scholarly journals Transposable Elements and DNA Methylation Create in Embryonic Stem Cells Human-Specific Regulatory Sequences Associated with Distal Enhancers and Noncoding RNAs

2015 ◽  
Vol 7 (6) ◽  
pp. 1432-1454 ◽  
Author(s):  
Gennadi V. Glinsky
Nature ◽  
2016 ◽  
Vol 532 (7599) ◽  
pp. 329-333 ◽  
Author(s):  
Tao P. Wu ◽  
Tao Wang ◽  
Matthew G. Seetin ◽  
Yongquan Lai ◽  
Shijia Zhu ◽  
...  

2021 ◽  
Author(s):  
Antoine Canat ◽  
Adeline Veillet ◽  
Robert Illingworth ◽  
Emmanuelle Fabre ◽  
Pierre Therizols

AbstractDNA methylation is essential for heterochromatin formation and repression of DNA repeat transcription, both of which are essential for genome integrity. Loss of DNA methylation is associated with disease, including cancer, but is also required for development. Alternative pathways to maintain heterochromatin are thus needed to limit DNA damage accumulation. Here, we find that DAXX, an H3.3 chaperone, protects pericentromeric heterochromatin and is essential for embryonic stem cells (ESCs) maintenance in the ground-state of pluripotency. Upon DNA demethylation-mediated damage, DAXX relocalizes to pericentromeric regions, and recruits PML and SETDB1, thereby promoting heterochromatin formation. In the absence of DAXX, the 3D-architecture and physical properties of pericentric heterochromatin are disrupted, resulting in derepression of major satellite DNA. Using epigenome editing tools, we demonstrate that H3.3, and specifically H3.3K9 modification, directly contribute to maintaining pericentromeric chromatin conformation. Altogether, our data reveal that DAXX and H3.3 unite DNA damage response and heterochromatin maintenance in ESCs.


2018 ◽  
Vol 32 (19-20) ◽  
pp. 1358-1358
Author(s):  
Ayala Tovy ◽  
Adam Spiro ◽  
Ryan McCarthy ◽  
Zohar Shipony ◽  
Yael Aylon ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Soonbong Baek ◽  
Hwan Choi ◽  
Hanseul Park ◽  
Byunguk Cho ◽  
Siyoung Kim ◽  
...  

2014 ◽  
Vol 139 (1) ◽  
pp. 142-161 ◽  
Author(s):  
Marie-Claude Senut ◽  
Arko Sen ◽  
Pablo Cingolani ◽  
Asra Shaik ◽  
Susan J. Land ◽  
...  

2012 ◽  
Vol 31 (6) ◽  
pp. 893-907 ◽  
Author(s):  
Albert G. Tsai ◽  
Debbie M. Chen ◽  
Mayin Lin ◽  
John C. F. Hsieh ◽  
Cindy Y. Okitsu ◽  
...  

Blood ◽  
2003 ◽  
Vol 102 (4) ◽  
pp. 1531-1533 ◽  
Author(s):  
Zhi Hong Lu ◽  
Jason T. Books ◽  
Richard M. Kaufman ◽  
Timothy J. Ley

Abstract The correction of mutant β-globin genes has long been a therapeutic goal for patients with β-thalassemia or hemoglobinopathies. The use of homologous recombination (HR) to achieve this goal is an attractive approach because it eliminates the need to include regulatory sequences in the therapeutic construct, and it eliminates mutagenesis induced by random integration. However, HR is a very inefficient process for gene correction, and its efficiency is probably locus dependent. The length of targeting arms is thought to be a determinant of targeting efficiency, so we compared the ability of standard (8-kb) versus very long (16-, 24-, and 110-kb) regions of homology to correct a mutant murine β-globin gene in embryonic stem cells. Increasing the length of the targeting sequences did not increase the efficiency of HR in this locus, suggesting that alternative approaches will be required to improve the efficiency of this approach for globin gene correction.


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