PuSH - Publication Server of Helmholtz Zentrum München

DNA methylation dynamics at transposable elements in mammals.

Essays Biochem. 63, 677-689 (2019)
DOI Order publishers version
Open Access Green as soon as Postprint is submitted to ZB.
Transposable elements dominate the mammalian genome, but their contribution to genetic and epigenetic regulation has been largely overlooked. This was in part due to technical limitations, which made the study of repetitive sequences at single copy resolution difficult. The advancement of next-generation sequencing assays in the last decade has greatly enhanced our understanding of transposable element function. In some instances, specific transposable elements are thought to have been co-opted into regulatory roles during both mouse and human development, while in disease such regulatory potential can contribute to malignancy. DNA methylation is arguably the best characterised regulator of transposable element activity. DNA methylation is associated with transposable element repression, and acts to limit their genotoxic potential. In specific developmental contexts, erasure of DNA methylation is associated with a burst of transposable element expression. Developmental regulation of DNA methylation enables transposon activation, ensuring their survival and propagation throughout the host genome, and also allows the host access to regulatory sequences encoded within the elements. Here I discuss DNA methylation at transposable elements, describing its function and dynamic regulation throughout murine and human development.
Additional Metrics?
Edit extra informations Login
Publication type Article: Journal article
Document type Review
Keywords Epigenetic Reprogramming ; Methylation ; Transposons; Male Germ-cells; Endogenous Retroviruses; Retrotransposable Elements; Infectious Progenitor; L1 Retrotransposon; Genome Activation; Line-1; Transcription; 5-methylcytosine; Expression
ISSN (print) / ISBN 0071-1365
e-ISSN 1744-1358
Quellenangaben Volume: 63, Issue: 6, Pages: 677-689 Article Number: , Supplement: ,
Publisher Portland Press
Publishing Place London
Reviewing status Peer reviewed