scholarly journals microRNAs as novel regulators of stem cell pluripotency and somatic cell reprogramming

BioEssays ◽  
2012 ◽  
Vol 34 (8) ◽  
pp. 670-680 ◽  
Author(s):  
Meng Amy Li ◽  
Lin He
EMBO Reports ◽  
2011 ◽  
Vol 12 (7) ◽  
pp. 720-726 ◽  
Author(s):  
Torben Redmer ◽  
Sebastian Diecke ◽  
Tamara Grigoryan ◽  
Angel Quiroga‐Negreira ◽  
Walter Birchmeier ◽  
...  

2017 ◽  
Vol 8 (5) ◽  
pp. 1366-1378 ◽  
Author(s):  
Christiana Hadjimichael ◽  
Konstantina Chanoumidou ◽  
Christoforos Nikolaou ◽  
Antonios Klonizakis ◽  
Gesthimani-Ioanna Theodosi ◽  
...  

2012 ◽  
Vol 72 (21) ◽  
pp. 5635-5645 ◽  
Author(s):  
Lan Yi ◽  
Chiwei Lu ◽  
Wenwei Hu ◽  
Yvonne Sun ◽  
Arnold J. Levine

2013 ◽  
Vol 13 (6) ◽  
pp. 676-690 ◽  
Author(s):  
Li Wang ◽  
Yi-Liang Miao ◽  
Xiaofeng Zheng ◽  
Brad Lackford ◽  
Bingying Zhou ◽  
...  

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Agnes Fütterer ◽  
Amaia Talavera-Gutiérrez ◽  
Tirso Pons ◽  
Jesús de Celis ◽  
Julio Gutiérrez ◽  
...  

AbstractEmbryonic stem cell (ESC) differentiation and somatic cell reprogramming are biological processes governed by antagonistic expression or repression of a largely common set of genes. Accurate regulation of gene expression is thus essential for both processes, and alterations in RNA processing are predicted to negatively affect both. We show that truncation of the DIDO gene alters RNA splicing and transcription termination in ESC and mouse embryo fibroblasts (MEF), which affects genes involved in both differentiation and reprogramming. We combined transcriptomic, protein interaction, and cellular studies to identify the underlying molecular mechanism. We found that DIDO3 interacts with the helicase DHX9, which is involved in R-loop processing and transcription termination, and that DIDO3-exon16 deletion increases nuclear R-loop content and causes DNA replication stress. Overall, these defects result in failure of ESC to differentiate and of MEF to be reprogrammed. MEF immortalization restored impaired reprogramming capacity. We conclude that DIDO3 has essential functions in ESC differentiation and somatic cell reprogramming by supporting accurate RNA metabolism, with its exon16-encoded domain playing the main role.


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