An NS-segment exonic splicing enhancer regulates influenza A virus replication in mammalian cells

Xiaofeng Huang, Min Zheng, Pui Wang, Bobo Wing-Yee Mok, Siwen Liu, Siu-Ying Lau, Pin Chen, Yen-Chin Liu, Honglian Liu, Yixin Chen, Wenjun Song, Kwok-Yung Yuen and Honglin Chen ()
Additional contact information
Xiaofeng Huang: State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong
Min Zheng: State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong
Pui Wang: State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong
Bobo Wing-Yee Mok: State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong
Siwen Liu: State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong
Siu-Ying Lau: State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong
Pin Chen: State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong
Yen-Chin Liu: State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong
Honglian Liu: State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong
Yixin Chen: National Institute of Diagnostics and Vaccine Development in Infectious Diseases, State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University
Wenjun Song: State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong
Kwok-Yung Yuen: State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong
Honglin Chen: State Key Laboratory for Emerging Infectious Diseases, The University of Hong Kong

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Influenza virus utilizes host splicing machinery to process viral mRNAs expressed from both M and NS segments. Through genetic analysis and functional characterization, we here show that the NS segment of H7N9 virus contains a unique G540A substitution, located within a previously undefined exonic splicing enhancer (ESE) motif present in the NEP mRNA of influenza A viruses. G540A supports virus replication in mammalian cells while retaining replication ability in avian cells. Host splicing regulator, SF2, interacts with this ESE to regulate splicing of NEP/NS1 mRNA and G540A substitution affects SF2–ESE interaction. The NS1 protein directly interacts with SF2 in the nucleus and modulates splicing of NS mRNAs during virus replication. We demonstrate that splicing of NEP/NS1 mRNA is regulated through a cis NEP-ESE motif and suggest a unique NEP-ESE may contribute to provide H7N9 virus with the ability to both circulate efficiently in avian hosts and replicate in mammalian cells.

Date: 2017
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms14751 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:8:y:2017:i:1:d:10.1038_ncomms14751

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

DOI: 10.1038/ncomms14751

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 ().