tetano
Editor, Senior Moderator
J Cell Sci. 2016 Mar 3. pii: jcs.188409. [Epub ahead of print]
[h=1]Influenza A virus ribonucleoproteins modulate host recycling by competing with Rab11 effectors.[/h] Vale-Costa S[SUP]1[/SUP], Alenquer M[SUP]1[/SUP], Sousa AL[SUP]2[/SUP], Kellen B[SUP]1[/SUP], Ramalho J[SUP]3[/SUP], Tranfield EM[SUP]2[/SUP], Amorim MJ[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A virus assembly is an unclear process, whereby individual virion components form an infectious particle. The segmented nature of influenza A genome, imposes a problem to assembly, as it requires packaging of eight distinct RNA particles (vRNPs). It also allows genome mixing from distinct parental strains, event associated with influenza pandemic outbreaks. It is important to public health to understand how segmented genomes assemble, a process dependent on the transport of components to assembly sites. Previously, it was shown that vRNPs are carried by recycling endosome (RE) vesicles, changing its distribution as a consequence. Here, we describe that vRNP binding to RE impairs its function, by competing with family-interacting-proteins for Rab11 binding, and that there is a causal relationship between Rab11 ability to recruit family-interacting-proteins and Rab11 redistribution. This competition reduces recycling sorting at an unclear step, resulting in clustering of single and double membrane vesicles. These morphological changes in Rab11 membranes are indicative of alterations in protein and lipid homeostasis during infection. Vesicular clustering creates hotspots of the vRNPs that need to interact to form an infectious particle.
? 2016. Published by The Company of Biologists Ltd.
PMID: 26940915 [PubMed - as supplied by publisher]
[h=1]Influenza A virus ribonucleoproteins modulate host recycling by competing with Rab11 effectors.[/h] Vale-Costa S[SUP]1[/SUP], Alenquer M[SUP]1[/SUP], Sousa AL[SUP]2[/SUP], Kellen B[SUP]1[/SUP], Ramalho J[SUP]3[/SUP], Tranfield EM[SUP]2[/SUP], Amorim MJ[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A virus assembly is an unclear process, whereby individual virion components form an infectious particle. The segmented nature of influenza A genome, imposes a problem to assembly, as it requires packaging of eight distinct RNA particles (vRNPs). It also allows genome mixing from distinct parental strains, event associated with influenza pandemic outbreaks. It is important to public health to understand how segmented genomes assemble, a process dependent on the transport of components to assembly sites. Previously, it was shown that vRNPs are carried by recycling endosome (RE) vesicles, changing its distribution as a consequence. Here, we describe that vRNP binding to RE impairs its function, by competing with family-interacting-proteins for Rab11 binding, and that there is a causal relationship between Rab11 ability to recruit family-interacting-proteins and Rab11 redistribution. This competition reduces recycling sorting at an unclear step, resulting in clustering of single and double membrane vesicles. These morphological changes in Rab11 membranes are indicative of alterations in protein and lipid homeostasis during infection. Vesicular clustering creates hotspots of the vRNPs that need to interact to form an infectious particle.
? 2016. Published by The Company of Biologists Ltd.
PMID: 26940915 [PubMed - as supplied by publisher]