In Vivo Control of CpG and Non-CpG DNA Methylation by DNA Methyltransferases

DSpace/Manakin Repository

In Vivo Control of CpG and Non-CpG DNA Methylation by DNA Methyltransferases

Citable link to this page

 

 
Title: In Vivo Control of CpG and Non-CpG DNA Methylation by DNA Methyltransferases
Author: Arand, Julia; Spieler, David; Karius, Tommy; Branco, Miguel R.; Meilinger, Daniela; Meissner, Alexander; Jenuwein, Thomas; Xu, Guoliang; Leonhardt, Heinrich; Wolf, Verena; Walter, Jörn

Note: Order does not necessarily reflect citation order of authors.

Citation: Arand, Julia, David Spieler, Tommy Karius, Miguel R. Branco, Daniela Meilinger, Alexander Meissner, Thomas Jenuwein, Guoliang Xu, Heinrich Leonhardt, Verena Wolf, and Jörn Walter. 2012. In vivo control of cpg and non-cpg dna methylation by dna methyltransferases. PLoS Genetics 8(6).
Full Text & Related Files:
Abstract: The enzymatic control of the setting and maintenance of symmetric and non-symmetric DNA methylation patterns in a particular genome context is not well understood. Here, we describe a comprehensive analysis of DNA methylation patterns generated by high resolution sequencing of hairpin-bisulfite amplicons of selected single copy genes and repetitive elements (LINE1, B1, IAP-LTR-retrotransposons, and major satellites). The analysis unambiguously identifies a substantial amount of regional incomplete methylation maintenance, i.e. hemimethylated CpG positions, with variant degrees among cell types. Moreover, non-CpG cytosine methylation is confined to ESCs and exclusively catalysed by Dnmt3a and Dnmt3b. This sequence position–, cell type–, and region-dependent non-CpG methylation is strongly linked to neighboring CpG methylation and requires the presence of Dnmt3L. The generation of a comprehensive data set of 146,000 CpG dyads was used to apply and develop parameter estimated hidden Markov models (HMM) to calculate the relative contribution of DNA methyltransferases (Dnmts) for de novo and maintenance DNA methylation. The comparative modelling included wild-type ESCs and mutant ESCs deficient for Dnmt1, Dnmt3a, Dnmt3b, or Dnmt3a/3b, respectively. The HMM analysis identifies a considerable de novo methylation activity for Dnmt1 at certain repetitive elements and single copy sequences. Dnmt3a and Dnmt3b contribute de novo function. However, both enzymes are also essential to maintain symmetrical CpG methylation at distinct repetitive and single copy sequences in ESCs.
Published Version: doi:10.1371/journal.pgen.1002750
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3386304/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11691835
Downloads of this work:

Show full Dublin Core record

This item appears in the following Collection(s)

 
 

Search DASH


Advanced Search
 
 

Submitters