Pathway for Ubiquinone Biosynthesis in Escherichia coli K-12: Gene-Enzyme Relationships and Intermediates

Young, Ian G.; Stroobant, Paul; Macdonald, Colin G.; Gibson, F.

doi:10.1128/jb.114.1.42-52.1973

Cited by 68 publications

(31 citation statements)

References 29 publications

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“…This demonstrates that the third open reading frame, the ubiH gene, is responsible for the observed altered plaque phenotype of SSW302. The ubiH gene product, UbiH, catalyzes the oxidation of 2-octaprenyl-6-methoxyphenol to 2-octaprenyl-6-methoxy-1,4-benzoquinol in the ubiquinol-8 biosynthetic pathway (43).…”

Section: Resultsmentioning

confidence: 99%

Impact of either Elevated or Decreased Levels of Cytochrome bd Expression on Shigella flexneri Virulence

et al. 1999

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Shigella spp. are the major cause of bacillary dysentery worldwide. The pathogenic process involves bacterial invasion and lysis of the phagocytic vacuole, followed by replication and movement within the cell cytoplasm and, ultimately, spread directly into adjacent cells. This study demonstrates that S. flexneri cytochrome bd expression is necessary for normal intracellular survival and virulence. Cytochrome bdis one of two terminal oxidases in the bacterial respiratory chain that reduce molecular oxygen to water, utilizing intermediates shuttled through the electron transport chain. S. flexneri mutants that contain a disruption in the cydC locus, which leads to defective cytochrome bd expression, or in the riboflavin (ribE) or ubiquinol-8 (ubiH) biosynthetic pathway, which leads to elevated cytochrome bd expression, were evaluated in intracellular survival and virulence assays. ThecydC mutant formed significantly smaller plaques, had significantly decreased intracellular survival, and had a 100-fold increase in lethal dose for mice compared with the wild type. TheribE and ubiH mutants each formed significantly larger plaques and had a 10-fold decrease in lethal dose for mice compared with the wild type. The data indicate that expression of cytochrome bd is required for S. flexneriintracellular survival and virulence.

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Section: Resultsmentioning

confidence: 99%

Impact of either Elevated or Decreased Levels of Cytochrome bd Expression on Shigella flexneri Virulence

et al. 1999

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“…S4C). As ubiH is involved in ubiquinone synthesis (Young, Stroobant, Macdonald, & Gibson, 1973), these data indicate that the SCV phenotype of the pepP mutant is also mediated by reduced activity of the ETC (rather than a direct effect of disrupting pepP function).…”

Section: Novel Genetic Targets Associated With the Etc Mediate Thmentioning

confidence: 82%

Macrophage adaptation leads to parallel evolution of genetically diverse Escherichia coli small‐colony variants with increased fitness in vivo and antibiotic collateral sensitivity

Ramiro

Costa

Gordo

2016

Evolutionary Applications

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Small‐colony variants (SCVs) are commonly observed in evolution experiments and clinical isolates, being associated with antibiotic resistance and persistent infections. We recently observed the repeated emergence of Escherichia coli SCVs during adaptation to the interaction with macrophages. To identify the genetic targets underlying the emergence of this clinically relevant morphotype, we performed whole‐genome sequencing of independently evolved SCV clones. We uncovered novel mutational targets, not previously associated with SCVs (e.g. cydA, pepP) and observed widespread functional parallelism. All SCV clones had mutations in genes related to the electron‐transport chain. As SCVs emerged during adaptation to macrophages, and often show increased antibiotic resistance, we measured SCV fitness inside macrophages and measured their antibiotic resistance profiles. SCVs had a fitness advantage inside macrophages and showed increased aminoglycoside resistance in vitro, but had collateral sensitivity to other antibiotics (e.g. tetracycline). Importantly, we observed similar results in vivo. SCVs had a fitness advantage upon colonization of the mouse gut, which could be tuned by antibiotic treatment: kanamycin (aminoglycoside) increased SCV fitness, but tetracycline strongly reduced it. Our results highlight the power of using experimental evolution as the basis for identifying the causes and consequences of adaptation during host‐microbe interactions.

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“…The mutations conferring zwittermicin A resistance on mutants MGZ05, MGZ07 and MGZ12 were mapped to the region at 87 map units on the E. coli chromosome (Table 1). Based on co‐transduction frequencies with other nearby markers (data not shown), the mutation in MGZ05 was localized counterclockwise from fadAB , in the vicinity of ubiB and ubiD (Cox et al ., 1969; Daniels et al ., 1992), which encode enzymes involved in the biosynthesis of the electron carrier, ubiquinone (Young et al ., 1973). Consistent with a disruption of ubiquinone biosynthesis, mutants MGZ05, MGZ07 and MGZ12 did not grow under ubiquinone‐dependent conditions, aerobically with malate or succinate as a carbon source, but grew well under conditions that do not require ubiquinone, aerobically or anaerobically on glucose or anaerobically on glycerol and nitrate (Cox et al ., 1968; Lin and Kuritzkes, 1987; Wissenbach et al ., 1990).…”

Section: Resultsmentioning

confidence: 99%

Genetic analysis of zwittermicin A resistance in Escherichia coli: effects on membrane potential and RNA polymerase

Stabb

Handelsman

1998

Molecular Microbiology

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SummaryZwittermicin A is a novel aminopolyol antibiotic that represents a new structural class of antibiotic and has diverse biological activities, including the suppression of plant disease and the ability to inhibit prokaryotic and eukaryotic cells. To enhance our fundamental understanding and applications of zwittermicin A, we elucidated mechanisms of zwittermicin A resistance in Escherichia coli. Two classes of zwittermicin Aresistant mutants of E. coli were selected and characterized. One class included mutants altered in hemA, hemB, hemL, ubi, cydAB or atp, which were defective in generating a proton motive force (PMF) and resistant to aminoglycosides. The mutant analysis, coupled with physiological data, indicated an association between the electrical membrane potential (⌬⌿) component of PMF and zwittermicin A sensitivity. A second class of zwittermicin A-resistant mutants was aminoglycoside sensitive and was affected in rpoB and rpoC, genes that encode subunits of RNA polymerase. The rpoB and rpoC mutants suggested that zwittermicin A might inhibit transcription, DNA replication, DNA gyrase or topoisomerase I; however, we found no further evidence to support any of these as the target for zwittermicin A. This study elucidated the genetic mechanisms of zwittermicin A resistance in E. coli. The results suggest that ⌬⌿ drives zwittermicin A uptake, and that, unlike other antibiotics for which resistance maps in rpoB or rpoC, zwittermicin A does not cause the rapid cessation of DNA or RNA synthesis, suggesting a unique mechanism of antibiosis.

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Pathway for Ubiquinone Biosynthesis in Escherichia coli K-12: Gene-Enzyme Relationships and Intermediates

Cited by 68 publications

References 29 publications

Impact of either Elevated or Decreased Levels of Cytochrome bd Expression on Shigella flexneri Virulence

Impact of either Elevated or Decreased Levels of Cytochrome bd Expression on Shigella flexneri Virulence

Macrophage adaptation leads to parallel evolution of genetically diverse Escherichia coli small‐colony variants with increased fitness in vivo and antibiotic collateral sensitivity

Genetic analysis of zwittermicin A resistance in Escherichia coli: effects on membrane potential and RNA polymerase

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