Evidence map›Paper›PMID 17542926›Full record

ArticleMolecular microbiology2007

The critical role of the linear plasmid lp36 in the infectious cycle of Borrelia burgdorferi.

Mollie W Jewett, Kevin Lawrence, Aaron C Bestor, Kit Tilly, Dorothee Grimm, Pamela Shaw, Mark VanRaden, Frank Gherardini, Patricia A Rosa

Open access · bronzeAbstract read
In one paragraph

Article in Molecular microbiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
5.9field-weighted citation impact, top 3% of its field
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

98 citing papers in PubMed, 117 citations in OpenAlex.

  1. Trial
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  19. The Infectivity GeneInfection and immunity · 2021
    Article
  20. Article

38 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

Mollie W JewettLaboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA. jewettm@niaid.nih.gov
Kevin Lawrence
Aaron C Bestor
Kit Tilly
Dorothee Grimm
Pamela Shaw
Mark VanRaden
Frank Gherardini
Patricia A Rosa
National Institutes of Health · USNational Institute of Allergy and Infectious Diseases · US

Funding

Molecular Genetic Basis of the Infectious Cycle of Borrelia burgdorferiZIAAI000917 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI ROSA, PATRICIA A · 2009 to 2023
$13.7M
The Roles of Key Transcription Factors on the Pathogenesis of B. Burgdorferi, the Causative Agent of Lyme DiseaseZIAAI000905 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI GHERARDINI, FRANK · 2009 to 2023
$12.4M
Molecular Genetics Of Infectious Borrelia BurgdorferiZ01AI000917 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI ROSA, PATRICIA A · 2002 to 2008
$2.2M
The Oxidative Stress Response In B. burgdorferiZ01AI000905 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI GHERARDINI, FRANK · 2002 to 2008
$744k
The Role Of Alternate Sigma Factors In The Transmission Cycle Of B. BurgdorferiZ01AI000906 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI GHERARDINI, FRANK · 2002 to 2008
$739k
The Role Of Alternate Sigma Factors In The Transmission Cycle Of B. BurgdorferiZIAAI000906 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI GHERARDINI, FRANK · 2009 to 2009
$105k
Intramural NIH HHS
6 · The paper itself

Abstract

Borrelia burgdorferi, the aetiological agent of Lyme disease, follows a life cycle that involves passage between the tick vector and the mammalian host. To investigate the role of the 36 kb linear plasmid, lp36 (also designated the B. burgdorferi K plasmid), in the infectious cycle of B. burgdorferi, we examined a clone lacking this plasmid, but containing all other plasmids known to be required for infectivity. Our results indicated that lp36 was not required for spirochete survival in the tick, but the clone lacking lp36 demonstrated low infectivity in the mammal. Restoration of lp36 to the mutant strain confirmed that the infectivity defect was due to loss of lp36. Moreover, spirochetes lacking lp36 exhibited a nearly 4-log increase in ID(50) relative to the isogenic lp36(+) clone. The infectivity defect of lp36-minus spirochetes was localized, in part, to loss of the bbk17 (adeC) gene, which encodes an adenine deaminase. This work establishes a vital role for lp36 in the infectious cycle of B. burgdorferi and identifies the bbk17 gene as a component of this plasmid that contributes to mammalian infectivity.

Indexed as

PlasmidsAnimalsAnimals, Outbred StrainsBorrelia burgdorferiLyme DiseaseMiceMice, Inbred C3HTicks

Identifiers

PMID17542926
PMCPMC1974800
OpenAlexW2143591164

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.