Evidence map›Paper›PMID 26069970›Full record

ArticlePloS one2015

Disruption of bbe02 by Insertion of a Luciferase Gene Increases Transformation Efficiency of Borrelia burgdorferi and Allows Live Imaging in Lyme Disease Susceptible C3H Mice.

Kamfai Chan, Laura Alter, Stephen W Barthold, Nikhat Parveen

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed.

  1. Article
  2. Article
  3. Long-term survival ofMicrobiology spectrum · 2025
    Article
  4. Article
  5. Infection and immunity · 2025
    Article
  6. Article
  7. Optimising Transformation Efficiency inInternational journal of molecular sciences · 2024
    Article
  8. Hitchhiker's Guide toJournal of bacteriology · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Genetic Manipulation ofCurrent issues in molecular biology · 2021
    Review
  15. Live Imaging.Current issues in molecular biology · 2021
    Review
  16. Article
  17. Article
  18. Protozoan ParasiteFrontiers in microbiology · 2019
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Kamfai ChanDepartment of Microbiology, Biochemistry and Molecular Genetics, Rutgers New Jersey Medical School, Newark, NJ, 07103, United States of America.
Laura AlterDepartment of Microbiology, Biochemistry and Molecular Genetics, Rutgers New Jersey Medical School, Newark, NJ, 07103, United States of America.
Stephen W BartholdDepartment of Pathology, Microbiology & Immunology, University of California School of Veterinary Medicine, Davis, CA, 95616, United States of America.
Nikhat ParveenDepartment of Microbiology, Biochemistry and Molecular Genetics, Rutgers New Jersey Medical School, Newark, NJ, 07103, United States of America.

Funding

Borrelia burgdorferi-glycosaminoglycan interactions and Lyme disease pathogenesisR01AI089921 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI PARVEEN, NIKHAT · 2011 to 2015
$1.7M
NIAID NIH HHS AI089921NIAID NIH HHS R01 AI089921
6 · The paper itself

Abstract

Lyme disease is the most prevalent tick-borne disease in North America and Europe. The causative agent, Borrelia burgdorferi persists in the white-footed mouse. Infection with B. burgdorferi can cause acute to persistent multisystemic Lyme disease in humans. Some disease manifestations are also exhibited in the mouse model of Lyme disease. Genetic manipulation of B. burgdorferi remains difficult. First, B. burgdorferi contains a large number of endogenous plasmids with unique sequences encoding unknown functions. The presence of these plasmids needs to be confirmed after each genetic manipulation. Second, the restriction modification defense systems, including that encoded by bbe02 gene lead to low transformation efficiency in B. burgdorferi. Therefore, studying the molecular basis of Lyme pathogenesis is a challenge. Furthermore, investigation of the role of a specific B. burgdorferi protein throughout infection requires a large number of mice, making it labor intensive and expensive. To overcome the problems associated with low transformation efficiency and to reduce the number of mice needed for experiments, we disrupted the bbe02 gene of a highly infectious and pathogenic B. burgdorferi strain, N40 D10/E9 through insertion of a firefly luciferase gene. The bbe02 mutant shows higher transformation efficiency and maintains luciferase activity throughout infection as detected by live imaging of mice. Infectivity and pathogenesis of this mutant were comparable to the wild-type N40 strain. This mutant will serve as an ideal parental strain to examine the roles of various B. burgdorferi proteins in Lyme pathogenesis in the mouse model in the future.

Indexed as

AnimalsBacterial ProteinsBorrelia burgdorferiDNA Restriction-Modification EnzymesFemaleGenetic VectorsLuciferasesLyme DiseaseMiceMice, Inbred C3HMutationRecombinant ProteinsTransformation, GeneticWhole Body ImagingBacterial ProteinsDNA Restriction-Modification EnzymesLuciferasesRecombinant Proteins

Identifiers

PMID26069970
PMCPMC4466376

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.