tetano
Editor, Senior Moderator
Nat Microbiol. 2016;2016. pii: 16069. Epub 2016 May 27.
[h=1]Influenza Virus mRNA Trafficking Through Host Nuclear Speckles.[/h] Mor A[SUP]1[/SUP], White A[SUP]1[/SUP], Zhang K[SUP]1[/SUP], Thompson M[SUP]2[/SUP], Esparza M[SUP]1[/SUP], Mu?oz-Moreno R[SUP]3[/SUP], Koide K[SUP]4[/SUP], Lynch KW[SUP]2[/SUP], Garc?a-Sastre A[SUP]5[/SUP], Fontoura BM[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A virus is a human pathogen whose genome is comprised of eight viral RNA segments that replicate in the nucleus. Two viral mRNAs are alternatively spliced. The unspliced M1 mRNA is translated into the matrix M1 protein while the ion channel M2 protein is generated after alternative splicing. These proteins are critical mediators of viral trafficking and budding. We show that influenza virus utilizes nuclear speckles to promote post-transcriptional splicing of its M1 mRNA. We assign previously unknown roles for the viral NS1 protein and cellular factors to an intranuclear trafficking pathway that targets the viral M1 mRNA to nuclear speckles, mediates splicing at these nuclear bodies, and exports the spliced M2 mRNA from the nucleus. Since nuclear speckles are storage sites for splicing factors, which leave these sites to splice cellular pre-mRNAs at transcribing genes, we reveal a functional subversion of nuclear speckles to promote viral gene expression.
[h=4]KEYWORDS:[/h] influenza virus; mRNA export; nuclear speckles; splicing
PMID: 27347430 PMCID: PMC4917225 [Available on 2016-11-27] DOI: 10.1038/nmicrobiol.2016.69
[PubMed]
[h=1]Influenza Virus mRNA Trafficking Through Host Nuclear Speckles.[/h] Mor A[SUP]1[/SUP], White A[SUP]1[/SUP], Zhang K[SUP]1[/SUP], Thompson M[SUP]2[/SUP], Esparza M[SUP]1[/SUP], Mu?oz-Moreno R[SUP]3[/SUP], Koide K[SUP]4[/SUP], Lynch KW[SUP]2[/SUP], Garc?a-Sastre A[SUP]5[/SUP], Fontoura BM[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A virus is a human pathogen whose genome is comprised of eight viral RNA segments that replicate in the nucleus. Two viral mRNAs are alternatively spliced. The unspliced M1 mRNA is translated into the matrix M1 protein while the ion channel M2 protein is generated after alternative splicing. These proteins are critical mediators of viral trafficking and budding. We show that influenza virus utilizes nuclear speckles to promote post-transcriptional splicing of its M1 mRNA. We assign previously unknown roles for the viral NS1 protein and cellular factors to an intranuclear trafficking pathway that targets the viral M1 mRNA to nuclear speckles, mediates splicing at these nuclear bodies, and exports the spliced M2 mRNA from the nucleus. Since nuclear speckles are storage sites for splicing factors, which leave these sites to splice cellular pre-mRNAs at transcribing genes, we reveal a functional subversion of nuclear speckles to promote viral gene expression.
[h=4]KEYWORDS:[/h] influenza virus; mRNA export; nuclear speckles; splicing
PMID: 27347430 PMCID: PMC4917225 [Available on 2016-11-27] DOI: 10.1038/nmicrobiol.2016.69
[PubMed]