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Kdm2b Regulates Somatic Reprogramming through Variant PRC1 Complex-Dependent Function.

Zhiwei Zhou1, Xuejie Yang1, Jiangping He2

  • 1CAS Key Laboratory of Regenerative Biology, Joint School of Life Sciences, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China; Guangzhou Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou 510530, China; University of Chinese Academy of Sciences, Beijing 100049, China.

Cell Reports
|November 23, 2017
PubMed
Summary
This summary is machine-generated.

Kdm2b recruits Polycomb repressive complex 1.1 (PRC1.1) to CpG islands, promoting somatic cell reprogramming. Bone morphogenetic protein (BMP) signaling represses this process by reducing PRC1.1 activity.

Keywords:
BMP signalingKdm2bPRC1Polycomb repressive complex 1epigenetic regulationiPSpluripotencyreprogrammingvariant PRC1

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Area of Science:

  • Epigenetics and developmental biology
  • Cellular reprogramming and differentiation

Background:

  • Polycomb repressive complex 1 (PRC1) is crucial for cell-fate determination.
  • Mammalian PRC1 exhibits diverse compositions, but the functional impact of variant PRC1 complexes on cell fate remains unclear.

Purpose of the Study:

  • To investigate the role of Kdm2b and variant PRC1 complexes in Oct4-induced somatic reprogramming.
  • To elucidate the mechanism by which bone morphogenetic protein (BMP) signaling influences somatic reprogramming.

Main Methods:

  • Investigated Kdm2b's role in recruiting variant PRC1 complexes (PRC1.1) to CpG islands (CGIs).
  • Analyzed the effect of BMP signaling on Oct4/Kdm2b-induced reprogramming.
  • Examined the impact of the BMP-SMAD pathway on PRC1.1 occupation and H2AK119 ubiquitination at developmental genes.

Main Results:

  • Kdm2b promotes Oct4-induced somatic reprogramming via PRC1.1 recruitment to CGIs.
  • BMP signaling selectively represses Oct4/Kdm2b-induced reprogramming.
  • BMP-SMAD signaling reduces PRC1.1 occupation and H2AK119 ubiquitination, leading to mesendodermal gene expression (e.g., Sox17) and suppressed reprogramming.

Conclusions:

  • PRC1.1 is involved in establishing pluripotency.
  • BMP4 signaling modulates PRC1.1 function, impacting somatic cell reprogramming and pluripotency maintenance.