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Ebola Virus GP Gene Polyadenylation Versus RNA Editing
Valentina A Volchkova1, Jaroslav Vorac1, Laurie Repiquet-Paire1
1Molecular Basis of Viral Pathogenicity, CIRI, INSERM, U1111-CNRS UMR5308, Université de Lyon, Université Claude Bernard Lyon 1, Ecole Normale Supérieure de Lyon, France.
The Journal of Infectious Diseases
|April 4, 2015
Summary
Ebola virus (EBOV) RNA editing creates truncated surface glycoprotein (GP) mRNA. This non-stop mRNA is surprisingly stable, impacting EBOV replication and pathogenicity.
Area of Science:
- Virology
- Molecular Biology
- Genetics
Background:
- Ebola virus (EBOV) surface glycoprotein (GP) synthesis relies on RNA editing.
- Previous understanding suggested standard mRNA processing pathways.
Purpose of the Study:
- To investigate the nature and implications of a shorter GP mRNA species observed during EBOV infection.
- To understand the regulatory mechanisms of EBOV surface GP expression.
Main Methods:
- Northern blot analysis of EBOV-infected cells.
- Sequence analysis of synthesized RNA species.
- In cellulo protein synthesis assays.
Main Results:
- A truncated, non-stop GP mRNA constitutes over 40% of total GP mRNA.
- This non-stop mRNA is polyadenylated at the editing site.
- Non-stop GP mRNA exhibits stability comparable to stop codon-containing mRNA, challenging non-stop decay theories.
- Protein synthesis from this truncated mRNA is tightly regulated and largely absent.
Conclusions:
- The EBOV RNA editing site acts as a cryptic transcription termination/polyadenylation site.
- This site rarely facilitates surface GP expression, indicating significant downregulation.
- These findings highlight the critical role of GP gene editing in EBOV replication and pathogenicity.
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