Evidence map›Paper›PMID 40811750›Full record

ArticlePLoS pathogens2025

Pore-C sequencing identifies episome-driven chromosome conformation perturbations differentiating pneumococcal epigenetic variants.

Tze Yee Lim, Samuel T Horsfield, Catherine M Troman, Stephen D Bentley, Min Jung Kwun, Nicholas J Croucher

Abstract read
In one paragraph

Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

6 authors.

Tze Yee LimMRC Centre for Global Infectious Disease Analysis, Department of Infectious Disease Epidemiology, School of Public Health, Imperial College London, London, United Kingdom.ORCID 0009-0004-4594-6382
Samuel T HorsfieldMRC Centre for Global Infectious Disease Analysis, Department of Infectious Disease Epidemiology, School of Public Health, Imperial College London, London, United Kingdom.ORCID 0000-0002-3859-4073
Catherine M TromanMRC Centre for Global Infectious Disease Analysis, Department of Infectious Disease Epidemiology, School of Public Health, Imperial College London, London, United Kingdom.ORCID 0000-0001-8584-7785
Stephen D BentleyParasites & Microbes, Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, United Kingdom.ORCID 0000-0001-8094-3751
Min Jung KwunMRC Centre for Global Infectious Disease Analysis, Department of Infectious Disease Epidemiology, School of Public Health, Imperial College London, London, United Kingdom.ORCID 0000-0003-1771-6913
Nicholas J CroucherMRC Centre for Global Infectious Disease Analysis, Department of Infectious Disease Epidemiology, School of Public Health, Imperial College London, London, United Kingdom.ORCID 0000-0001-6303-8768

Funding

Wellcome Trust
6 · The paper itself

Abstract

Streptococcus pneumoniae (pneumococcus) is a genetically diverse opportunistic bacterial pathogen that expresses two phase-variable loci encoding restriction-modification systems. Comparisons of two genetically-distinct pairs of epigenetically-distinct variants, each distinguished by a stabilised arrangement of one of these phase-variable loci, found the consequent changes in genome-wide DNA methylation patterns were associated with differential expression of mobile genetic elements (MGEs). This relationship was hypothesised to be mediated through changes in xenogenic silencing (XS) or nucleoid organisation. Therefore the chromosomal conformation of both variants of each pair were characterised using Illumina Hi-C, and Nanopore Pore-C, sequencing. Both methods concurred that the organisation of the pneumococcal chromosome was dominated by small-scale structures, with most pairwise interactions between loci <25 kb apart. Neither found substantial evidence for higher-order structure or XS in the pneumococcal genome, with more complex contact patterns only evident around the replication origin. Comparisons between the variants identified phage-related chromosomal islands (PRCIs) as the foci of differential contact densities between the variants. This was driven by copy number variation, resulting from variable excision and replication of the episomal PRCIs. However, the methods were discordant in their identification of the variant in which the PRCI was more actively replicating in both pairs. Validatory experiments demonstrated that the prevalence of circular PRCIs was not determined by DNA modification, but instead varied stochastically between colonies in both backgrounds, and was metastable during vegetative growth. PRCI excision was inducible by mitomycin C, but independent of the presence of a prophage. Yet transcriptional activation of these elements was affected by both signals, indicating transcription and replication are separately regulated. Therefore pneumococcal MGEs do not appear to be subject to XS, resulting in heterogeneity being generated within these bacterial populations through the frequent local disruption of chromosome conformation resulting from the stochastic excision and reintegration of episomal elements.

Indexed as

Chromosomes, BacterialEpigenesis, GeneticPlasmidsStreptococcus pneumoniaeDNA Copy Number VariationsDNA MethylationGenetic VariationGenome, Bacterial

Identifiers

PMID40811750
PMCPMC12416852

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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.