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Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a

Author

Listed:
  • Kun-Yong Kim

    (Yale School of Medicine)

  • Yoshiaki Tanaka

    (Yale School of Medicine)

  • Juan Su

    (Yale School of Medicine
    the Second Military Medical University)

  • Bilal Cakir

    (Yale School of Medicine)

  • Yangfei Xiang

    (Yale School of Medicine)

  • Benjamin Patterson

    (Yale School of Medicine)

  • Junjun Ding

    (Icahn School of Medicine at Mount Sinai)

  • Yong-Wook Jung

    (CHA University)

  • Ji-Hyun Kim

    (Yale School of Medicine)

  • Eriona Hysolli

    (Yale School of Medicine)

  • Haelim Lee

    (Yale School of Medicine)

  • Rana Dajani

    (Hashemite University
    Harvard University)

  • Jonghwan Kim

    (the University of Texas at Austin)

  • Mei Zhong

    (Yale School of Medicine)

  • Jeong-Heon Lee

    (Indiana University-Purdue University Indianapolis)

  • David Skalnik

    (Indiana University-Purdue University Indianapolis)

  • Jeong Mook Lim

    (Seoul National University)

  • Gareth J. Sullivan

    (University of Oslo
    Oslo University Hospital and University of Oslo)

  • Jianlong Wang

    (Icahn School of Medicine at Mount Sinai)

  • In-Hyun Park

    (Yale School of Medicine)

Abstract

Embryonic stem cells (ESCs) maintain pluripotency through unique epigenetic states. When ESCs commit to a specific lineage, epigenetic changes in histones and DNA accompany the transition to specialized cell types. Investigating how epigenetic regulation controls lineage specification is critical in order to generate the required cell types for clinical applications. Uhrf1 is a widely known hemi-methylated DNA-binding protein, playing a role in DNA methylation through the recruitment of Dnmt1 and in heterochromatin formation alongside G9a, Trim28, and HDACs. Although Uhrf1 is not essential in ESC self-renewal, it remains elusive how Uhrf1 regulates cell specification. Here we report that Uhrf1 forms a complex with the active trithorax group, the Setd1a/COMPASS complex, to maintain bivalent histone marks, particularly those associated with neuroectoderm and mesoderm specification. Overall, our data demonstrate that Uhrf1 safeguards proper differentiation via bivalent histone modifications.

Suggested Citation

  • Kun-Yong Kim & Yoshiaki Tanaka & Juan Su & Bilal Cakir & Yangfei Xiang & Benjamin Patterson & Junjun Ding & Yong-Wook Jung & Ji-Hyun Kim & Eriona Hysolli & Haelim Lee & Rana Dajani & Jonghwan Kim & Me, 2018. "Uhrf1 regulates active transcriptional marks at bivalent domains in pluripotent stem cells through Setd1a," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04818-0
    DOI: 10.1038/s41467-018-04818-0
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