ArticleInfection and immunity2013
Borrelia burgdorferi linear plasmid 28-3 confers a selective advantage in an experimental mouse-tick infection model.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Article
- Article
- Large-Scale Sequencing ofGenes · 2022Review
- Article
- Article
- Genetic Manipulation ofCurrent issues in molecular biology · 2021Review
- New Insights Into CRASP-Mediated Complement Evasion in the Lyme Disease Enzootic Cycle.Frontiers in cellular and infection microbiology · 2020Review
- Primordial origin and diversification of plasmids in Lyme disease agent bacteria.BMC genomics · 2018Article
- Plasmid diversity and phylogenetic consistency in the Lyme disease agent Borrelia burgdorferi.BMC genomics · 2017Article
- Borrelia burgdorferi: Carbon Metabolism and the Tick-Mammal Enzootic Cycle.Microbiology spectrum · 2015Article
- Apparent role for Borrelia burgdorferi LuxS during mammalian infection.Infection and immunity · 2015Article
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Authors and funding
3 authors.
Funding
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-kb linear plasmids, lp28-3, we generated strains specifically lacking lp28-3 and assayed the contribution of genes carried by lp28-3 to B. burgdorferi infection. We found that lp28-3 does not carry 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 coinjected into a mouse, and this advantage was reflected in the population of spirochetes acquired by feeding ticks. Our data demonstrate that genes carried by lp28-3, although not essential, contribute to the fitness of B. burgdorferi during infection.
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