scholarly journals X-chromosome epigenetic reprogramming in pluripotent stem cells via noncoding genes

2011 ◽  
Vol 22 (4) ◽  
pp. 336-342 ◽  
Author(s):  
Daniel H. Kim ◽  
Yesu Jeon ◽  
Montserrat C. Anguera ◽  
Jeannie T. Lee
2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Antonia A. Dominguez ◽  
H. Rosaria Chiang ◽  
Meena Sukhwani ◽  
Kyle E. Orwig ◽  
Renee A. Reijo Pera

Development ◽  
2016 ◽  
Vol 143 (16) ◽  
pp. 2958-2964 ◽  
Author(s):  
Shin Kobayashi ◽  
Yusuke Hosoi ◽  
Hirosuke Shiura ◽  
Kazuo Yamagata ◽  
Saori Takahashi ◽  
...  

2020 ◽  
Vol 14 (5) ◽  
pp. 745-754 ◽  
Author(s):  
Susmita Mandal ◽  
Deepshikha Chandel ◽  
Harman Kaur ◽  
Sudeshna Majumdar ◽  
Maniteja Arava ◽  
...  

2017 ◽  
Vol 4 (7) ◽  
pp. 54-54 ◽  
Author(s):  
Shafqat A. Khan ◽  
Pauline N. C. B. Audergon ◽  
Bernhard Payer

2012 ◽  
Vol 371 (2) ◽  
pp. 146-155 ◽  
Author(s):  
Masahito Tachibana ◽  
Hong Ma ◽  
Michelle L. Sparman ◽  
Hyo-Sang Lee ◽  
Cathy M. Ramsey ◽  
...  

2018 ◽  
Author(s):  
Juan Song ◽  
Adrian Janiszewski ◽  
Natalie De Geest ◽  
Lotte Vanheer ◽  
Irene Talon ◽  
...  

ABSTRACTDuring early mammalian development, the two X-chromosomes in female cells are active. Dosage compensation between XX female and XY male cells is then achieved by X-chromosome inactivation in female cells. Reprogramming female mouse somatic cells into induced pluripotent stem cells (iPSCs) leads to X-chromosome reactivation. The extent to which increased X-chromosome dosage (X-dosage) in female iPSCs leads to differences in the molecular and cellular properties of XX and XY iPSCs is still unclear. We show that chromatin accessibility in mouse iPSCs is modulated by X-dosage. Specific sets of transcriptional regulator motifs are enriched in chromatin with increased accessibility in XX or XY iPSCs. We show that the transcriptome, growth and pluripotency exit are also modulated by X-dosage in iPSCs. To understand the mechanisms by which increased X-dosage modulates the molecular and cellular properties of mouse pluripotent stem cells, we used heterozygous deletions of the X-linked gene Dusp9 in XX embryonic stem cells. We show that X-dosage regulates the transcriptome, open chromatin landscape, growth and pluripotency exit largely independently of global DNA methylation. Our results uncover new insights into X-dosage in pluripotent stem cells, providing principles of how gene dosage modulates the epigenetic and genetic mechanisms regulating cell identity.


2020 ◽  
Vol 160 (6) ◽  
pp. 283-294 ◽  
Author(s):  
Paola Rebuzzini ◽  
Maurizio Zuccotti ◽  
Silvia Garagna

X dosage compensation between XX female and XY male mammalian cells is achieved by a process known as X-chromosome inactivation (XCI). XCI initiates early during preimplantation development in female cells, and it is subsequently stably maintained in somatic cells. However, XCI is a reversible process that occurs in vivo in the inner cell mass of the blastocyst, in primordial germ cells or in spermatids during reprogramming. Erasure of transcriptional gene silencing can occur though a mechanism named X-chromosome reactivation (XCR). XCI and XCR have been substantially deciphered in the mouse, whereas they still remain debated in the human. In this review, we summarized the recent advances in the knowledge of X-linked gene dosage compensation during mouse and human preimplantation development and in pluripotent stem cells.


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