@article{Chelmicki_Dundar_Turley-MOF_compl_ensur-2014,
author = {Chelmicki, Tomasz and Dundar, Friederike and Turley, 
          Matthew and Khanam, Tasneem and Aktas, Tugce and Ramirez, 
          Fidel and Gendrel, Anne-Valerie and Wright, Patrick R. and 
          Videm, Pavankumar and Backofen, Rolf and Heard, Edith and 
          Manke, Thomas and Akhtar, Asifa},
title = {{MOF}-associated complexes ensure stem cell identity and 
         {Xist} repression},
journal = {Elife},
year = {2014},
doi = {10.7554/eLife.02024},
volume = {3},
user = {backofen},
pmid = {24842875},
pages = {e02024},
number = {},
issn = {2050-084X},
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 as well as 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.}
}