Kyungjin Boo1,*, Jinhyuk Bhin2,*, Yoon Jeon3, Joomyung Kim1, Hi-Jai R. Shin1, Jong-Eun Park4, Kyeongkyu Kim1, Chang Rok Kim1, Hyonchol Jang3, In-Hoo Kim3, V. Narry Kim4, Daehee Hwang2,5, Ho Lee3 & Sung Hee Baek1
1 Creative Research Initiative Center for Chromatin Dynamics, School of Biological Sciences, Seoul National University, Seoul 151-742, South Korea. 2 Department of Chemical Engineering, POSTECH, Pohang 790-784, South Korea. 3 Research Institute, Graduate School of Cancer Science and Policy, National Cancer Center, Gyeonggi-do 410-769, South Korea. 4 Institute for Basic Science, School of Biological Sciences, Seoul National University, Seoul 151-742, South Korea. 5 Department of New Biology and Center for Plant Aging Research, Institute for Basic Science, DGIST, Daegu 711-873, South Korea.
* These authors contributed equally to this work.
Correspondence to : Daehee Hwang or Ho Lee or Sung Hee Baek
The actions of transcription factors, chromatin modifiers and noncoding RNAs are crucial for the programming of cell states. Although the importance of various epigenetic machineries for controlling pluripotency of embryonic stem (ES) cells has been previously studied, how chromatin modifiers cooperate with specific transcription factors still remains largely elusive. Here, we find that Pontin chromatin remodelling factor plays an essential role as a coactivator for Oct4 for maintenance of pluripotency in mouse ES cells. Genome-wide analyses reveal that Pontin and Oct4 share a substantial set of target genes involved in ES cell maintenance. Intriguingly, we find that the Oct4-dependent coactivator function of Pontin extends to the transcription of large intergenic noncoding RNAs (lincRNAs) and in particular linc1253, a lineage programme repressing lincRNA, is a Pontin-dependent Oct4 target lincRNA. Together, our findings demonstrate that the Oct4-Pontin module plays critical roles in the regulation of genes involved in ES cell fate determination.