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Updated: Jan 10, 2026
An Assay for Quantifying Protein-RNA Binding in Bacteria
Published on: June 12, 2019
mRNA poly(A)-tail length is a battleground for coronavirus-host competition
Arash Latifkar1,2,3, Yevgen Levdansky4, Amer Balabaki1,2,3
1Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.
Abstract:
Most eukaryotic mRNAs contain a poly(A) tail, which in post-embryonic cells enhances their stability. Many cytoplasmic RNA viruses also harbor poly(A) tails on their genomic RNA and mRNAs. Here, we report that coronavirus infection causes cytoplasmic poly(A)-binding protein (PABPC) activity to become limiting, which preferentially destabilizes short-tailed host mRNAs, occurring before the action of virally encoded mRNA-decay factor nsp1. In this environment hostile to poly(A) tails, viral RNAs maintain a narrow tail-length distribution centering on 70-80 nucleotides across infection cycles. They do this through two mechanisms. First, viral tails are extended during RNA synthesis within double-membrane vesicles; second, viral tails are capped by a complex that includes PABPC1 and CSDE1 and slows tail shortening. Our findings suggest poly(A)-tail length is an arena of host-virus conflict, in which preserving tail lengths of viral mRNAs promotes their cytoplasmic dominance.
Insights
Coronavirus infection limits cytoplasmic poly(A)-binding protein (PABPC) activity, destabilizing host mRNAs. Viral RNAs maintain their poly(A) tail length via extension and capping, ensuring cytoplasmic dominance.
Area of Science:
- Molecular Biology
- Virology
- Cell Biology
Background:
- Eukaryotic mRNAs possess poly(A) tails for stability.
- Cytoplasmic RNA viruses often have poly(A) tails on their RNA.
Purpose of the Study:
- To investigate the impact of coronavirus infection on poly(A) tail dynamics.
- To understand how viral RNAs maintain poly(A) tails during infection.
Main Methods:
- Analysis of host and viral mRNA poly(A) tail lengths during coronavirus infection.
- Investigation of poly(A)-binding protein (PABPC) activity and its role.
- Identification of viral RNA tail-capping mechanisms.
Main Results:
- Coronavirus infection limits PABPC activity, leading to preferential destabilization of short-tailed host mRNAs.
- Viral RNAs maintain a consistent poly(A) tail length (70-80 nucleotides).
- Two mechanisms contribute to viral poly(A) tail maintenance: extension during RNA synthesis and capping by a PABPC1/CSDE1 complex.
Conclusions:
- Poly(A) tail length is a critical battleground in host-virus interactions.
- Viruses actively manage poly(A) tail length to ensure their mRNA stability and cytoplasmic dominance.
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