@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},
  volume =	 {3},
  number =	 {},
  pages =	 {e02024},
  user =	 {backofen},
  pmid =	 {24842875},
  doi = 	 {10.7554/eLife.02024},
  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.}
}