Zinc Finger RNA-Binding Protein Zn72D Regulates ADAR-Mediated RNA Editing in Neurons

被引:15
作者
Sapiro, Anne L. [1 ]
Freund, Emily C. [1 ]
Restrepo, Lucas [2 ]
Qiao, Huan-Huan [4 ]
Bhate, Amruta [1 ]
Li, Qin [1 ]
Ni, Jian-Quan [3 ]
Mosca, Timothy J. [2 ]
Li, Jin Billy [1 ]
机构
[1] Stanford Univ, Dept Genet, Stanford, CA 94305 USA
[2] Thomas Jefferson Univ, Dept Neurosci, Philadelphia, PA 19107 USA
[3] Tsinghua Univ, Sch Med, Gene Regulatory Lab, Beijing, Peoples R China
[4] Tianjin Univ, Acad Med Engn & Translat Med, Tianjin Key Lab Brain Sci & Neural Engn, Tianjin, Peoples R China
基金
美国国家科学基金会;
关键词
TRANSGENIC RNAI; DROSOPHILA; MELANOGASTER; IDENTIFICATION; ADENOSINE; MUTATIONS; DATABASE; NUCLEAR; BRAINS; SCREEN;
D O I
10.1016/j.celrep.2020.107654
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Adenosine-to-inosine RNA editing, catalyzed by adenosine deaminase acting on RNA (ADAR) enzymes, alters RNA sequences from those encoded by DNA. These editing events are dynamically regulated, but few trans regulators of ADARs are known in vivo. Here, we screen RNA-binding proteins for roles in editing regulation with knockdown experiments in the Drosophila brain. We identify zinc-finger protein at 72D (Zn72D) as a regulator of editing levels at a majority of editing sites in the brain. Zn72D both regulates ADAR protein levels and interacts with ADAR in an RNA-dependent fashion, and similar to ADAR, Zn72D is necessary to maintain proper neuro-muscular junction architecture and fly mobility. Furthermore, Zn72D's regulatory role in RNA editing is conserved because the mammalian homolog of Zn72D, Zfr, regulates editing in mouse primary neurons. The broad and conserved regulation of ADAR editing by Zn72D in neurons sustains critically important editing events.
引用
收藏
页数:18
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