Evidence map›Paper›PMID 31388080›Full record

ArticleScientific reports2019

Genome-wide Phenotypic Profiling Identifies and Categorizes Genes Required for Mycobacterial Low Iron Fitness.

Marte S Dragset, Thomas R Ioerger, Yanjia J Zhang, Mali Mærk, Zekarias Ginbot, James C Sacchettini, Trude H Flo, Eric J Rubin, Magnus Steigedal

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 52 citations in OpenAlex.

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  14. Review
  15. Vaccines · 2023
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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

9 authors at 3 institutions in 3 countries.

Marte S DragsetNTNU Norwegian University of Science and Technology, Centre of Molecular Inflammation Research and Department of Clinical and Molecular Medicine, Trondheim, 7491, Norway. marte.dragset@ntnu.no.ORCID http://orcid.org/0000-0003-1546-4329
Thomas R IoergerTexas A&M University, Department of Computer Science, College Station, TX, 77843, USA.
Yanjia J ZhangHarvard T.H. Chan School of Public Health, Department of Immunology and Infectious Diseases, Boston, MA, 02115, USA.
Mali MærkNTNU Norwegian University of Science and Technology, Centre of Molecular Inflammation Research and Department of Clinical and Molecular Medicine, Trondheim, 7491, Norway.
Zekarias GinbotNTNU Norwegian University of Science and Technology, Centre of Molecular Inflammation Research and Department of Clinical and Molecular Medicine, Trondheim, 7491, Norway.
James C SacchettiniTexas A&M University, Department of Biochemistry and Biophysics, College Station, TX, 77843, USA.
Trude H FloNTNU Norwegian University of Science and Technology, Centre of Molecular Inflammation Research and Department of Clinical and Molecular Medicine, Trondheim, 7491, Norway.ORCID http://orcid.org/0000-0002-2569-0381
Eric J RubinHarvard T.H. Chan School of Public Health, Department of Immunology and Infectious Diseases, Boston, MA, 02115, USA.
Magnus SteigedalNTNU Norwegian University of Science and Technology, Centre of Molecular Inflammation Research and Department of Clinical and Molecular Medicine, Trondheim, 7491, Norway.
Harvard University · USNorwegian University of Science and Technology · NOTexas A&M University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron is vital for nearly all living organisms, but during infection, not readily available to pathogens. Infectious bacteria therefore depend on specialized mechanisms to survive when iron is limited. These mechanisms make attractive targets for new drugs. Here, by genome-wide phenotypic profiling, we identify and categorize mycobacterial genes required for low iron fitness. Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), can scavenge host-sequestered iron by high-affinity iron chelators called siderophores. We take advantage of siderophore redundancy within the non-pathogenic mycobacterial model organism M. smegmatis (Msmeg), to identify genes required for siderophore dependent and independent fitness when iron is low. In addition to genes with a potential function in recognition, transport or utilization of mycobacterial siderophores, we identify novel putative low iron survival strategies that are separate from siderophore systems. We also identify the Msmeg in vitro essential gene set, and find that 96% of all growth-required Msmeg genes have a mutual ortholog in Mtb. Of these again, nearly 90% are defined as required for growth in Mtb as well. Finally, we show that a novel, putative ferric iron ABC transporter contributes to low iron fitness in Msmeg, in a siderophore independent manner.

Indexed as

Antitubercular AgentsATP-Binding Cassette TransportersBacterial ProteinsDrug DevelopmentGene Knockdown TechniquesGenes, BacterialGenes, EssentialGenetic ProfileHumansIronMycobacterium smegmatisMycobacterium tuberculosisSiderophoresTuberculosisAntitubercular AgentsATP-Binding Cassette TransportersBacterial ProteinsIronSiderophores

Identifiers

PMID31388080
PMCPMC6684656
OpenAlexW2965016808

What OpenQuestion holds

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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.