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An Assay for Quantifying Protein-RNA Binding in Bacteria
Published on: June 12, 2019
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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.
Biorxiv : the Preprint Server for Biology
|November 24, 2025
Summary
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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