Evidence map›Paper›PMID 39745890›Full record

ArticleThe ISME journal2025

Escherichia coli phage-inducible chromosomal island aids helper phage replication and represses the locus of enterocyte effacement pathogenicity island.

Kat Pick, Lauren Stadel, Tracy L Raivio

Abstract read
In one paragraph

Article in The ISME journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

3 authors.

Kat PickDepartment of Biological Sciences, CW 405 Biological Sciences Building, University of Alberta, Edmonton, AB T6G 2E9, Canada.
Lauren StadelDepartment of Biological Sciences, CW 405 Biological Sciences Building, University of Alberta, Edmonton, AB T6G 2E9, Canada.
Tracy L RaivioDepartment of Biological Sciences, CW 405 Biological Sciences Building, University of Alberta, Edmonton, AB T6G 2E9, Canada.

Funding

CIHR CIHR 185971National Sciences and Engineering Research Council RGPIN-2021-02710NSERC Postgraduate Scholarship -Doctoral
6 · The paper itself

Abstract

In this study, we identify and characterize a novel phage-inducible chromosomal island (PICI) found in commensal Escherichia coli MP1. This novel element, EcCIMP1, is induced and mobilized by the temperate helper phage vB_EcoP_Kapi1. EcCIMP1 contributes to superinfection immunity against its helper phage, impacting bacterial competition outcomes. Genetic analysis of EcCIMP1 led us to uncover a putative transcriptional repressor, which silences virulence gene expression in the murine pathogen Citrobacter rodentium. We also found a putative excisionase encoded by EcCIMP1 which paradoxically does not promote excision of EcCIMP1 but rather supports excision of the helper phage. Another putative excisionase encoded by a presumed integrative conjugative element can also support the excision of vB_EcoP_Kapi1, demonstrating crosstalk between excisionases from multiple classes of mobile genetic elements within the same cell. Although phylogenetically distant from other characterized PICIs, EcCIMP1 and EcCIMP1-like elements are prevalent in both pathogenic and commensal isolates of E. coli from around the world, underscoring the importance of characterizing these abundant genetic elements.

Indexed as

BacteriophagesColiphagesEscherichia coliGenomic IslandsHelper VirusesVirus ReplicationAnimalsCitrobacter rodentiumGene Expression Regulation, BacterialMicebacterial competitioncrosstalkexcisionaselysogenymobile genetic elementsphage-inducible chromosomal islandtemperate bacteriophagevirulence

Identifiers

PMID39745890
PMCPMC11773190

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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.