期刊
NATURE GENETICS
卷 50, 期 3, 页码 443-451出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41588-018-0060-9
关键词
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资金
- US National Institutes of Health (NIH) [1R01-GM095942, R21HD087722, R01HL112294]
- Empire State Stem Cell Fund through the New York State Department of Health (NYSTEM) [C028103, C028121]
- Irma T. Hirschl and Weill-Caulier Trusts Career Scientist Award
- Ministerio de Economia y Competitividad of Spain [2014-16779]
- National Natural Science Foundation of China [31471219, 31428010]
- Center for Life Sciences (CLS) at Tsinghua University
- Agencia Estatal de Investigacion [BFU2016-80899-P]
- Conselleria de Cultura, Educacion e Ordenacion Universitaria [ED431F 2016/016]
Ten-eleven translocation (TET) proteins play key roles in the regulation of DNA-methylation status by oxidizing 5-methylcytosine (5mC) to generate 5-hydroxymethylcytosine (5hmC), which can both serve as a stable epigenetic mark and participate in active demethylation. Unlike the other members of the TET family, TET2 does not contain a DNA-binding domain, and it remains unclear how it is recruited to chromatin. Here we show that TET2 is recruited by the RNA-binding protein Paraspeckle component 1 (PSPC1) through transcriptionally active loci, including endogenous retroviruses (ERVs) whose long terminal repeats (LTRs) have been co-opted by mammalian genomes as stage-and tissue-specific transcriptional regulatory modules. We found that PSPC1 and TET2 contribute to ERVL and ERVL-associated gene regulation by both transcriptional repression via histone deacetylases and post-transcriptional destabilization of RNAs through 5hmC modification. Our findings provide evidence for a functional role of transcriptionally active ERVs as specific docking sites for RNA epigenetic modulation and gene regulation.
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