Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41467-020-14621-5
Title: Cis- and trans-regulations of pre-mRNA splicing by RNA editing enzymes influence cancer development
Authors: Tang, Sze Jing 
Shen, Haoqing
An, Omer 
Hong, HuiQi 
Li, Jia 
Song, Yangyang 
Han, Jian 
Tay, Daryl Jin Tai 
Ng, Vanessa Hui En 
Bellido Molias, Fernando 
Leong, Ka Wai 
Pitcheshwar, Priyankaa
Yang, Henry 
Chen, Leilei 
Keywords: Science & Technology
Multidisciplinary Sciences
Science & Technology - Other Topics
TO-INOSINE RNA
ADENOSINE DEAMINASES
GLUR-B
BINDING
ADARS
GENE
TRANSCRIPTOME
COMPETITION
POSITION
EVENTS
Issue Date: 7-Feb-2020
Publisher: NATURE PUBLISHING GROUP
Citation: Tang, Sze Jing, Shen, Haoqing, An, Omer, Hong, HuiQi, Li, Jia, Song, Yangyang, Han, Jian, Tay, Daryl Jin Tai, Ng, Vanessa Hui En, Bellido Molias, Fernando, Leong, Ka Wai, Pitcheshwar, Priyankaa, Yang, Henry, Chen, Leilei (2020-02-07). Cis- and trans-regulations of pre-mRNA splicing by RNA editing enzymes influence cancer development. NATURE COMMUNICATIONS 11 (1). ScholarBank@NUS Repository. https://doi.org/10.1038/s41467-020-14621-5
Abstract: © 2020, The Author(s). RNA editing and splicing are the two major processes that dynamically regulate human transcriptome diversity. Despite growing evidence of crosstalk between RNA editing enzymes (mainly ADAR1) and splicing machineries, detailed mechanistic explanations and their biological importance in diseases, such as cancer are still lacking. Herein, we identify approximately a hundred high-confidence splicing events altered by ADAR1 and/or ADAR2, and ADAR1 or ADAR2 protein can regulate cassette exons in both directions. We unravel a binding tendency of ADARs to dsRNAs that involves GA-rich sequences for editing and splicing regulation. ADAR1 edits an intronic splicing silencer, leading to recruitment of SRSF7 and repression of exon inclusion. We also present a mechanism through which ADAR2 binds to dsRNA formed between GA-rich sequences and polypyrimidine (Py)-tract and precludes access of U2AF65 to 3′ splice site. Furthermore, we find these ADARs-regulated splicing changes per se influence tumorigenesis, not merely byproducts of ADARs editing and binding.
Source Title: NATURE COMMUNICATIONS
URI: https://scholarbank.nus.edu.sg/handle/10635/168507
ISSN: 2041-1723
DOI: 10.1038/s41467-020-14621-5
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