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Epigenetics

VTRNA2-1: an environment-sensitive human epiallele

Silver MJ, Kessler NJ, Hennig BJ, et al. · Genome biology · 2015

Open access · cc by · source: Europe PMC

Independent genome-wide methylation screens converge on VTRNA2-1 as a systemic metastable epiallele shaped by periconceptional environment and stable for years.

How this study connects

Role on claims

Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.

  • SupportsEpigeneticsconcept

    VTRNA2-1 shows concordant multi-tissue methylation differences, is partly set by periconceptional environment, and remains stable ≥10 years; ME regions are depleted for CGIs/SINEs and enriched for LINEs/ERVs.

    Evidence for the claim as stated.

  • SupportsBisulfite Sequencingmethod

    Independent genome-wide screens for systemic interindividual methylation converged on VTRNA2-1: concordant multi-tissue differences, partly set by periconceptional environment (season of conception in Gambian infants), and stable for at least 10 years. Metastable epiallele regions were depleted for CGIs/SINEs and enriched for LINEs/ERVs. Epiallele status is not itself proof of disease causation in every tissue.

    Evidence for the claim as stated.

  • SupportsBisulfite Sequencingmethod

    Bisulfite designs here are not one map. VTRNA2-1 is a multi-tissue epiallele stable ≥10 years and sensitive to periconceptional season; the ageing paper compresses 102 AR-CpGs into a 3-site blood clock (MAD 3.34 years); Yoruba 27K arrays link methylation to genetics and expression in 77 LCLs. A clock CpG is not an environment-set metastable epiallele.

    Evidence for the claim as stated.

Open questions

Tensions this paper is part of

From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.

  • Scope difference — different assays, populations, or outcomes

    Bisulfite designs here are not one map. VTRNA2-1 is a multi-tissue epiallele stable ≥10 years and sensitive to periconceptional season; the ageing paper compresses 102 AR-CpGs into a 3-site blood clock (MAD 3.34 years); Yoruba 27K arrays link methylation to genetics and expression in 77 LCLs. A clock CpG is not an environment-set metastable epiallele.

Study at a glance

Design
Other — Multi-tissue metastable-epiallele screens plus Gambian season-of-conception methylation analyses
N
N=215 · Season-of-conception contrast: 110 dry-season vs 105 rainy-season conceptions; additional multi-tissue discovery screens
Population
Human multi-tissue DNA methylomes and Gambian infant cohorts
Outcome
Systemic interindividual methylation at VTRNA2-1 and periconceptional environment effects

Structured fields used in claim comparison tables when every cited study has a complete layer.

Inspect source passages

VTRNA2-1: an environment-sensitive human epiallele

These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.

Methylation at this epiallele is stable over at least 10 years.

Further, we demonstrated that this is partially determined by periconceptional environment, and is stable over at least 10 years.

Why screen multiple embryonic-lineage tissues?

screening for concordant variation in multiple tissues representing different embryonic lineages, is unique in enabling the identification of systemic interindividual variation [].
Read passages in the original paper

Key findings

VTRNA2-1 shows concordant multi-tissue methylation differences, is partly set by periconceptional environment, and remains stable ≥10 years; ME regions are depleted for CGIs/SINEs and enriched for LINEs/ERVs.

Methodology

Authors screened multi-tissue DNA methylomes for systemic interindividual variation, then tested season-of-conception effects in Gambian infants, converging on VTRNA2-1.

Limitations

Epiallele status is not itself proof of disease causation in every tissue; screens have genomic biases despite being genomewide.

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