PHC1 maintains pluripotency by organizing genome-wide chromatin interactions of the Nanog locus

Li Chen, Qiaoqiao Tong, Xiaowen Chen, Penglei Jiang, Hua Yu, Qianbing Zhao, Lingang Sun, Chao Liu, Bin Gu, Yuping Zheng, Lijiang Fei, Xiao Jiang, Wenjuan Li, Giacomo Volpe, Mazid MD. Abdul, Guoji Guo, Jin Zhang, Pengxu Qian, Qiming Sun, Dante Neculai, Miguel A. Esteban, Chen Li (), Feiqiu Wen () and Junfeng Ji ()
Additional contact information
Li Chen: Zhejiang University School of Medicine
Qiaoqiao Tong: Zhejiang University School of Medicine
Xiaowen Chen: Division of Hematology and Oncology, Shenzhen Children’s Hospital
Penglei Jiang: Zhejiang University School of Medicine
Hua Yu: Zhejiang University School of Medicine
Qianbing Zhao: Zhejiang University School of Medicine
Lingang Sun: Zhejiang University School of Medicine
Chao Liu: Zhejiang University School of Medicine
Bin Gu: Hospital for Sick Children
Yuping Zheng: Zhejiang University
Lijiang Fei: Zhejiang University School of Medicine
Xiao Jiang: Zhejiang University School of Medicine
Wenjuan Li: Chinese Academy of Sciences
Giacomo Volpe: Chinese Academy of Sciences
Mazid MD. Abdul: Chinese Academy of Sciences
Guoji Guo: Zhejiang University School of Medicine
Jin Zhang: Zhejiang University School of Medicine
Pengxu Qian: Zhejiang University School of Medicine
Qiming Sun: Zhejiang University School of Medicine
Dante Neculai: Zhejiang University
Miguel A. Esteban: Chinese Academy of Sciences
Chen Li: Zhejiang University School of Medicine
Feiqiu Wen: Division of Hematology and Oncology, Shenzhen Children’s Hospital
Junfeng Ji: Zhejiang University School of Medicine

Nature Communications, 2021, vol. 12, issue 1, 1-13

Abstract: Abstract Polycomb group (PcG) proteins maintain cell identity by repressing gene expression during development. Surprisingly, emerging studies have recently reported that a number of PcG proteins directly activate gene expression during cell fate determination process. However, the mechanisms by which they direct gene activation in pluripotency remain poorly understood. Here, we show that Phc1, a subunit of canonical polycomb repressive complex 1 (cPRC1), can exert its function in pluripotency maintenance via a PRC1-independent activation of Nanog. Ablation of Phc1 reduces the expression of Nanog and overexpression of Nanog partially rescues impaired pluripotency caused by Phc1 depletion. We find that Phc1 interacts with Nanog and activates Nanog transcription by stabilizing the genome-wide chromatin interactions of the Nanog locus. This adds to the already known canonical function of PRC1 in pluripotency maintenance via a PRC1-dependent repression of differentiation genes. Overall, our study reveals a function of Phc1 to activate Nanog transcription through regulating chromatin architecture and proposes a paradigm for PcG proteins to maintain pluripotency.

Date: 2021
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/s41467-021-22871-0 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-22871-0

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-021-22871-0

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().