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Your search keyword '"Lucas, R."' showing total 3 results
Start Over Author "Lucas, R." Topic pseudomonas aeruginosa Journal molecular microbiology
3 results on '"Lucas, R."'

1. Growth phenotypes of Pseudomonas aeruginosa lasR mutants adapted to the airways of cystic fibrosis patients.

Author

D'Argenio DA, Wu M, Hoffman LR, Kulasekara HD, Déziel E, Smith EE, Nguyen H, Ernst RK, Larson Freeman TJ, Spencer DH, Brittnacher M, Hayden HS, Selgrade S, Klausen M, Goodlett DR, Burns JL, Ramsey BW, and Miller SI

Subjects
Alleles, Amides pharmacology, Amino Acid Sequence, Amino Acids pharmacology, Bacterial Proteins chemistry, Ceftazidime pharmacology, Cell Lineage drug effects, Child, Child, Preschool, DNA-Binding Proteins chemistry, Humans, Infant, Molecular Sequence Data, Mutant Proteins metabolism, Phenotype, Pseudomonas Infections, Pseudomonas aeruginosa cytology, Pseudomonas aeruginosa drug effects, Pseudomonas aeruginosa isolation & purification, Quinolines metabolism, Respiratory System drug effects, Succinic Acid pharmacology, Trans-Activators chemistry, Transcription Factors metabolism, Transcription, Genetic drug effects, beta-Lactamases metabolism, Adaptation, Biological drug effects, Bacterial Proteins metabolism, Cystic Fibrosis microbiology, DNA-Binding Proteins metabolism, Mutation genetics, Pseudomonas aeruginosa growth & development, Respiratory System microbiology, Trans-Activators metabolism
Abstract

The opportunistic pathogen Pseudomonas aeruginosa undergoes genetic change during chronic airway infection of cystic fibrosis (CF) patients. One common change is a mutation inactivating lasR, which encodes a transcriptional regulator that responds to a homoserine lactone signal to activate expression of acute virulence factors. Colonies of lasR mutants visibly accumulated the iridescent intercellular signal 4-hydroxy-2-heptylquinoline. Using this colony phenotype, we identified P. aeruginosa lasR mutants that emerged in the airway of a CF patient early during chronic infection, and during growth in the laboratory on a rich medium. The lasR loss-of-function mutations in these strains conferred a growth advantage with particular carbon and nitrogen sources, including amino acids, in part due to increased expression of the catabolic pathway regulator CbrB. This growth phenotype could contribute to selection of lasR mutants both on rich medium and within the CF airway, supporting a key role for bacterial metabolic adaptation during chronic infection. Inactivation of lasR also resulted in increased beta-lactamase activity that increased tolerance to ceftazidime, a widely used beta-lactam antibiotic. Loss of LasR function may represent a marker of an early stage in chronic infection of the CF airway with clinical implications for antibiotic resistance and disease progression.

Published
2007
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2. Growth phenotypes of Pseudomonas aeruginosa lasR mutants adapted to the airways of cystic fibrosis patients

Author

Mikkel Klausen, Hemantha D. Kulasekara, Bonnie W. Ramsey, David H. Spencer, Hillary S. Hayden, Robert K. Ernst, Manhong Wu, Eric E. Smith, Mitchell J. Brittnacher, Lucas R. Hoffman, Jane L. Burns, Samuel I. Miller, Theodore J. Larson Freeman, Sara E. Selgrade, David R. Goodlett, David A. D'Argenio, Eric Déziel, and Hai Nguyen

Subjects
biology, Pseudomonas aeruginosa, Mutant, Homoserine, Virulence, biochemical phenomena, metabolism, and nutrition, respiratory system, biology.organism_classification, medicine.disease_cause, medicine.disease, Microbiology, Cystic fibrosis, Phenotype, chemistry.chemical_compound, Chronic infection, chemistry, medicine, Molecular Biology, Pseudomonadaceae
Abstract

The opportunistic pathogen Pseudomonas aeruginosa undergoes genetic change during chronic airway infection of cystic fibrosis (CF) patients. One common change is a mutation inactivating lasR, which encodes a transcriptional regulator that responds to a homoserine lactone signal to activate expression of acute virulence factors. Colonies of lasR mutants visibly accumulated the iridescent intercellular signal 4-hydroxy-2-heptylquinoline. Using this colony phenotype, we identified P. aeruginosa lasR mutants that emerged in the airway of a CF patient early during chronic infection, and during growth in the laboratory on a rich medium. The lasR loss-of-function mutations in these strains conferred a growth advantage with particular carbon and nitrogen sources, including amino acids, in part due to increased expression of the catabolic pathway regulator CbrB. This growth phenotype could contribute to selection of lasR mutants both on rich medium and within the CF airway, supporting a key role for bacterial metabolic adaptation during chronic infection. Inactivation of lasR also resulted in increased beta-lactamase activity that increased tolerance to ceftazidime, a widely used beta-lactam antibiotic. Loss of LasR function may represent a marker of an early stage in chronic infection of the CF airway with clinical implications for antibiotic resistance and disease progression.

Published
2007

3. Growth phenotypes of Pseudomonas aeruginosa lasR mutants adapted to the airways of cystic fibrosis patients

Author

David A, D'Argenio, Manhong, Wu, Lucas R, Hoffman, Hemantha D, Kulasekara, Eric, Déziel, Eric E, Smith, Hai, Nguyen, Robert K, Ernst, Theodore J, Larson Freeman, David H, Spencer, Mitchell, Brittnacher, Hillary S, Hayden, Sara, Selgrade, Mikkel, Klausen, David R, Goodlett, Jane L, Burns, Bonnie W, Ramsey, and Samuel I, Miller

Subjects
Cystic Fibrosis, Transcription, Genetic, Molecular Sequence Data, Respiratory System, Adaptation, Biological, Succinic Acid, Ceftazidime, beta-Lactamases, Article, Bacterial Proteins, Humans, Cell Lineage, Pseudomonas Infections, Amino Acid Sequence, Amino Acids, Child, Alleles, Infant, biochemical phenomena, metabolism, and nutrition, respiratory system, Amides, DNA-Binding Proteins, Phenotype, Child, Preschool, Mutation, Pseudomonas aeruginosa, Quinolines, Trans-Activators, Mutant Proteins, Transcription Factors
Abstract

The opportunistic pathogen Pseudomonas aeruginosa undergoes genetic change during chronic airway infection of cystic fibrosis (CF) patients. One common change is a mutation inactivating lasR, which encodes a transcriptional regulator that responds to a homoserine lactone signal to activate expression of acute virulence factors. Colonies of lasR mutants visibly accumulated the iridescent intercellular signal 4-hydroxy-2-heptylquinoline. Using this colony phenotype, we identified P. aeruginosa lasR mutants that emerged in the airway of a CF patient early during chronic infection, and during growth in the laboratory on a rich medium. The lasR loss-of-function mutations in these strains conferred a growth advantage with particular carbon and nitrogen sources, including amino acids, in part due to increased expression of the catabolic pathway regulator CbrB. This growth phenotype could contribute to selection of lasR mutants both on rich medium and within the CF airway, supporting a key role for bacterial metabolic adaptation during chronic infection. Inactivation of lasR also resulted in increased beta-lactamase activity that increased tolerance to ceftazidime, a widely used beta-lactam antibiotic. Loss of LasR function may represent a marker of an early stage in chronic infection of the CF airway with clinical implications for antibiotic resistance and disease progression.

Published
2007

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