tetano
Editor, Senior Moderator
Mol Cell Proteomics. 2018 Jul 6. pii: mcp.RA117.000364. doi: 10.1074/mcp.RA117.000364. [Epub ahead of print]
[h=1]Influenza A virus induces autophagosomal targeting of ribosomal proteins.[/h] Becker AC[SUP]1[/SUP], Gannage M[SUP]2[/SUP], Giese S[SUP]1[/SUP], Hu Z[SUP]3[/SUP], Abou-Eid S[SUP]3[/SUP], Roubaty C[SUP]4[/SUP], Paul P[SUP]5[/SUP], B?hler LK[SUP]6[/SUP], Gretzmeier C[SUP]1[/SUP], Dumit VI[SUP]1[/SUP], Kaeser-Pebernard S[SUP]3[/SUP], Schwemmle M[SUP]7[/SUP], M?nz C[SUP]5[/SUP], Dengjel J[SUP]8[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Seasonal epidemics of influenza A virus are a major cause of severe illness and are of high socio-economic relevance. For the design of effective anti-viral therapies, a detailed knowledge of pathways perturbed by virus infection is critical. We performed comprehensive expression and organellar proteomics experiments to study the cellular consequences of influenza A virus infection using three human epithelial cell lines derived from human lung carcinomas: A549, Calu-1 and NCI-H1299. As a common response, the type I interferon pathway was upregulated upon infection. Interestingly, influenza A virus infection led to numerous cell line-specific responses affecting both protein abundance as well as subcellular localization. In A549 cells, the vesicular compartment appeared expanded after virus infection. In particular, the composition of autophagsomes was altered by targeting of ribosomes, viral mRNA and proteins to these double membrane vesicles. Thus, autophagy may support viral protein translation by promoting the clustering of the respective molecular machinery in autophagosomes in a cell line-dependent manner.
[h=4]KEYWORDS:[/h] Autophagy; Cell biology*; Ribosomes*; SILAC; Viruses; autophagosome; cell line; organelle; proteomics; vesicle
PMID: 29980615 DOI: 10.1074/mcp.RA117.000364
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[h=1]Influenza A virus induces autophagosomal targeting of ribosomal proteins.[/h] Becker AC[SUP]1[/SUP], Gannage M[SUP]2[/SUP], Giese S[SUP]1[/SUP], Hu Z[SUP]3[/SUP], Abou-Eid S[SUP]3[/SUP], Roubaty C[SUP]4[/SUP], Paul P[SUP]5[/SUP], B?hler LK[SUP]6[/SUP], Gretzmeier C[SUP]1[/SUP], Dumit VI[SUP]1[/SUP], Kaeser-Pebernard S[SUP]3[/SUP], Schwemmle M[SUP]7[/SUP], M?nz C[SUP]5[/SUP], Dengjel J[SUP]8[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Seasonal epidemics of influenza A virus are a major cause of severe illness and are of high socio-economic relevance. For the design of effective anti-viral therapies, a detailed knowledge of pathways perturbed by virus infection is critical. We performed comprehensive expression and organellar proteomics experiments to study the cellular consequences of influenza A virus infection using three human epithelial cell lines derived from human lung carcinomas: A549, Calu-1 and NCI-H1299. As a common response, the type I interferon pathway was upregulated upon infection. Interestingly, influenza A virus infection led to numerous cell line-specific responses affecting both protein abundance as well as subcellular localization. In A549 cells, the vesicular compartment appeared expanded after virus infection. In particular, the composition of autophagsomes was altered by targeting of ribosomes, viral mRNA and proteins to these double membrane vesicles. Thus, autophagy may support viral protein translation by promoting the clustering of the respective molecular machinery in autophagosomes in a cell line-dependent manner.
[h=4]KEYWORDS:[/h] Autophagy; Cell biology*; Ribosomes*; SILAC; Viruses; autophagosome; cell line; organelle; proteomics; vesicle
PMID: 29980615 DOI: 10.1074/mcp.RA117.000364
Free full text