Evidence map›Paper›PMID 33891594›Full record

ArticlePLoS biology2021

A functional bacteria-derived restriction modification system in the mitochondrion of a heterotrophic protist.

David S Milner, Jeremy G Wideman, Courtney W Stairs, Cory D Dunn, Thomas A Richards

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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  8. Selfish gene leaves bacteria behind.Nature reviews. Microbiology · 2021
    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

5 authors at 4 institutions in 5 countries.

David S MilnerDepartment of Zoology, University of Oxford, Oxford, United Kingdom.ORCID 0000-0003-3669-7463
Jeremy G WidemanBiodesign Center for Mechanisms of Evolution, School of Life Sciences, Arizona State University, Tempe, Arizona, United States of America.ORCID 0000-0002-4426-9533
Courtney W StairsDepartment of Biology, Lund University, Lund, Sweden.ORCID 0000-0001-6650-0970
Cory D DunnInstitute of Biotechnology, Helsinki Institute of Life Science, University of Helsinki, Helsinki, Finland.
Thomas A RichardsDepartment of Zoology, University of Oxford, Oxford, United Kingdom.ORCID 0000-0002-9692-0973
University of Oxford · GBInstitute for Advanced Study · DELund University · SEUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The overarching trend in mitochondrial genome evolution is functional streamlining coupled with gene loss. Therefore, gene acquisition by mitochondria is considered to be exceedingly rare. Selfish elements in the form of self-splicing introns occur in many organellar genomes, but the wider diversity of selfish elements, and how they persist in the DNA of organelles, has not been explored. In the mitochondrial genome of a marine heterotrophic katablepharid protist, we identify a functional type II restriction modification (RM) system originating from a horizontal gene transfer (HGT) event involving bacteria related to flavobacteria. This RM system consists of an HpaII-like endonuclease and a cognate cytosine methyltransferase (CM). We demonstrate that these proteins are functional by heterologous expression in both bacterial and eukaryotic cells. These results suggest that a mitochondrion-encoded RM system can function as a toxin-antitoxin selfish element, and that such elements could be co-opted by eukaryotic genomes to drive biased organellar inheritance.

Indexed as

Evolution, MolecularBacteriaBase SequenceDNA, MitochondrialDNA Restriction-Modification EnzymesEscherichia coliEukaryotaGene Transfer, HorizontalGenome, MitochondrialMitochondriaOrganisms, Genetically ModifiedPhylogenyRepetitive Sequences, Nucleic AcidSaccharomyces cerevisiaeSequence Analysis, DNADNA, MitochondrialDNA Restriction-Modification Enzymes

Identifiers

PMID33891594
PMCPMC8099122
OpenAlexW3155828211

What OpenQuestion holds

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LicenceCC BY
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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.