Evidence map›Paper›PMID 26845436›Full record

ArticlePLoS genetics2016

Adaptive Remodeling of the Bacterial Proteome by Specific Ribosomal Modification Regulates Pseudomonas Infection and Niche Colonisation.

Richard H Little, Lucia Grenga, Gerhard Saalbach, Alexandra M Howat, Sebastian Pfeilmeier, Eleftheria Trampari, Jacob G Malone

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
18.5field-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

42 citing papers in PubMed, 60 citations in OpenAlex.

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  10. tRNA epitranscriptome determines pathogenicity of the opportunistic pathogenProceedings of the National Academy of Sciences of the United States of America · 2024
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  19. Systematic analysis of lysine malonylation inFrontiers in cellular and infection microbiology · 2022
    Article
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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

7 authors at 2 institutions in 1 country.

Richard H LittleDepartment of Molecular Microbiology, John Innes Centre, Norwich Research Park, Norwich, United Kingdom.
Lucia GrengaDepartment of Molecular Microbiology, John Innes Centre, Norwich Research Park, Norwich, United Kingdom.
Gerhard SaalbachDepartment of Molecular Microbiology, John Innes Centre, Norwich Research Park, Norwich, United Kingdom.
Alexandra M HowatSchool of Biological Sciences, University of East Anglia, Norwich Research Park, Norwich, United Kingdom.
Sebastian PfeilmeierDepartment of Molecular Microbiology, John Innes Centre, Norwich Research Park, Norwich, United Kingdom.
Eleftheria TrampariDepartment of Molecular Microbiology, John Innes Centre, Norwich Research Park, Norwich, United Kingdom.
Jacob G MaloneDepartment of Molecular Microbiology, John Innes Centre, Norwich Research Park, Norwich, United Kingdom.
John Innes Centre · GBNorwich Research Park · GB

Funding

Biotechnology and Biological Sciences Research Council BB/J004553/1Biotechnology and Biological Sciences Research Council BB/M002586/1
6 · The paper itself

Abstract

Post-transcriptional control of protein abundance is a highly important, underexplored regulatory process by which organisms respond to their environments. Here we describe an important and previously unidentified regulatory pathway involving the ribosomal modification protein RimK, its regulator proteins RimA and RimB, and the widespread bacterial second messenger cyclic-di-GMP (cdG). Disruption of rimK affects motility and surface attachment in pathogenic and commensal Pseudomonas species, with rimK deletion significantly compromising rhizosphere colonisation by the commensal soil bacterium P. fluorescens, and plant infection by the pathogens P. syringae and P. aeruginosa. RimK functions as an ATP-dependent glutamyl ligase, adding glutamate residues to the C-terminus of ribosomal protein RpsF and inducing specific effects on both ribosome protein complement and function. Deletion of rimK in P. fluorescens leads to markedly reduced levels of multiple ribosomal proteins, and also of the key translational regulator Hfq. In turn, reduced Hfq levels induce specific downstream proteomic changes, with significant increases in multiple ABC transporters, stress response proteins and non-ribosomal peptide synthetases seen for both ΔrimK and Δhfq mutants. The activity of RimK is itself controlled by interactions with RimA, RimB and cdG. We propose that control of RimK activity represents a novel regulatory mechanism that dynamically influences interactions between bacteria and their hosts; translating environmental pressures into dynamic ribosomal changes, and consequently to an adaptive remodeling of the bacterial proteome.

Indexed as

Adaptation, PhysiologicalBacterial ProteinsCyclic GMPGene Expression Regulation, BacterialHumansModels, BiologicalMovementMutationPlant RootsProtein BindingProteomePseudomonasPseudomonas InfectionsRegulonRhizosphereRibosomesBacterial Proteinsbis(3',5')-cyclic diguanylic acidCyclic GMPProteome

Identifiers

PMID26845436
PMCPMC4741518
OpenAlexW2292172688

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.