ncbi.nlm.nih.gov/pubmed/23753630 Infect Immun. 2013 Jun 10. [Epub ahead of print] Borrelia burgdorferi linear plasmid 28-3 confers a selective advantage in an experimental mouse-tick infection model. Dulebohn DP, Bestor A, Rosa PA. Source Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, Division of Intramural Research, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, MT 59840, USA. Abstract Borrelia burgdorferi, the bacterium that causes Lyme disease, has a unique segmented genome consisting of numerous linear and circular plasmids and a linear chromosome. Many of these genetic elements have been found to encode factors critical for B. burgdorferi to complete the infectious cycle. However, several plasmids remain poorly characterized and their roles during infection with B. burgdorferi have not been elucidated. To more fully characterize the role of one of the four 28-kilobase linear plasmids, lp28-3, we generated strains specifically lacking lp28-3 and assayed the contribution of lp28-3-encoded genes to B. burgdorferi infection. We found that lp28-3 does not encode any genes that are strictly required for infection of a mouse or tick and that lp28-3-deficient spirochetes are competent at causing a disseminated infection. Interestingly, spirochetes containing lp28-3 were at a selective advantage compared to lp28-3-deficient spirochetes when co-injected into a mouse, and this advantage was reflected in the population of spirochetes acquired by feeding ticks. Our data demonstrate that lp28-3-encoded genes, although not essential, contribute to the fitness of B. burgdorferi during infection.
Posted on: Thu, 13 Jun 2013 06:38:28 +0000
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