Evidence map›Paper›PMID 27793092›Full record

ArticleBMC genomics2016

In-silico prediction and deep-DNA sequencing validation indicate phase variation in 115 Neisseria meningitidis genes.

Emilio Siena, Romina D'Aurizio, David Riley, Hervé Tettelin, Silvia Guidotti, Giulia Torricelli, E Richard Moxon, Duccio Medini

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 25 citations in OpenAlex.

  1. Frontiers in cellular and infection microbiology · 2025
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  14. Proceedings of the National Academy of Sciences of the United States of America · 2018
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  16. Review
  17. Regulation ofFEBS open bio · 2017
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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

8 authors at 4 institutions in 3 countries.

Emilio SienaGSK Vaccines, 53100, Siena, Italy. emilio.x.siena@gsk.com.
Romina D'AurizioGSK Vaccines, 53100, Siena, Italy.
David RileyInstitute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Hervé TettelinInstitute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Silvia GuidottiGSK Vaccines, 53100, Siena, Italy.
Giulia TorricelliGSK Vaccines, 53100, Siena, Italy.
E Richard MoxonMedical Sciences Division, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, OX3 9DS, UK.
Duccio MediniGSK Vaccines, 53100, Siena, Italy. duccio.x.medini@gsk.com.
Human Genome Sciences (United States) · USInstitute of Informatics and Telematics · ITJohn Radcliffe Hospital · GBUniversity of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Neisseria meningitidis (Nm) chromosome shows a high abundance of simple sequence DNA repeats (SSRs) that undergo stochastic, reversible mutations at high frequency. This mechanism is reflected in an extensive phenotypic diversity that facilitates Nm adaptation to dynamic environmental changes. To date, phase-variable phenotypes mediated by SSRs variation have been experimentally confirmed for 26 Nm genes.

resultsHere we present a population-scale comparative genomic analysis that identified 277 genes and classified them into 52 strong, 60 moderate and 165 weak candidates for phase variation. Deep-coverage DNA sequencing of single colonies grown overnight under non-selective conditions confirmed the presence of high-frequency, stochastic variation in 115 of them, providing circumstantial evidence for their phase variability. We confirmed previous observations of a predominance of variable SSRs within genes for components located on the cell surface or DNA metabolism. However, in addition we identified an unexpectedly broad spectrum of other metabolic functions, and most of the variable SSRs were predicted to induce phenotypic changes by modulating gene expression at a transcriptional level or by producing different protein isoforms rather than mediating on/off translational switching through frameshifts. Investigation of the evolutionary history of SSR contingency loci revealed that these loci were inherited from a Nm ancestor, evolved independently within Nm, or were acquired by Nm through lateral DNA exchange.

conclusionsOverall, our results have identified a broader and qualitatively different phenotypic diversification of SSRs-mediated stochastic variation than previously documented, including its impact on central Nm metabolism.

Indexed as

DNA, BacterialGenes, BacterialHigh-Throughput Nucleotide SequencingMicrosatellite RepeatsPhenotypeGene Expression Regulation, BacterialGenotypeHumansNeisseria meningitidisPolymorphism, GeneticSelection, GeneticDNA, BacterialComparative genomicsContingency lociHost-pathogen interactionNeisseria meningitidisPhase variation

Identifiers

PMID27793092
PMCPMC5084427
OpenAlexW2541900524

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.