Evidence map›Paper›PMID 27868255›Full record

ReviewMolecular microbiology2017

Regulatory gene mutation: a driving force behind group a Streptococcus strain- and serotype-specific variation.

Poulomee Sarkar, Paul Sumby

Abstract readReview
In one paragraph

Review in Molecular microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

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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

2 authors.

Poulomee SarkarDepartment of Microbiology & Immunology, University of Nevada, Reno School of Medicine, Reno, Nevada, USA.
Paul SumbyDepartment of Microbiology & Immunology, University of Nevada, Reno School of Medicine, Reno, Nevada, USA.

Funding

Delineation of the molecular mechanisms underlying group A Streptococcus virulencR01AI087747 · NIAID · UNIVERSITY OF NEVADA RENO · PI SUMBY, PAUL · 2010 to 2014
$1.8M
NIAID NIH HHS R01 AI087747
6 · The paper itself

Abstract

Data from multiple bacterial pathogens are consistent with regulator-encoding genes having higher mutation frequencies than the genome average. Such mutations drive both strain- and type- (e.g., serotype, haplotype) specific phenotypic heterogeneity, and may challenge public health due to the potential of variants to circumvent established treatment and/or preventative regimes. Here, using the human bacterial pathogen the group A Streptococcus (GAS; S. pyogenes) as a model organism, we review the types and regulatory-, phenotypic-, and disease-specific consequences of naturally occurring regulatory gene mutations. Strain-specific regulator mutations that will be discussed include examples that transform isolates into hyper-invasive forms by enhancing expression of immunomodulatory virulence factors, and examples that promote asymptomatic carriage of the organism. The discussion of serotype-specific regulator mutations focuses on serotype M3 GAS isolates, and how the identified rewiring of regulatory networks in this serotype may be contributing to a decades old epidemiological association of M3 isolates with particularly severe invasive infections. We conclude that mutation plays an outsized role in GAS pathogenesis and has clinical relevance. Given the phenotypic variability associated with regulatory gene mutations, the rapid examination of these genes in infecting isolates may inform with respect to potential patient complications and treatment options.

Indexed as

Gene Expression Regulation, BacterialGenes, RegulatorGenome, BacterialHumansMutationSerogroupStreptococcal InfectionsStreptococcus pyogenesVirulence FactorsVirulence Factors

Identifiers

PMID27868255
PMCPMC5296365

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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.