Giuseppe
Emeritus
J Gen Virol. 2008 Dec;89(Pt 12):3097-101.
The influenza A virus spliced messenger RNA M mRNA3 is not required for viral replication in tissue culture.
Jackson D, Lamb RA. - Howard Hughes Medical Institute and Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, Evanston, IL 60208-3500, USA.
Influenza A virus genome RNA segment 7 encodes three known mRNAs, two of which, M2 mRNA and M mRNA3, are derived by alternative splicing of the primary collinear mRNA transcript using alternative 5' splice sites.
The function of M mRNA3 is currently unknown, therefore we attempted to determine whether it is essential for virus replication.
Recombinant viruses unable to produce M mRNA3 and/or M2 mRNA were created by mutating the shared 3' splice site.
Growth of the mutant viruses in M2-expressing MDCK cells was not significantly affected by the lack of M mRNA3.
During the course of a wild-type virus infection, levels of M mRNA3 began to decrease while those of M2 mRNA increased, which may indicate a potential mechanism of alternative splicing control.
These data suggest that neither M mRNA3 nor any potential protein product are essential for influenza virus replication in tissue culture.
PMID: 19008398 [PubMed - in process
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The influenza A virus spliced messenger RNA M mRNA3 is not required for viral replication in tissue culture.
Jackson D, Lamb RA. - Howard Hughes Medical Institute and Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, Evanston, IL 60208-3500, USA.
Influenza A virus genome RNA segment 7 encodes three known mRNAs, two of which, M2 mRNA and M mRNA3, are derived by alternative splicing of the primary collinear mRNA transcript using alternative 5' splice sites.
The function of M mRNA3 is currently unknown, therefore we attempted to determine whether it is essential for virus replication.
Recombinant viruses unable to produce M mRNA3 and/or M2 mRNA were created by mutating the shared 3' splice site.
Growth of the mutant viruses in M2-expressing MDCK cells was not significantly affected by the lack of M mRNA3.
During the course of a wild-type virus infection, levels of M mRNA3 began to decrease while those of M2 mRNA increased, which may indicate a potential mechanism of alternative splicing control.
These data suggest that neither M mRNA3 nor any potential protein product are essential for influenza virus replication in tissue culture.
PMID: 19008398 [PubMed - in process
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