Evidence map›Paper›PMID 26007654›Full record

ArticleNucleic acids research2015

Regulation of the Type I-F CRISPR-Cas system by CRP-cAMP and GalM controls spacer acquisition and interference.

Adrian G Patterson, James T Chang, Corinda Taylor, Peter C Fineran

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

45 citing papers in PubMed, 80 citations in OpenAlex.

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  6. The H-NS homologues MvaT and MvaU repress CRISPR-Cas inPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
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  19. Mechanisms regulating the CRISPR-Cas systems.Frontiers in microbiology · 2023
    Review
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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 at 1 institution in 1 country.

Adrian G PattersonDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand.
James T ChangDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand.
Corinda TaylorDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand.
Peter C FineranDepartment of Microbiology and Immunology, University of Otago, PO Box 56, Dunedin 9054, New Zealand peter.fineran@otago.ac.nz.
University of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The CRISPR-Cas prokaryotic 'adaptive immune systems' represent a sophisticated defence strategy providing bacteria and archaea with protection from invading genetic elements, such as bacteriophages or plasmids. Despite intensive research into their mechanism and application, how CRISPR-Cas systems are regulated is less clear, and nothing is known about the regulation of Type I-F systems. We used Pectobacterium atrosepticum, a Gram-negative phytopathogen, to study CRISPR-Cas regulation, since it contains a single Type I-F system. The CRP-cAMP complex activated the cas operon, increasing the expression of the adaptation genes cas1 and cas2-3 in addition to the genes encoding the Csy surveillance complex. Mutation of crp or cyaA (encoding adenylate cyclase) resulted in reductions in both primed spacer acquisition and interference. Furthermore, we identified a galactose mutarotase, GalM, which reduced cas operon expression in a CRP- and CyaA-dependent manner. We propose that the Type I-F system senses metabolic changes, such as sugar availability, and regulates cas genes to initiate an appropriate defence response. Indeed, elevated glucose levels reduced cas expression in a CRP- and CyaA-dependent manner. Taken together, these findings highlight that a metabolite-sensing regulatory pathway controls expression of the Type I-F CRISPR-Cas system to modulate levels of adaptation and interference.

Indexed as

CRISPR-Cas SystemsGene Expression Regulation, BacterialBinding SitesCarbohydrate EpimerasesCRISPR-Associated ProteinsCyclic AMPCyclic AMP Receptor ProteinGlucoseMutationOperonPectobacteriumPromoter Regions, GeneticTranscriptional ActivationCarbohydrate EpimerasesCRISPR-Associated ProteinsCyclic AMPCyclic AMP Receptor Proteingalactose mutarotaseGlucose

Identifiers

PMID26007654
PMCPMC4499141
OpenAlexW1613849333

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.