scholarly journals Going retro: Transposable elements, embryonic stem cells, and the mammalian placenta (retrospective on DOI 10.1002/bies.201300059)

BioEssays ◽  
2015 ◽  
Vol 37 (11) ◽  
pp. 1154-1154 ◽  
Author(s):  
David Haig
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Transposable Elements ◽  
Embryonic Stem

Transposable elements have rewired the core regulatory network of human embryonic stem cells

2010 ◽  
Vol 42 (7) ◽  
pp. 631-634 ◽  
Author(s):  
Galih Kunarso ◽  
Na-Yu Chia ◽  
Justin Jeyakani ◽  
Catalina Hwang ◽  
Xinyi Lu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Transposable Elements ◽  
Human Embryonic Stem Cells ◽  
Regulatory Network ◽  
Embryonic Stem ◽  
The Core

scholarly journals Functional dissection of the enhancer repertoire in human embryonic stem cells

2017 ◽  
Author(s):  
Tahsin Stefan Barakat ◽  
Florian Halbritter ◽  
Man Zhang ◽  
André F. Rendeiro ◽  
Christoph Bock ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Transposable Elements ◽  
Histone Modifications ◽  
Human Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Housekeeping Genes ◽  
List Type ◽  
Enhancer Activity ◽  
Enhancer Function

SummaryEnhancers are genetic elements that regulate spatiotemporal gene expression. Enhancer function requires transcription factor (TF) binding and correlates with histone modifications. However, the extent to which TF binding and histone modifications can functionally define active enhancers remains unclear. Here we combine chromatin immunoprecipitation with a massively parallel reporter assay to identify functional enhancers in human embryonic stem cells (hESCs) genome-wide in a quantitative unbiased manner. While active enhancers associate with TFs, only a minority of regions marked by NANOG, OCT4, H3K27ac and H3K4me1 function as enhancers, with activity changing markedly with culture conditions. Our analysis also reveals a novel enhancer set associated with housekeeping genes. Moreover, while transposable elements associate with putative enhancers only some exhibit activity. Similarly, within super-enhancers, large tracts are non-functional, with activity restricted to small sub-domains. This catalogue of validated enhancers provides a valuable resource for further functional dissection of the regulatory genome.HighlightsA catalog of functional enhancers in hESCs including a novel housekeeping classActive enhancers feature specific transcription factors and transposable elementsMajor shifts in enhancer activity occur during induction of naive pluripotencySuper-enhancers consist of small units with enhancer function

scholarly journals Endogenous retroviruses co-opted into divergently transcribed regulatory elements shape the regulatory landscape of embryonic stem cells

2021 ◽  
Author(s):  
Stylianos Bakoulis ◽  
Robert Krautz ◽  
Nicolas Alcaraz ◽  
Marco Salvatore ◽  
Robin Andersson
Keyword(s):  
Stem Cells ◽  
Transcription Factors ◽  
Embryonic Stem Cells ◽  
Transposable Elements ◽  
Embryonic Stem ◽  
Regulatory Elements ◽  
Endogenous Retroviruses ◽  
Gene Promoters ◽  
Specific Regulation ◽  
Regulatory Landscape

Transcription factor binding to regulatory elements is the key process underlying gene regulation during cellular differentiation. Although the specific regulation of genes by transcription factors is generally conserved, regulatory elements themselves are associated with high evolutionary turnover, a process that has been attributed to transposable elements. However, it is unclear how frequent co-option of transposable elements into regulatory elements is and to which regulatory programs they contribute. Here, we report an in-depth characterization of the transposon-derived regulatory landscape of mouse embryonic stem cells. We demonstrate that a substantial number of endogenous retroviral elements are divergently transcribed into unstable RNAs, and that these elements contribute to a sizable proportion of active enhancers and gene promoters. We further show that transposon subfamilies contribute to specific regulatory programs through their enrichment of binding sites for transcription factors, shedding light on the formation of regulatory programs and the origins of regulatory elements.

scholarly journals Enrichment of Short interspersed transposable elements (SINEs) in hypomethylated genic regions in embryonic stem cells

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Hiroki Muramoto ◽  
Shintaro Yagi ◽  
Keiji Hirabayashi ◽  
Shinya Sato ◽  
Jun Ohgane ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Transposable Elements ◽  
Embryonic Stem

scholarly journals The role of MORC3 in silencing transposable elements in mouse embryonic stem cells

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Varsha P. Desai ◽  
Jihed Chouaref ◽  
Haoyu Wu ◽  
William A. Pastor ◽  
Ryan L. Kan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Transposable Elements ◽  
Embryonic Stem ◽  
Chromatin Accessibility ◽  
Mouse Embryonic Stem Cells ◽  
Endogenous Retroviruses ◽  
Direct Role ◽  
Developmental Abnormalities

Abstract Background Microrchidia proteins (MORCs) are involved in epigenetic gene silencing in a variety of eukaryotic organisms. Deletion of MORCs result in several developmental abnormalities and their dysregulation has been implicated in developmental disease and multiple cancers. Specifically, mammalian MORC3 mutations are associated with immune system defects and human cancers such as bladder, uterine, stomach, lung, and diffuse large B cell lymphomas. While previous studies have shown that MORC3 binds to H3K4me3 in vitro and overlaps with H3K4me3 ChIP-seq peaks in mouse embryonic stem cells, the mechanism by which MORC3 regulates gene expression is unknown. Results In this study, we identified that mutation in Morc3 results in a suppressor of variegation phenotype in a Modifiers of murine metastable epialleles Dominant (MommeD) screen. We also find that MORC3 functions as an epigenetic silencer of transposable elements (TEs) in mouse embryonic stem cells (mESCs). Loss of Morc3 results in upregulation of TEs, specifically those belonging to the LTR class of retrotransposons also referred to as endogenous retroviruses (ERVs). Using ChIP-seq we found that MORC3, in addition to its known localization at H3K4me3 sites, also binds to ERVs, suggesting a direct role in regulating their expression. Previous studies have shown that these ERVs are marked by the repressive histone mark H3K9me3 which plays a key role in their silencing. However, we found that levels of H3K9me3 showed only minor losses in Morc3 mutant mES cells. Instead, we found that loss of Morc3 resulted in increased chromatin accessibility at ERVs as measured by ATAC-seq. Conclusions Our results reveal MORC3 as a novel regulator of ERV silencing in mouse embryonic stem cells. The relatively minor changes of H3K9me3 in the Morc3 mutant suggests that MORC3 acts mainly downstream of, or in a parallel pathway with, the TRIM28/SETDB1 complex that deposits H3K9me3 at these loci. The increased chromatin accessibility of ERVs in the Morc3 mutant suggests that MORC3 may act at the level of chromatin compaction to effect TE silencing.

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