Evidence map›Paper›PMID 42013857›Full record

ArticleCell reports methods2026

Genetic modification of intractable bacterial clones by heat shock-facilitated phage transduction.

Lukas Schulze, Jens Stahl, Nastassia J Knödlseder, Sophia Krauss, Theresa Harbig, Kay Nieselt, Holger Brüggemann, Bernhard Krismer, Andreas Peschel

Abstract read
In one paragraph

Article in Cell reports methods, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Lukas SchulzeDepartment of Infection Biology, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany; Cluster of Excellence EXC 2124, Controlling Microbes to Fight Infections, Tübingen, Germany; German Center for Infection Research (DZIF), Partner Site Tübingen, Tübingen, Germany.
Jens StahlDepartment of Infection Biology, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany; Cluster of Excellence EXC 2124, Controlling Microbes to Fight Infections, Tübingen, Germany; German Center for Infection Research (DZIF), Partner Site Tübingen, Tübingen, Germany.
Nastassia J KnödlsederDepartment of Biomedicine, Aarhus University, Aarhus, Denmark; Department of Medicine and Life Sciences, Universitat Pompeu Fabra, Barcelona, Spain.
Sophia KraussDepartment of Infection Biology, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany; Cluster of Excellence EXC 2124, Controlling Microbes to Fight Infections, Tübingen, Germany; German Center for Infection Research (DZIF), Partner Site Tübingen, Tübingen, Germany.
Theresa HarbigInstitute for Bioinformatics and Medical Informatics, University of Tübingen, Tübingen, Germany.
Kay NieseltInstitute for Bioinformatics and Medical Informatics, University of Tübingen, Tübingen, Germany.
Holger BrüggemannDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Bernhard KrismerDepartment of Infection Biology, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany; Cluster of Excellence EXC 2124, Controlling Microbes to Fight Infections, Tübingen, Germany; German Center for Infection Research (DZIF), Partner Site Tübingen, Tübingen, Germany. Electronic address: b.krismer@uni-tuebingen.de.
Andreas PeschelDepartment of Infection Biology, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, Germany; Cluster of Excellence EXC 2124, Controlling Microbes to Fight Infections, Tübingen, Germany; German Center for Infection Research (DZIF), Partner Site Tübingen, Tübingen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing recognition of commensal bacteria as essential for microbiome integrity and pathogen exclusion underscores the urgency of molecularly characterizing commensal interactions. However, many commensals cannot be transformed using available methodologies due to barriers imposed by restriction-modification (RM) systems. We developed a method for introducing plasmid DNA into otherwise intractable non-Staphylococcus aureus (NAS) staphylococci, important commensals of the human nasal and skin microbiomes, via phage transduction. We demonstrate that exposing recipient bacteria to a pulse of elevated temperature prior to phage exposure renders NAS isolates effectively and transiently amenable to transduction. Transduction of NAS mutants lacking RM systems did not respond to heat shock, indicating that transient deactivation of RM enzymes enables transduction. Our method also facilitates the transduction of representatives from other Bacillota and Actinomycetota taxa, suggesting that this approach will support research on diverse bacterial groups across a range of ecosystems.

Indexed as

BacteriophagesHeat-Shock ResponseStaphylococcus aureusTransduction, GeneticHumansPlasmidsbacteriophagesCP: microbiologyCP: molecular biologygenetic manipulationheat shockrestriction barrierrestriction-modificationstaphylococcitransduction

Identifiers

PMID42013857
PMCPMC13198106

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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.