Cell Reports (Nov 2017)

Kdm2b Regulates Somatic Reprogramming through Variant PRC1 Complex-Dependent Function

  • Zhiwei Zhou,
  • Xuejie Yang,
  • Jiangping He,
  • Jing Liu,
  • Fang Wu,
  • Shengyong Yu,
  • Yuting Liu,
  • Runxia Lin,
  • He Liu,
  • Yuanbin Cui,
  • Chunhua Zhou,
  • Xiaoshan Wang,
  • Jian Wu,
  • Shangtao Cao,
  • Lin Guo,
  • Lihui Lin,
  • Tao Wang,
  • Xiaozhong Peng,
  • Boqing Qiang,
  • Andrew P. Hutchins,
  • Duanqing Pei,
  • Jiekai Chen

DOI
https://doi.org/10.1016/j.celrep.2017.10.091
Journal volume & issue
Vol. 21, no. 8
pp. 2160 – 2170

Abstract

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Polycomb repressive complex 1 (PRC1) plays essential roles in cell-fate determination. Recent studies have found that the composition of mammalian PRC1 is particularly varied and complex; however, little is known about the functional consequences of these variant PRC1 complexes on cell-fate determination. Here, we show that Kdm2b promotes Oct4-induced somatic reprogramming through recruitment of a variant PRC1 complex (PRC1.1) to CpG islands (CGIs). Furthermore, we find that bone morphogenetic protein (BMP) represses Oct4/Kdm2b-induced somatic reprogramming selectively. Mechanistically, BMP-SMAD pathway attenuates PRC1.1 occupation and H2AK119 ubiquitination at genes linked to development, resulting in the expression of mesendodermal factors such as Sox17 and a consequent suppression of somatic reprogramming. These observations reveal that PRC1.1 participates in the establishment of pluripotency and identify BMP4 signaling as a modulator of PRC1.1 function.

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