Oestrogen receptor β regulates epigenetic patterns at specific genomic loci through interaction with thymine DNA glycosylase
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- 作者：Yun Liu ; William Duong ; Claudia Krawczyk ; Nancy Bretschneider…
- 关键词：Oestrogen receptor β ; Thymine DNA glycosylase ; DNA methylation ; Reduced representation bisulfite sequencing ; Mouse embryonic fibroblasts ; Mouse embryonic stem cells
- 刊名：Epigenetics & Chromatin
- 出版年：2016
- 出版时间：December 2016
- 年：2016
- 卷：9
- 期：1
- 全文大小：2,228 KB
- 刊物主题：Animal Genetics and Genomics; Human Genetics; Plant Genetics & Genomics; Cell Biology;
- 出版者：BioMed Central
- ISSN：1756-8935
文摘
Background DNA methylation is one way to encode epigenetic information and plays a crucial role in regulating gene expression during embryonic development. DNA methylation marks are established by the DNA methyltransferases and, recently, a mechanism for active DNA demethylation has emerged involving the ten-eleven translocator proteins and thymine DNA glycosylase (TDG). However, so far it is not clear how these enzymes are recruited to, and regulate DNA methylation at, specific genomic loci. A number of studies imply that sequence-specific transcription factors are involved in targeting DNA methylation and demethylation processes. Oestrogen receptor beta (ERβ) is a ligand-inducible transcription factor regulating gene expression in response to the female sex hormone oestrogen. Previously, we found that ERβ deficiency results in changes in DNA methylation patterns at two gene promoters, implicating an involvement of ERβ in DNA methylation. In this study, we set out to explore this involvement on a genome-wide level, and to investigate the underlying mechanisms of this function.