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

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, Mei Zhong, Jeong-Heon Lee, David Skalnik, Jeong Mook Lim, Gareth J. Sullivan, Jianlong Wang and In-Hyun Park ()
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Kun-Yong Kim: Yale School of Medicine
Yoshiaki Tanaka: Yale School of Medicine
Juan Su: Yale School of Medicine
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
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
Jianlong Wang: Icahn School of Medicine at Mount Sinai
In-Hyun Park: Yale School of Medicine

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-04818-0

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