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Title 

DNA methylation: an epigenetic mark of cellular memory

Authors 

Mirang KimJ Costello

Publisher 

Korean Society of Medical Biochemistry

Issue Date 

2017

Citation 

Experimental and Molecular Medicine

Keywords 

DNA memoryFetal brainGenome-wide association studiesInduced pluripotent stem cellsMethylation quantitative trait lociNon-coding variantsSchizophrenia

Abstract 

Genome-wide association studies (GWAS) have remarkably advanced insight into the genetic basis of schizophrenia (SCZ). Still, most of the functional variance in disease risk remains unexplained. Hence, there is a growing need to map genetic variability-to-genes-to-functions for understanding the pathophysiology of SCZ and the development of better treatments. Genetic variation can regulate various cellular functions including DNA methylation, an epigenetic mark with important roles in transcription and the mediation of environmental influences. Methylation quantitative trait loci (meQTLs) are derived by mapping levels of DNA methylation in genetically different, genotyped individuals and define loci at which DNA methylation is influenced by genetic variation. Recent evidence points to an abundance of meQTLs in brain tissues whose functional contributions to development and mental diseases are still poorly understood. Interestingly, fetal meQTLs reside in regulatory domains affecting methylome reconfiguration during early brain development and are enriched in loci identified by GWAS for SCZ. Moreover, fetal meQTLs are preserved in the adult brain and could trace early epigenomic deregulation during vulnerable periods. Overall, these findings highlight the role of fetal meQTLs in the genetic risk for and in the possible neurodevelopmental origin of SCZ.

ISSN 

1226-3613

Link 

http://dx.doi.org/10.3390/genes7120104

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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