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Effects of 6‐hydroxynicotinate 3‐monooxygenase gene knockout (∆nicC) on nicotinate degradation and virulence modulation in Bordetella pertussis (LB266)
Author(s) -
Chiaranunt Pailin,
Sprano Jacob,
Daniels Abigail,
Snider Mark
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb266
Subject(s) - bordetella pertussis , virulence , adenylate cyclase toxin , pertussis toxin , microbiology and biotechnology , whooping cough , gene knockout , mutant , bordetella , strain (injury) , gene , biology , chemistry , bacteria , biochemistry , virology , receptor , genetics , g protein , vaccination , anatomy
Due to increased incidence of whooping cough, further investigation of the pathogenic mechanisms of its causative agent, Bordetella pertussis, is of medical importance. Previous in vitro assays indicate a correlation between elevated nicotinate concentrations and the down‐regulation of virulent toxins (e.g. pertussis toxin and adenylate cyclase) in B. pertussis. Furthermore, recent genomic analyses reveal a unique nicotinate degradation pathway in B. pertussis. This study analyzes the effects of disrupting the gene that codes for 6‐hydroxynicotinate 3‐monooxygenase (NicC), the enzyme predicted to catalyze the committed step in this pathway. A nicC knockout strain (ΔnicC) of B. pertussis Tohama I was created by insertion of a chloramphenicol‐resistance (CmR) gene via allelic exchange. Analyses by HPLC assays and RT‐PCR of nicotinate degradation and the resulting effects on virulence modulation, respectively, in ΔnicC and the wildtype Tohama I strains of B. pertussis are ongoing.