Acquisition and Role of Molybdate in Pseudomonas aeruginosa

Pederick, Victoria G.; Eijkelkamp, Bart A.; Ween, Miranda P.; Begg, Stephanie L.; Paton, James C.; McDevitt, Christopher A.

doi:10.1128/aem.02465-14

Cited by 36 publications

(69 citation statements)

References 52 publications

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“…Molybdate is the oxyanion form of molybdenum, an important metal cofactor for many molybdoenzymes involved in carbon, sulphur, and nitrogen metabolism . In Pseudomonas aeruginosa and Mycobacterium tuberculosis , molybdenum and the ModABC transport system have been implicated in virulence such as biofilm formation and intracellular survival in macrophages . It is possible that molybdenum may also be important for B. pertussis virulence.…”

Section: Discussionmentioning

confidence: 99%

Proteomic Adaptation of Australian Epidemic Bordetella pertussis

et al. 2018

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Bordetella pertussis causes whooping cough. The predominant strains in Australia changed to single nucleotide polymorphism (SNP) cluster I (pertussis toxin promoter allele ptxP3/pertactin gene allele prn2) from cluster II (non-ptxP3/non-prn2). Cluster I was mostly responsible for the 2008-2012 Australian epidemic and was found to have higher fitness compared to cluster II using an in vivo mouse competition assay, regardless of host's immunization status. This study aimed to identify proteomic differences that explain higher fitness in cluster I using isobaric tags for relative and absolute quantification (iTRAQ), and high-resolution multiple reaction monitoring (MRM-hr). A few key differences in the whole cell and secretome were identified between the cluster I and II strains tested. In the whole cell, nine proteins were upregulated (>1.2 fold change, q < 0.05) and three were downregulated (<0.8 fold change, q < 0.05) in cluster I. One downregulated protein was BP1569, a TLR2 agonist for Th1 immunity. In the secretome, 12 proteins were upregulated and 1 was downregulated which was Bsp22, a type III secretion system (T3SS) protein. Furthermore, there was a trend of downregulation in three T3SS effectors and other virulence factors. Three proteins were upregulated in both whole cell and supernatant: BP0200, molybdate ABC transporter (ModB), and tracheal colonization factor A (TcfA). Important expression differences in lipoprotein, T3SS, and transport proteins between the cluster I and II strains were identified. These differences may affect immune evasion, virulence and metabolism, and play a role in increased fitness of cluster I.

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Section: Discussionmentioning

confidence: 99%

Proteomic Adaptation of Australian Epidemic Bordetella pertussis

et al. 2018

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“…For import across the cytoplasmic membrane, only one transporter has been identified in P. aeruginosa, the ABC transporter ModABC (PA1861-1863) (Figure 1, Table 3) (Pederick et al, 2014). Nothing is known concerning the way in which Mo crosses the outer membrane in P. aeruginosa and Gram-negative bacteria.…”

Section: Molybdate (Mo)mentioning

confidence: 99%

“…ModA is the periplasmic binding protein of this transport system, ModC the ATPase and ModB the permease. Orthologous operons of modABC can be found in many other Pseudomonas species, including P. fluorecens, P. putida and P. syringae (Pederick et al, 2014). As W has no known role in Pseudomonas, this interaction is most likely non-physiological.…”

Section: Molybdate (Mo)mentioning

confidence: 99%

An overview of the biological metal uptake pathways in Pseudomonas aeruginosa

Schalk

Cunrath

2016

Environmental Microbiology

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Biological metal ions, including Co, Cu, Fe, Mg, Mn, Mo, Ni and Zn ions, are necessary for the survival and the growth of all microorganisms. Their biological functions are linked to their particular chemical properties: they play a role in structuring macromolecules and/or act as co-factors catalyzing diverse biochemical reactions. These metal ions are also essential for microbial pathogens during infection: they are involved in bacterial metabolism and various virulence factor functions. Therefore, during infection, bacteria need to acquire biological metal ions from the host such that there is competition for these ions between the bacterium and the host. Evidence is increasingly emerging of "nutritional immunity" against pathogens in the hosts; this includes strategies making access to metals difficult for infecting bacteria. It is clear that biological metals play key roles during infection and in the battle between the pathogens and the host. Here, we summarize current knowledge about the strategies used by Pseudomonas aeruginosa to access the various biological metals it requires. P. aeruginosa is a medically significant Gram-negative bacterial opportunistic pathogen that can cause severe chronic lung infections in cystic fibrosis patients and that is responsible for nosocomial infections worldwide.

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“…Also, a mutation converting a stop codon to lysine (*241K) in LpsB, a highly conserved glycosyltransferase that is involved in the biosynthesis of the LPS core (12) and is potentially important for A. baumannii virulence and colistin resistance (13), was observed in the Cst r strain Ab249. Interestingly, in the second Cst r strain Ab347, we observed the loss of a 47,969-bp genomic region containing, among others, the genes mrkC, mrkD, modA, modB, modC, modD, and ppk, which have been previously associated with biofilm production in Enterobacteriaceae and in Pseudomonas strains (14)(15)(16). Of note is the removal of the genes mrkC (pilin) and mrkD (assembly chaperone), which are part of chaperone-usher (CU) system assembling pili.…”

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confidence: 95%

Colistin-Resistant Acinetobacter baumannii Clinical Strains with Deficient Biofilm Formation

Dafopoulou

Xavier

Hotterbeekx

et al. 2016

Antimicrob Agents Chemother

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In two pairs of clinical colistin-susceptible/colistin-resistant (Cst s /Cst r ) Acinetobacter baumannii strains, the Cst r strains showed significantly decreased biofilm formation in static and dynamic assays (P < 0.001) and lower relative fitness (P < 0.05) compared with those of the Cst s counterparts. The whole-genome sequencing comparison of strain pairs identified a mutation converting a stop codon to lysine (*241K) in LpsB (involved in lipopolysaccharide [LPS] synthesis) in one Cst r strain and a frameshift mutation in CarO and the loss of a 47,969-bp element containing multiple genes associated with biofilm production in the other. Colistin-resistant (Cst r ) Acinetobacter baumannii clinical isolates are increasingly recovered worldwide (1), which is causing major clinical concerns. Thus far, two primary colistin resistance mechanisms have been described in A. baumannii, (i) modification of the lipid A moiety of lipopolysaccharide (LPS) mediated by mutations and/or overexpression in the two-component regulatory system pmrAB and (ii) loss of LPS caused by either mutations or insertional inactivation of lipid A biosynthesis genes (2).The development of colistin resistance in clinical and laboratory-derived Cst r A. baumannii due to changes in the PmrAB system has been correlated with impaired fitness and virulence (3, 4) and lower infectivity (5, 6). Also, reduced biofilm formation has been observed in laboratory-generated Cst r A. baumannii (7,8). We previously reported the characteristics of two pairs of colistin-susceptible (Cst s )/Cst r A. baumannii clinical strains (Ab248/ Ab249 and Ab299/Ab347; colistin MICs of 0.5/128 and 0.5/32 g/ml, respectively) sequentially obtained from two patients after prolonged colistin exposure (6). Briefly, compared to Cst s strains, Cst r strains harbored a single pmrB mutation (P233S for Ab249 and P170L for Ab347) and had significantly slower growth. Strains within each pair had identical pulsed-field gel electrophoresis (PFGE) profiles, and all were assigned to the international clone 2. Important differences in the antibiotic resistance phenotypes other than colistin were not observed (6). One Cst r strain underexpressed the CsuA/B and CsuC proteins, which are involved in biofilm formation (6). In the present follow-up study, we compared these strain pairs in terms of fitness, biofilm-forming ability, and whole-genome sequencing (WGS) focusing specifically on genes involved in virulence and biofilm formation.In vitro competition assays were performed in triplicate at 5 h and 20 h (4), and relative fitness was calculated as previously described (9). To study adhesion (6 h) and biofilm formation (24 h) under static conditions, the crystal violet method was used (10) with some modifications. Briefly, inoculum was prepared by adjusting exponential cultures grown in Luria-Bertani (LB) broth to a 0.5 McFarland standard, and this was followed by a 1:10 dilution in LB broth. Then, 200-l aliquots (approximately 2 ϫ 10 6 CFU) were loaded into a 96-well polystyrene microplate (...

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Acquisition and Role of Molybdate in Pseudomonas aeruginosa

Cited by 36 publications

References 52 publications

Proteomic Adaptation of Australian Epidemic Bordetella pertussis

Proteomic Adaptation of Australian Epidemic Bordetella pertussis

An overview of the biological metal uptake pathways in Pseudomonas aeruginosa

Colistin-Resistant Acinetobacter baumannii Clinical Strains with Deficient Biofilm Formation

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