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RNF219 interacts with CCR4–NOT in regulating stem cell differentiation
Hao Du1,† , Chen Chen1,† , Yan Wang1,† , Yang Yang2 , Zhuanzhuan Che1 , Xiaoxu Liu1 , Siyan Meng1 , Chenghao Guo1 , Manman Xu1 , Haitong Fang1 , Fengchao Wang3 , Chengqi Lin1,4,* , Zhuojuan Luo1,4,*
1School of Life Science and Technology, The Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China
2Department of Biological Sciences, Center for Systems Biology, the University of Texas at Dallas, Richardson, TX 75080, USA
3Institute of Combined Injury of PLA, State Key Laboratory of Trauma, Burns and Combined Injury, Army Medical University, Chongqing 400038, China
4Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, China
†These authors contributed equally to this work.
*Correspondence to:Chengqi Lin , Email:cqlin@seu.edu.cn Zhuojuan Luo , Email:zjluo@seu.edu.cn
J Mol Cell Biol, Volume 12, Issue 11, November 2020, 894-905,  https://doi.org/10.1093/jmcb/mjaa061
Keyword: RNF219, CCR4–NOT, protein complex, stem cell differentiation, deadenylation

Regulation of RNA stability plays a crucial role in gene expression control. Deadenylation is the initial rate-limiting step for the majority of RNA decay events. Here, we show that RING finger protein 219 (RNF219) interacts with the CCR4–NOT deadenylase complex. RNF219–CCR4–NOT exhibits deadenylation activity in vitro. RNA-seq analyses identify some of the 2-cell-specific genes and the neuronal genes significantly downregulated upon RNF219 knockdown, while upregulated after depletion of the CCR4–NOT subunit CNOT10 in mouse embryonic stem (ES) cells. RNF219 depletion leads to impaired neuronal lineage commitment during ES cell differentiation. Our study suggests that RNF219 is a novel interacting partner of CCR4–NOT and required for maintenance of ES cell pluripotency.


Volume 12, Issue 11
November 2020