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  MOF-associated complexes ensure stem cell identity and Xist repression

Chelmicki, T., Dündar, F., Turley, M. J., Khanam, T., Aktas, T., Ramírez, F., et al. (2014). MOF-associated complexes ensure stem cell identity and Xist repression. eLife, 3, e02024.

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https://www.ncbi.nlm.nih.gov/pubmed/24842875 (Publisher version)
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 Creators:
Chelmicki, Tomasz1, Author
Dündar, Friederike1, Author              
Turley, Matthew James1, Author
Khanam, Tasneem1, Author
Aktas, Tugce2, Author
Ramírez, Fidel2, Author
Gendrel, Anne-Valerie2, Author
Wright, Patrick Rudolf2, Author
Videm, Pavankumar2, Author
Backofen, Rolf2, Author
Heard, Edith2, Author
Manke, Thomas1, Author              
Akhtar, Asifa1, Author              
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1Department of Epigenetics, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243644              
2External Organizations, ou_persistent22              

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 Abstract: Histone acetyl transferases (HATs) play distinct roles in many cellular processes and are frequently misregulated in cancers. Here, we study the regulatory potential of MYST1-(MOF)-containing MSL and NSL complexes in mouse embryonic stem cells (ESCs) and neuronal progenitors. We find that both complexes influence transcription by targeting promoters and TSS-distal enhancers. In contrast to flies, the MSL complex is not exclusively enriched on the X chromosome, yet it is crucial for mammalian X chromosome regulation as it specifically regulates Tsix, the major repressor of Xist lncRNA. MSL depletion leads to decreased Tsix expression, reduced REX1 recruitment, and consequently, enhanced accumulation of Xist and variable numbers of inactivated X chromosomes during early differentiation. The NSL complex provides additional, Tsix-independent repression of Xist by maintaining pluripotency. MSL and NSL complexes therefore act synergistically by using distinct pathways to ensure a fail-safe mechanism for the repression of X inactivation in ESCs.

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Language(s): eng - English
 Dates: 2014
 Publication Status: Published in print
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 Rev. Type: Peer
 Identifiers: eDoc: 701055
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Title: eLife
Source Genre: Journal
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Pages: - Volume / Issue: 3 Sequence Number: - Start / End Page: e02024 Identifier: -