary tract infection (UTI) in the developed world. The major factors associated with virulence of UPEC are fimbrial adhesins, which mediate attachment to specific receptors, enhance persistence and trigger innate host responses. UPEC produce a range of fimbrial adhesins, with type 1 and P fimbriae of the chaperone-usher subclass being the best characterized. The prototype UPEC strain CFT073 contains ten gene clusters that contain genes characteristic of this class of fimbriae. However, only five of these gene clusters have been characterized in detail. In this study the F9 fimbrial gene cluster (c1931–c1936) from CFT073 has been characterized. The F9 fimbriae-encoding genes were PCR amplified, cloned and expressed in a K-12 background devoid of type 1 fimbriae. While F9 fimbrial expression was not associated with any haemagglutination or cellular adherence properties, a role in biofilm formation was observed. E. coli K-12 cells expressing F9 fimbriae produced a dense and uniform biofilm in both microtitre plate and continuous-flow biofilm model systems. In wild-type UPEC CFT073, expression of the F9 major subunit-encoding gene was detected during exponential growth in M9 minimal medium. F9 expression could also be detected following selection and enrichment for pellicle growth in a CFT073fim foc double mutant. The F9 genes appear to be common in UPEC and other types of pathogenic E. coli. However, their precise contribution to disease remains to be determined.
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Analysis of the aerobactin and ferric hydroxamate uptake systems of Yersinia pestis
More LessYersinia pestis genomes contain genes homologous to the aerobactin receptor (iutA) and biosynthetic genes (iucABCD) as well as the ferric hydroxamate uptake system (fhuCDB) of Escherichia coli. However, iucA is disrupted by a frameshift mutation. An E. coli strain carrying the cloned Y. pestis aerobactin region was unable to produce aerobactin, but could use the siderophore as an iron source. Repair of the frameshift mutation in iucA did not allow aerobactin production in E. coli or Y. pestis. In contrast, a Y. pestis strain with a plasmid encoding the iucABCD-iutA genes from Shigella flexneri or pColV-K30 did produce and secrete the siderophore. In addition, Yersinia pseudotuberculosis PB1, which encodes the iucABCD-iutA locus without the Y. pestis-specific frameshift mutation, also failed to produce aerobactin. The Y. pestis fhuCDB operon, encoding an ABC transporter for a range of hydroxamate siderophores, was able to complement a strain of E. coli with a transposon insertion in fhuC, allowing utilization of aerobactin and ferrichrome. Y. pestis KIM6, a strain deficient in the production of the siderophore yersiniabactin, was able to use both the ferrichrome and the aerobactin siderophores as a source of iron. Mutations in iutA or the fhu operon abolished the ability of KIM6 to use aerobactin. Mutations in the fhu operon, but not in iutA, affected the ability of KIM6 to use ferrichrome. This demonstrates that Y. pestis uses both ferrichrome and aerobactin, but has lost the ability to synthesize aerobactin.
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Unequal contribution of ALS9 alleles to adhesion between Candida albicans and human vascular endothelial cells
More LessThe Candida albicans ALS (agglutinin-like sequence) family includes eight genes (ALS1 to ALS7, and ALS9) that share a common general organization, consisting of a relatively conserved 5′ domain, a central domain of tandemly repeated sequence units, and a 3′ domain of relatively variable length and sequence. To test the hypothesis that the cell-surface glycoproteins encoded by the ALS genes mediate contact between the fungal cell and host surfaces, a set of C. albicans mutant strains was systematically constructed, each lacking one of the ALS sequences. Phenotypes of the mutant strains were evaluated, primarily using adhesion assays. ALS9 is unique within the ALS family due to extensive allelic sequence variation within the 5′ domain that may result in functional differences between proteins encoded by ALS9-1 and ALS9-2. Deletion of ALS9 significantly reduces C. albicans adhesion to human vascular endothelial cell monolayers. The mutation was complemented by reintegration of a wild-type copy of ALS9-2, but not ALS9-1, suggesting allelic functional differences. Complementation of the mutation with a gene fusion between the 5′ domain of ALS9-2 and the tandem repeats and 3′ domain of ALS9-1 also restored wild-type adhesion levels. Analysis of the als9Δ/als9Δ mutant phenotype in other assays demonstrated no significant difference from a control strain for adhesion to buccal epithelial cells or laminin-coated plastic plates. The als9Δ/als9Δ mutant did not show significant differences from the control for adhesion to or destruction of cells in the reconstituted human epithelium (RHE) disease model, or for cell-wall defects, germ-tube formation or biofilm formation in a catheter model. Analysis of ALS9 allelic frequency in a collection of geographically diverse clinical isolates showed a distinct preference for ALS9-2 allelic sequences, within both the 5′ and the 3′ domain of the ALS9 coding region. These data suggest greater selective pressure to maintain the ALS9-2 allele in C. albicans isolates and imply its greater relative importance in host–pathogen interactions.
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Role of the Vps34p-interacting protein Ade5,7p in hyphal growth and virulence of Candida albicans
The phosphatidylinositol (PtdIns) 3-kinase Vps34p of the human pathogenic yeast Candida albicans participates in virulence and in protein transport. In order to dissect these two functions, a search for proteins interacting with C. albicans Vps34p was performed using a yeast two-hybrid system. This study demonstrates the physical interaction between Vps34p and Ade5,7p, which is the bifunctional enzyme of the de novo purine nucleotide biosynthetic pathway. The interaction initially observed in a yeast two-hybrid system was confirmed in vitro with recombinant proteins. Given the complex formation between Ade5,7p and the virulence-regulating Vps34p, it was of interest to characterize the function of Ade5,7p in C. albicans. To this end, ade5,7 null mutants were generated. The resulting mutants were adenine deficient, and sensitive to the presence of metal ions. In addition, the ade5,7 null mutants were avirulent in a mouse model of systemic candidiasis, and showed reduced hyphal growth in an agar matrix under embedded conditions. In summary, Ade5,7p interacts with the multifunctional virulence regulator PtdIns 3-kinase Vps34p, and ade5,7 and vps34 null mutant strains show similar phenotypes regarding sensitivity to metal ions, hyphal growth and virulence.
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nadA and nadB of Shigella flexneri 5a are antivirulence loci responsible for the synthesis of quinolinate, a small molecule inhibitor of Shigella pathogenicity
The evolution of bacterial pathogens from commensal organisms involves virulence gene acquisition followed by pathoadaptation to the new host, including inactivation of antivirulence loci (AVL). AVL are core ancestral genes whose expression is incompatible with the pathogenic lifestyle. Previous studies identified cadA (encoding lysine decarboxylase) as an AVL of Shigella spp. In this study, AVL of Shigella were identified by examining a phenotypic difference from its non-pathogenic ancestor, Escherichia coli. Unlike most E. coli strains, Shigella spp. are nicotinic acid auxotrophs, the pathway for the de novo synthesis of NAD being uniformly defective. In Shigella flexneri, this defect is due to alterations in the nadA and/or nadB genes encoding the enzyme complex that converts l-aspartate to quinolinate, a precursor to NAD synthesis. Quinolinate was found to inhibit invasion and cell-to-cell spread of Sh. flexneri 5a and its ability to induce polymorphonuclear neutrophil transepithelial migration. Virulence of other Shigella species was also inhibited by quinolinate. Introduction of functional nadA and nadB genes from E. coli K-12 into Sh. flexneri 5a restored its ability to synthesize quinolinate but also resulted in strong attenuation of virulence in this strain. The results define nadA and nadB as AVL in Shigella and validate the concept of pathoadaptive evolution of bacteria from commensal ancestors by inactivation of AVL. They also suggest that studies focusing on this form of bacterial evolution can identify novel inhibitors of virulence in other bacterial pathogens.
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- Physiology
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σ s-Dependent carbon-starvation induction of pbpG (PBP 7) is required for the starvation-stress response in Salmonella enterica serovar Typhimurium
Carbon-energy source starvation is a commonly encountered stress that can influence the epidemiology and virulence of Salmonella enterica serovars. Salmonella responds to C-starvation by eliciting the starvation-stress response (SSR), which allows for long-term C-starvation survival and cross-resistance to other stresses. The stiC locus was identified as a C-starvation-inducible, σ S-dependent locus required for a maximal SSR. We report here that the stiC locus is an operon composed of the yohC (putative transport protein) and pbpG (penicillin-binding protein-7/8) genes. yohC pbpG transcription is initiated from a σ S–dependent C-starvation-inducible promoter upstream of yohC. Another (σ S-independent) promoter, upstream of pbpG, drives lower constitutive pbpG transcription, primarily during exponential phase. C-starvation-inducible pbpG expression was required for development of the SSR in 5 h, but not 24 h, C-starved cells; yohC was dispensable for the SSR. Furthermore, the yohC pbpG operon is induced within MDCK epithelial cells, but was not essential for oral virulence in BALB/c mice. Thus, PBP 7 is required for physiological changes, occurring within the first few hours of C-starvation, essential for the development of the SSR. Lack of PBP 7, however, can be compensated for by further physiological changes developed in 24 h C-starved cells. This supports the dynamic overlapping and distinct nature of resistance pathways within the Salmonella SSR.
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The glgX gene product of Corynebacterium glutamicum is required for glycogen degradation and for fast adaptation to hyperosmotic stress
More LessCorynebacterium glutamicum cells growing in medium containing sugars accumulate glycogen in the early exponential-growth phase, and start to degrade this polymer at entry into the stationary phase. In a first attempt to investigate glycogen degradation, the C. glutamicum glgX gene, which encodes a protein with 46 % identity to the isoamylase-type debranching enzyme of Escherichia coli, was analysed, expressed and inactivated. The purified C. glutamicum gene product showed debranching activity towards glycogen, amylopectin and starch. Chromosomal inactivation of glgX in C. glutamicum wild-type led to slower growth and to a higher intracellular glycogen pool throughout growth, when compared to those in the parental strain. This result suggests that glycogen synthesis and degradation occur simultaneously in C. glutamicum. When exposed to hyperosmotic shock, C. glutamicum rapidly degrades glycogen, and at the same time, synthesizes the osmoprotectant trehalose. The glgX mutant, however, synthesized only minor amounts of trehalose throughout cultivation, and its growth ceased after hyperosmotic shock. Taken together, the results indicate that the glgX gene product is essential for glycogen degradation in C. glutamicum, that glycogen is constantly recycled in C. glutamicum, and that it serves as a carbon store for trehalose synthesis via the TreYZ pathway after hyperosmotic shock.
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- Plant-Microbe Interactions
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Quorum-sensing-regulated transcriptional initiation of plasmid transfer and replication genes in Rhizobium leguminosarum biovar viciae
More LessTransfer of the Rhizobium leguminosarum biovar viciae symbiosis plasmid pRL1JI is regulated by a cascade of gene induction involving three LuxR-type quorum-sensing regulators, TraR, BisR and CinR. TraR induces the plasmid transfer traI-trb operon in a population-density-dependent manner in response to N-acylhomoserine lactones (AHLs) made by TraI. Expression of the traR gene is primarily induced by BisR in response to AHLs made by CinI, and expression of cinI is induced by CinR and repressed by BisR. Analysis of transcription initiation of cinI, traR and traI identified potential regulatory domains recognized by the CinR, BisR and TraR regulators. Deletion and mutation of the cinI promoter identified potential recognition motifs for activation by CinR and repression by BisR. Analysis of the DNA sequence upstream of traI and expression of transcriptional gene fusions revealed a predicted TraR-binding (tra-box) domain. Two transcript initiation sites were identified upstream of the plasmid replication gene repA, which is divergently transcribed from traI; one of these repA transcripts requires the quorum-sensing cascade mediated via BisR and TraR, showing that the pRL1JI plasmid replication genes are co-regulated with the plasmid transfer genes.
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