Pyruvate metabolism in Campylobacter spp.

Mendz, George L.; Ball, Graham E.; Meek, David J. J.

doi:10.1016/s0304-4165(96)00107-9

Cited by 47 publications

(47 citation statements)

References 14 publications

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“…C. jejuni cannot use glucose as a primary carbon source; however, genome sequence and experimental data indicate that C. jejuni possesses an EmbdenMeyerhof (glycolysis and gluconeogenesis) pathway that is likely to be largely gluconeogenic (49,58,73). C. jejuni requires gluconeogenesis to generate glucose-derived polysaccharides and can also incorporate glycolysis end products like pyruvate into the TCA cycle via anaplerotic enzymes like pyruvate carboxylase (49,73).…”

Section: -Gs and 11168-o Appear Identical By Current Molecular Gmentioning

confidence: 99%

The Genome-Sequenced Variant of Campylobacter jejuni NCTC 11168 and the Original Clonal Clinical Isolate Differ Markedly in Colonization, Gene Expression, and Virulence-Associated Phenotypes

Gaynor

Cawthraw²,

Manning³

et al. 2004

J Bacteriol

174

131

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The genome sequence of the enteric bacterial pathogen Campylobacter jejuni NCTC 11168 (11168-GS) was published in 2000, providing a valuable resource for the identification of C. jejuni-specific colonization and virulence factors. Surprisingly, the 11168-GS clone was subsequently found to colonize 1-day-old chicks following oral challenge very poorly compared to other strains. In contrast, we have found that the original clinical isolate from which 11168-GS was derived, 11168-O, is an excellent colonizer of chicks. Other marked phenotypic differences were also identified: 11168-O invaded and translocated through tissue culture cells far more efficiently and rapidly than 11168-GS, was significantly more motile, and displayed a different morphology. Serotyping, multiple high-resolution molecular genotyping procedures, and subtractive hybridization did not yield observable genetic differences between the variants, suggesting that they are clonal. However, microarray transcriptional profiling of these strains under microaerobic and severely oxygen-limited conditions revealed dramatic expression differences for several gene families. Many of the differences were in respiration and metabolism genes and operons, suggesting that adaptation to different oxygen tensions may influence colonization potential. This correlates biologically with our observation that anaerobically priming 11168-GS or aerobically passaging 11168-O caused an increase or decrease, respectively, in colonization compared to the parent strain. Expression differences were also observed for several flagellar genes and other less well-characterized genes that may participate in motility. Targeted sequencing of the sigma factors revealed specific DNA differences undetected by the other genomic methods. These observations highlight the capacity of C. jejuni to adapt to multiple environmental niches, the likelihood that this adaptation involves genetic evolution, and provides the first whole-genome molecular exploration of the effect of laboratory culture and storage on colonization and virulence properties of this pathogen.

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Section: -Gs and 11168-o Appear Identical By Current Molecular Gmentioning

confidence: 99%

The Genome-Sequenced Variant of Campylobacter jejuni NCTC 11168 and the Original Clonal Clinical Isolate Differ Markedly in Colonization, Gene Expression, and Virulence-Associated Phenotypes

Gaynor

Cawthraw²,

Manning³

et al. 2004

J Bacteriol

174

131

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“…This pattern of acetate production followed by utilization is characteristic of a bacterial mechanism known as the 'acetate switch' which occurs when bacteria deplete their environment of acetogenic carbon sources, such as L-serine or pyruvate, and begin to scavenge for acetate (Wolfe, 2005). The production of acetate by C. jejuni as a result of L-serine and pyruvate catabolism has been reported elsewhere (Mendz et al, 1997). However, to our knowledge, this is the first time that subsequent reassimilation of acetate during the later stages of the C. jejuni growth cycle has been described.…”

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confidence: 80%

“…The production of acetate is indicative of the presence of a mixed acid fermentation pathway in C. jejuni (Mendz et al, 1997). Acetate excretion is thought to result from the need to recycle CoA, required for the conversion of pyruvate into acetyl-CoA.…”

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confidence: 99%

Metabolite and transcriptome analysis of Campylobacter jejuni in vitro growth reveals a stationary-phase physiological switch

et al. 2009

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Campylobacter jejuni is a prevalent cause of food-borne diarrhoeal illness in humans. Understanding of the physiological and metabolic capabilities of the organism is limited. We report a detailed analysis of the C. jejuni growth cycle in batch culture. Combined transcriptomic, phenotypic and metabolic analysis demonstrates a highly dynamic 'stationary phase', characterized by a peak in motility, numerous gene expression changes and substrate switching, despite transcript changes that indicate a metabolic downshift upon the onset of stationary phase. Video tracking of bacterial motility identifies peak activity during stationary phase. Amino acid analysis of culture supernatants shows a preferential order of amino acid utilization. Proton NMR ( 1 H-NMR) highlights an acetate switch mechanism whereby bacteria change from acetate excretion to acetate uptake, most probably in response to depletion of other substrates. Acetate production requires pta (Cj0688) and ackA (Cj0689), although the acs homologue (Cj1537c) is not required. Insertion mutants in Cj0688 and Cj0689 maintain viability less well during the stationary and decline phases of the growth cycle than wild-type C. jejuni, suggesting that these genes, and the acetate pathway, are important for survival. INTRODUCTIONCampylobacter jejuni is the major cause of food-borne bacterial gastroenteritis worldwide, with an estimated 1 in 100 individuals in both the USA and the UK developing Campylobacter-related illness each year (Gaynor et al., 2004;Gillespie et al., 2002). Although most cases are selflimiting, C. jejuni can cause severe post-infection complications including the peripheral neuropathies GuillainBarré and Miller-Fisher syndromes (Nachamkin et al., 2000). Despite the significance of C. jejuni as a food-borne pathogen, our understanding of its basic biochemistry and physiology, gene regulation, colonization, virulence and environmental survival mechanisms lags behind that of many other pathogenic and non-pathogenic bacteria, and many questions regarding C. jejuni physiology and pathogenesis remain (Young et al., 2007). Research has been hampered by a lack of genetic tools, the difficulty of growing the bacteria in the laboratory and the absence of a suitable animal model that mimics human disease.C. jejuni is a fastidious bacterium, with a limited capacity for biosynthesis, and requires complex growth media (Kelly, 2001). Establishing the metabolic capabilities of C. jejuni is central to comprehension of environmental persistence and host colonization. The microaerophilic nature, complex nutritional requirements and relative difficulty of culturing C. jejuni have all contributed to the limited understanding of metabolism (Kelly, 2001(Kelly, , 2005Sellars et al., 2002). C. jejuni is unable to catabolize glucose and other hexose sugars due to the absence of the key glycolytic enzyme 6-phosphofructokinase (Parkhill et al., 2000;Velayudhan & Kelly, 2002 The importance of each amino acid in C. jejuni metabolism is yet to be fully established, however, and i...

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“…Respiratory activities (as measured by O 2 uptake) were similar to those of the parent strain for all respiratory substrates tested except for ␣-ketoglutarate (Table 6). ␣-Ketoglutarate is a tricarboxylic acid (TCA) cycle intermediate and the entry point for many amino acids into central carbon metabolism, making it especially important in an asaccharolytic organism such as C. jejuni that garners most of its carbon and energy from amino acids (18,22,35). OOR (encoded by oorDABC [Cj0535 to Cj0538]) is a functional equivalent to ␣-ketoglutarate dehydrogenase in that it catalyzes the decarboxylation of ␣-ketoglutarate to form succinyl-CoA (16).…”

Section: Discussionmentioning

confidence: 99%

“…The physiology of C. jejuni has adapted to take advantage of life in the lower avian cecum, where C. jejuni predominates (3). Anaerobic fermentation appears to be the dominant lifestyle in the cecum (20), and C. jejuni utilizes fermentation by-products such as small organic acids as both carbon and energy sources (18,22,23,35,38). C. jejuni itself is nonfermentative and uses oxidative phosphorylation for all its energy demands.…”

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confidence: 99%

TheCampylobacter jejuniNADH:Ubiquinone Oxidoreductase (Complex I) Utilizes Flavodoxin Rather than NADH

Weerakoon

Olson

2008

J Bacteriol

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Campylobacter jejuni encodes 12 of the 14 subunits that make up the respiratory enzyme NADH:ubiquinone oxidoreductase (also called complex I). The two nuo genes not present in C. jejuni encode the NADH dehydrogenase, and in their place in the operon are the novel genes designated Cj1575c and Cj1574c. A series of mutants was generated in which each of the 12 nuo genes (homologues to known complex I subunits) was disrupted or deleted. Each of the nuo mutants will not grow in amino acid-based medium unless supplemented with an alternative respiratory substrate such as formate. Unlike the nuo genes, Cj1574c is an essential gene and could not be disrupted unless an intact copy of the gene was provided at an unrelated site on the chromosome. A nuo deletion mutant can efficiently respire formate but is deficient in ␣-ketoglutarate respiratory activity compared to the wild type. In C. jejuni, ␣-ketoglutarate respiration is mediated by the enzyme 2-oxoglutarate:acceptor oxidoreductase; mutagenesis of this enzyme abolishes ␣-ketoglutarate-dependent O 2 uptake and fails to reduce the electron transport chain. The electron acceptor for 2-oxoglutarate:acceptor oxidoreductase was determined to be flavodoxin, which was also determined to be an essential protein in C. jejuni. A model is presented in which CJ1574 mediates electron flow into the respiratory transport chain from reduced flavodoxin and through complex I.

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Pyruvate metabolism in Campylobacter spp.

Cited by 47 publications

References 14 publications

The Genome-Sequenced Variant of Campylobacter jejuni NCTC 11168 and the Original Clonal Clinical Isolate Differ Markedly in Colonization, Gene Expression, and Virulence-Associated Phenotypes

The Genome-Sequenced Variant of Campylobacter jejuni NCTC 11168 and the Original Clonal Clinical Isolate Differ Markedly in Colonization, Gene Expression, and Virulence-Associated Phenotypes

Metabolite and transcriptome analysis of Campylobacter jejuni in vitro growth reveals a stationary-phase physiological switch

TheCampylobacter jejuniNADH:Ubiquinone Oxidoreductase (Complex I) Utilizes Flavodoxin Rather than NADH

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