Genetic transformation of the Lyme disease agent Borrelia burgdorferi with coumarin-resistant gyrB.
AUTOR(ES)
Samuels, D S
RESUMO
No useful method to genetically manipulate Borrelia burgdorferi, the causative agent of Lyme disease, has been developed previously. We have used resistance to the coumarin antibiotic coumermycin A1, an inhibitor of DNA gyrase, as a genetic marker to monitor the transformation of B. burgdorferi by electroporation. Introduction of site-directed mutations into the gyrB gene demonstrated that transformation was successful, provided evidence that homologous recombination occurs on the chromosome, and established that mutations at Arg-133 of DNA gyrase B confer coumermycin A1 resistance in B. burgdorferi. The coumermycin A1-resistant gyrB marker and genetic transformation can now be applied toward dissecting the physiology and pathogenesis of the Lyme disease agent on a molecular genetic level.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=196823Documentos Relacionados
- gyrB mutations in coumermycin A1-resistant Borrelia burgdorferi.
- groEL Expression in gyrB Mutants of Borrelia burgdorferi
- Plasmid analysis of Borrelia burgdorferi, the Lyme disease agent.
- Transformation of the Lyme Disease Spirochete Borrelia burgdorferi with Heterologous DNA
- Ticks and biting insects infected with the etiologic agent of Lyme disease, Borrelia burgdorferi.