Evidence map›Paper›PMID 21829394›Full record

ArticlePLoS genetics2011

Identification of functional toxin/immunity genes linked to contact-dependent growth inhibition (CDI) and rearrangement hotspot (Rhs) systems.

Stephen J Poole, Elie J Diner, Stephanie K Aoki, Bruce A Braaten, Claire t'Kint de Roodenbeke, David A Low, Christopher S Hayes

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
10.0field-weighted citation impact, top 1% 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

139 citing papers in PubMed, 184 citations in OpenAlex.

  1. Article
  2. Article
  3. Hypermutable hotspot enables the rapid evolution of self/non-self recognition genes inProceedings of the National Academy of Sciences of the United States of America · 2025
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  4. Predicting clinical outcome ofMicrobial genomics · 2025
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  6. Frontiers in cellular and infection microbiology · 2025
    Review
  7. Journal of oral microbiology · 2025
    Article
  8. Article
  9. Article
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  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

79 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

7 authors at 1 institution in 1 country.

Stephen J PooleDepartment of Molecular, Cellular, and Developmental Biology, University of California Santa Barbara, Santa Barbara, California, USA. poole@lifesci.ucsb.edu
Elie J Diner
Stephanie K Aoki
Bruce A Braaten
Claire t'Kint de Roodenbeke
David A Low
Christopher S Hayes
University of California, Santa Barbara · US

Funding

Vaccines and Diagnostics TrialsU54AI065359 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI BARBOUR, ALAN G. · 2005 to 2013
$88.8M
NIAID NIH HHS U54 AI065359
6 · The paper itself

Abstract

Bacterial contact-dependent growth inhibition (CDI) is mediated by the CdiA/CdiB family of two-partner secretion proteins. Each CdiA protein exhibits a distinct growth inhibition activity, which resides in the polymorphic C-terminal region (CdiA-CT). CDI(+) cells also express unique CdiI immunity proteins that specifically block the activity of cognate CdiA-CT, thereby protecting the cell from autoinhibition. Here we show that many CDI systems contain multiple cdiA gene fragments that encode CdiA-CT sequences. These "orphan" cdiA-CT genes are almost always associated with downstream cdiI genes to form cdiA-CT/cdiI modules. Comparative genome analyses suggest that cdiA-CT/cdiI modules are mobile and exchanged between the CDI systems of different bacteria. In many instances, orphan cdiA-CT/cdiI modules are fused to full-length cdiA genes in other bacterial species. Examination of cdiA-CT/cdiI modules from Escherichia coli EC93, E. coli EC869, and Dickeya dadantii 3937 confirmed that these genes encode functional toxin/immunity pairs. Moreover, the orphan module from EC93 was functional in cell-mediated CDI when fused to the N-terminal portion of the EC93 CdiA protein. Bioinformatic analyses revealed that the genetic organization of CDI systems shares features with rhs (rearrangement hotspot) loci. Rhs proteins also contain polymorphic C-terminal regions (Rhs-CTs), some of which share significant sequence identity with CdiA-CTs. All rhs genes are followed by small ORFs representing possible rhsI immunity genes, and several Rhs systems encode orphan rhs-CT/rhsI modules. Analysis of rhs-CT/rhsI modules from D. dadantii 3937 demonstrated that Rhs-CTs have growth inhibitory activity, which is specifically blocked by cognate RhsI immunity proteins. Together, these results suggest that Rhs plays a role in intercellular competition and that orphan gene modules expand the diversity of toxic activities deployed by both CDI and Rhs systems.

Indexed as

Amino Acid SequenceBase SequenceCell ProliferationContact InhibitionEscherichia coliEscherichia coli ProteinsGene Expression Regulation, BacterialGene OrderMembrane ProteinsMolecular Sequence DataCdiA protein, E coliCdiI protein, E coliEscherichia coli ProteinsMembrane Proteins

Identifiers

PMID21829394
PMCPMC3150448
OpenAlexW2001348075

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.