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Cell Rep. 2015 Jan 6;10(1):20-8. doi: 10.1016/j.celrep.2014.12.004. Epub 2014 Dec 24.

TRIM28 represses transcription of endogenous retroviruses in neural progenitor cells.

Author information

1
Laboratory of Molecular Neurogenetics, Department of Experimental Medical Science, Wallenberg Neuroscience Center and Lund Stem Cell Center, Lund University, 221 84 Lund, Sweden.
2
School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.
3
Science for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, 751 23 Uppsala, Sweden.
4
IRCM, Institut de Recherche en Cancérologie de Montpellier, INSERM, U896, Université Montpellier; Institut Régional du Cancer Montpellier, Montpellier 34298, France.
5
Laboratory of Molecular Neurogenetics, Department of Experimental Medical Science, Wallenberg Neuroscience Center and Lund Stem Cell Center, Lund University, 221 84 Lund, Sweden. Electronic address: johan.jakobsson@med.lu.se.

Abstract

TRIM28 is a corepressor that mediates transcriptional silencing by establishing local heterochromatin. Here, we show that deletion of TRIM28 in neural progenitor cells (NPCs) results in high-level expression of two groups of endogenous retroviruses (ERVs): IAP1 and MMERVK10C. We find that NPCs use TRIM28-mediated histone modifications to dynamically regulate transcription and silencing of ERVs, which is in contrast to other somatic cell types using DNA methylation. We also show that derepression of ERVs influences transcriptional dynamics in NPCs through the activation of nearby genes and the expression of long noncoding RNAs. These findings demonstrate a unique dynamic transcriptional regulation of ERVs in NPCs. Our results warrant future studies on the role of ERVs in the healthy and diseased brain.

PMID:
25543143
PMCID:
PMC4434221
DOI:
10.1016/j.celrep.2014.12.004
[Indexed for MEDLINE]
Free PMC Article

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