Evidence map›Paper›PMID 22792059›Full record

ArticlePLoS computational biology2012

Predicting signatures of "synthetic associations" and "natural associations" from empirical patterns of human genetic variation.

Diana Chang, Alon Keinan

Abstract read
In one paragraph

Article in PLoS computational biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. A Variant in theJournal of dental research · 2023
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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.

Diana ChangDepartment of Biological Statistics and Computational Biology, Cornell University, Ithaca, New York, United States of America.
Alon Keinan

Funding

Tri-Institutional Training Program in Computational Biology & MedicineT32GM083937 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHRISTINI, DAVID J. · 2009 to 2018
$3.1M
Population Structure Admixture and Selection across the 1000 Genomes Data SetU01HG005715 · NHGRI · STANFORD UNIVERSITY · PI BUSTAMANTE, CARLOS DANIEL, CLARK, ANDREW G · 2010 to 2012
$1.1M
NHGRI NIH HHS U01 HG005715NHGRI NIH HHS U01-HG005715NIGMS NIH HHS T32 GM083937NIGMS NIH HHS T32GM083937
6 · The paper itself

Abstract

Genome-wide association studies (GWAS) have in recent years discovered thousands of associated markers for hundreds of phenotypes. However, associated loci often only explain a relatively small fraction of heritability and the link between association and causality has yet to be uncovered for most loci. Rare causal variants have been suggested as one scenario that may partially explain these shortcomings. Specifically, Dickson et al. recently reported simulations of rare causal variants that lead to association signals of common, tag single nucleotide polymorphisms, dubbed "synthetic associations". However, an open question is what practical implications synthetic associations have for GWAS. Here, we explore the signatures exhibited by such "synthetic associations" and their implications based on patterns of genetic variation observed in human populations, thus accounting for human evolutionary history -a force disregarded in previous simulation studies. This is made possible by human population genetic data from HapMap 3 consisting of both resequencing and array-based genotyping data for the same set of individuals from multiple populations. We report that synthetic associations tend to be further away from the underlying risk alleles compared to "natural associations" (i.e. associations due to underlying common causal variants), but to a much lesser extent than previously predicted, with both the age and the effect size of the risk allele playing a part in this phenomenon. We find that while a synthetic association has a lower probability of capturing causal variants within its linkage disequilibrium block, sequencing around the associated variant need not extend substantially to have a high probability of capturing at least one causal variant. We also show that the minor allele frequency of synthetic associations is lower than of natural associations for most, but not all, loci that we explored. Finally, we find the variance in associated allele frequency to be a potential indicator of synthetic associations.

Indexed as

Genetic VariationModels, GeneticComputer SimulationDatabases, GeneticEvolution, MolecularGene FrequencyGenome-Wide Association StudyGenomicsHapMap ProjectHumansLinkage DisequilibriumPolymorphism, Single Nucleotide

Identifiers

PMID22792059
PMCPMC3390358

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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.