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Polyadenylation of ribonucleic acids in mouse L cells infected by encephalomyocarditis virus
Abstract:
Polyadenylation of cytoplasmic RNAs was investigated in L cells infected with encephalomyocarditis virus. During the early stage of infection, the mean size of newly made poly(A) chains attached to cell mRNAs decreased gradually, in parallel with the shut-off of RNA synthesis. Later on, poly(A) segments, an average of 50 nucleotides long, were associated with viral RNA isolated either from polysomes or whole cytoplasm. These segments seemed to be processed differently in the course of time, and RNA molecules containing short poly(A) tracts (less than 20 bases) were incorporated into the virions.
Insights
Encephalomyocarditis virus infection alters polyadenylation in L cells, shortening poly(A) tails on cellular mRNA and incorporating short poly(A) tracts into viral RNA.
Area of Science:
- Virology
- Molecular Biology
- Biochemistry
Background:
- Polyadenylation is a crucial post-transcriptional modification of eukaryotic messenger RNA (mRNA).
- Encephalomyocarditis virus (EMCV) is a positive-sense single-stranded RNA virus that replicates in the cytoplasm of host cells.
Purpose of the Study:
- To investigate the impact of encephalomyocarditis virus (EMCV) infection on the polyadenylation of cytoplasmic RNAs in L cells.
- To characterize the changes in poly(A) tail length and processing during viral infection.
Main Methods:
- Infection of L cells with EMCV.
- Analysis of poly(A) chain size on cellular and viral RNA.
- Isolation of RNA from polysomes and whole cytoplasm.
Main Results:
- A gradual decrease in the mean size of newly synthesized poly(A) chains on cellular mRNAs was observed during early EMCV infection, coinciding with RNA synthesis shut-off.
- Viral RNA isolated from polysomes and cytoplasm later in infection was associated with poly(A) segments averaging 50 nucleotides.
- Evidence suggests differential processing of these poly(A) segments over time, with short poly(A) tracts (<20 bases) being incorporated into progeny virions.
Conclusions:
- EMCV infection significantly affects host cell mRNA polyadenylation, leading to shorter poly(A) tails.
- Viral RNA acquires poly(A) segments that undergo dynamic processing during infection.
- The incorporation of truncated poly(A) tails into virions may be a mechanism employed by EMCV.