Evidence map›Paper›PMID 25019935›Full record

ArticlePloS one2014

Characterization of genome-methylome interactions in 22 nuclear pedigrees.

Nongluk Plongthongkum, Kristel R van Eijk, Simone de Jong, Tina Wang, Jae Hoon Sul, Marco P M Boks, René S Kahn, Ho-Lim Fung, Roel A Ophoff, Kun Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Article
  6. Review
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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

10 authors at 4 institutions in 2 countries.

Nongluk PlongthongkumDepartment of Bioengineering, University of California San Diego, La Jolla, California, United States of America.
Kristel R van EijkDepartment of Psychiatry, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, Utrecht, The Netherlands.
Simone de JongCenter for Neurobehavioral Genetics, Semel Institute for Neuroscience and Behavior, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America.
Tina WangCenter for Neurobehavioral Genetics, Semel Institute for Neuroscience and Behavior, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America.
Jae Hoon SulDepartment of Computer Science, University of California Los Angeles, Los Angeles, California, United States of America.
Marco P M BoksDepartment of Psychiatry, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, Utrecht, The Netherlands.
René S KahnDepartment of Psychiatry, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, Utrecht, The Netherlands.
Ho-Lim FungDepartment of Bioengineering, University of California San Diego, La Jolla, California, United States of America.
Roel A OphoffCenter for Neurobehavioral Genetics, Semel Institute for Neuroscience and Behavior, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America; Department of Psychiatry, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, Utrecht, The Netherlands.
Kun ZhangDepartment of Bioengineering, University of California San Diego, La Jolla, California, United States of America.
University of California, Los Angeles · USUniversity of California, San Diego · USUtrecht University · NLUniversity Medical Center Utrecht · NL

Funding

Minority Action PlanP50HG003233 · NHGRI · JOHNS HOPKINS UNIVERSITY · PI FEINBERG, ANDREW P. · 2004 to 2013
$22.4M
Genomic Studies of Bipolar Disorder in a Large Cohort from The NetherlandsR01MH090553 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI OPHOFF, ROEL A · 2010 to 2014
$6.0M
Epigenetics and disease: the role of DNA methylation in schizophrenia susceptibilR01DA028526 · NIDA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI OPHOFF, ROEL A · 2009 to 2013
$2.5M
Genome-methylome InteractionsR01GM097253 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHANG, KUN · 2011 to 2014
$1.4M
NHGRI NIH HHS HG003233NHGRI NIH HHS P50 HG003233NIDA NIH HHS DA028526NIDA NIH HHS R01 DA028526NIGMS NIH HHS GM097253NIGMS NIH HHS R01 GM097253NIMH NIH HHS MH090553NIMH NIH HHS R01 MH090553
6 · The paper itself

Abstract

Genetic polymorphisms can shape the global landscape of DNA methylation, by either changing substrates for DNA methyltransferases or altering the DNA binding affinity of cis-regulatory proteins. The interactions between CpG methylation and genetic polymorphisms have been previously investigated by methylation quantitative trait loci (mQTL) and allele-specific methylation (ASM) analysis. However, it remains unclear whether these approaches can effectively and comprehensively identify all genetic variants that contribute to the inter-individual variation of DNA methylation levels. Here we used three independent approaches to systematically investigate the influence of genetic polymorphisms on variability in DNA methylation by characterizing the methylation state of 96 whole blood samples in 52 parent-child trios from 22 nuclear pedigrees. We performed targeted bisulfite sequencing with padlock probes to quantify the absolute DNA methylation levels at a set of 411,800 CpG sites in the human genome. With mid-parent offspring analysis (MPO), we identified 10,593 CpG sites that exhibited heritable methylation patterns, among which 70.1% were SNPs directly present in methylated CpG dinucleotides. We determined the mQTL analysis identified 49.9% of heritable CpG sites for which regulation occurred in a distal cis-regulatory manner, and that ASM analysis was only able to identify 5%. Finally, we identified hundreds of clusters in the human genome for which the degree of variation of CpG methylation, as opposed to whether or not CpG sites were methylated, was associated with genetic polymorphisms, supporting a recent hypothesis on the genetic influence of phenotypic plasticity. These results show that cis-regulatory SNPs identified by mQTL do not comprise the full extent of heritable CpG methylation, and that ASM appears overall unreliable. Overall, the extent of genome-methylome interactions is well beyond what is detectible with the commonly used mQTL and ASM approaches, and is likely to include effects on plasticity.

Indexed as

DNA MethylationNuclear FamilyPedigreeCpG IslandsFemaleGenome, HumanGenomicsHumansMalePolymorphism, Single NucleotideQuantitative Trait Loci

Identifiers

PMID25019935
PMCPMC4096397
OpenAlexW2010191835

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.