Evidence map›Paper›PMID 37246713›Full record

ArticleNucleic acids research2023

DUF2285 is a novel helix-turn-helix domain variant that orchestrates both activation and antiactivation of conjugative element transfer in proteobacteria.

William J Jowsey, Calum R P Morris, Drew A Hall, John T Sullivan, Robert D Fagerlund, Karina Y Eto, Paul D Solomon, Joel P Mackay, Charles S Bond, Joshua P Ramsay and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.9field-weighted citation impact, top 20% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

11 authors at 4 institutions in 2 countries.

William J JowseyDepartment of Microbiology and Immunology, University of Otago, Dunedin 9016, New Zealand.
Calum R P MorrisDepartment of Microbiology and Immunology, University of Otago, Dunedin 9016, New Zealand.
Drew A HallSchool of Molecular Sciences, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia.
John T SullivanDepartment of Microbiology and Immunology, University of Otago, Dunedin 9016, New Zealand.
Robert D FagerlundDepartment of Microbiology and Immunology, University of Otago, Dunedin 9016, New Zealand.
Karina Y EtoCurtin Medical School and Curtin Health Innovation Research Institute, Curtin University, Perth, WA 6102, Australia.
Paul D SolomonSchool of Life and Environmental Sciences, University of Sydney, Sydney, NSW 2006, Australia.
Joel P MackaySchool of Life and Environmental Sciences, University of Sydney, Sydney, NSW 2006, Australia.
Charles S BondSchool of Molecular Sciences, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia.ORCID 0000-0002-9584-6783
Joshua P RamsayCurtin Medical School and Curtin Health Innovation Research Institute, Curtin University, Perth, WA 6102, Australia.ORCID 0000-0002-1301-7077
Clive W RonsonDepartment of Microbiology and Immunology, University of Otago, Dunedin 9016, New Zealand.ORCID 0000-0002-2217-9676
University of Otago · NZCurtin University · AUThe University of Sydney · AUThe University of Western Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Horizontal gene transfer is tightly regulated in bacteria. Often only a fraction of cells become donors even when regulation of horizontal transfer is coordinated at the cell population level by quorum sensing. Here, we reveal the widespread 'domain of unknown function' DUF2285 represents an 'extended-turn' variant of the helix-turn-helix domain that participates in both transcriptional activation and antiactivation to initiate or inhibit horizontal gene transfer. Transfer of the integrative and conjugative element ICEMlSymR7A is controlled by the DUF2285-containing transcriptional activator FseA. One side of the DUF2285 domain of FseA has a positively charged surface which is required for DNA binding, while the opposite side makes critical interdomain contacts with the N-terminal FseA DUF6499 domain. The QseM protein is an antiactivator of FseA and is composed of a DUF2285 domain with a negative surface charge. While QseM lacks the DUF6499 domain, it can bind the FseA DUF6499 domain and prevent transcriptional activation by FseA. DUF2285-domain proteins are encoded on mobile elements throughout the proteobacteria, suggesting regulation of gene transfer by DUF2285 domains is a widespread phenomenon. These findings provide a striking example of how antagonistic domain paralogues have evolved to provide robust molecular control over the initiation of horizontal gene transfer.

Indexed as

Conjugation, GeneticProteobacteriaBacterial ProteinsGene Transfer, HorizontalMesorhizobiumQuorum SensingTranscriptional ActivationTranscription FactorsBacterial ProteinsTranscription Factors

Identifiers

PMID37246713
PMCPMC10359603
OpenAlexW4378640499

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.