Evidence map›Paper›PMID 22773786›Full record

ArticleJournal of bacteriology2012

TolC-dependent secretion of an ankyrin repeat-containing protein of Rickettsia typhi.

Simran J Kaur, M Sayeedur Rahman, Nicole C Ammerman, Magda Beier-Sexton, Shane M Ceraul, Joseph J Gillespie, Abdu F Azad

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bacteriology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. crANKing up the infection: ankyrin domains inInfection and immunity · 2024
    Review
  4. Article
  5. mSphere · 2023
    Article
  6. Review
  7. Article
  8. bioRxiv : the preprint server for biology · 2023
    Article
  9. Type 1 secretion system and effectors in Rickettsiales.Frontiers in cellular and infection microbiology · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

7 authors at 2 institutions in 1 country.

Simran J KaurDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
M Sayeedur Rahman
Nicole C Ammerman
Magda Beier-Sexton
Shane M Ceraul
Joseph J Gillespie
Abdu F Azad
University of Maryland, Baltimore · USVirginia Tech · US

Funding

MURINE TYPHUS: VECTOR BIOLOGY AND TRANSMISSIONR01AI017828 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI RAHMAN, MOHAMMED SAYEEDUR · 1985 to 2022
$10.2M
Murine Typhus: Vector Biology &TransmissionR37AI017828 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI AZAD, ABDU F · 1998 to 2007
$3.6M
Generation of Genetically Attenuated RickettsiaeR01AI059118 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI AZAD, ABDU F · 2005 to 2009
$2.1M
NIAID NIH HHS AI017828NIAID NIH HHS AI059118NIAID NIH HHS HHSN272200900040CNIAID NIH HHS R01 AI017828NIAID NIH HHS R01 AI059118NIAID NIH HHS R37 AI017828
6 · The paper itself

Abstract

Rickettsia typhi, the causative agent of murine (endemic) typhus, is an obligate intracellular pathogen with a life cycle involving both vertebrate and invertebrate hosts. In this study, we characterized a gene (RT0218) encoding a C-terminal ankyrin repeat domain-containing protein, named Rickettsia ankyrin repeat protein 1 (RARP-1), and identified it as a secreted effector protein of R. typhi. RT0218 showed differential transcript abundance at various phases of R. typhi intracellular growth. RARP-1 was secreted by R. typhi into the host cytoplasm during in vitro infection of mammalian cells. Transcriptional analysis revealed that RT0218 was cotranscribed with adjacent genes RT0217 (hypothetical protein) and RT0216 (TolC) as a single polycistronic mRNA. Given one of its functions as a facilitator of extracellular protein secretion in some Gram-negative bacterial pathogens, we tested the possible role of TolC in the secretion of RARP-1. Using Escherichia coli C600 and an isogenic tolC insertion mutant as surrogate hosts, our data demonstrate that RARP-1 is secreted in a TolC-dependent manner. Deletion of either the N-terminal signal peptide or the C-terminal ankyrin repeats abolished RARP-1 secretion by wild-type E. coli. Importantly, expression of R. typhi tolC in the E. coli tolC mutant restored the secretion of RARP-1, suggesting that TolC has a role in RARP-1 translocation across the outer membrane. This work implies that the TolC component of the putative type 1 secretion system of R. typhi is involved in the secretion process of RARP-1.

Indexed as

Ankyrin RepeatAnimalsBacterial Outer Membrane ProteinsBacterial ProteinsCell LineEscherichia coliEscherichia coli ProteinsGene DeletionGene Expression ProfilingGenetic Complementation TestHumansMembrane Transport ProteinsMutagenesis, InsertionalRickettsia typhiTranscription, GeneticBacterial Outer Membrane ProteinsBacterial ProteinsEscherichia coli ProteinsMembrane Transport ProteinstolC protein, E coli

Identifiers

PMID22773786
PMCPMC3430354
OpenAlexW2127681689

What OpenQuestion holds

Textmetadata
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.