scholarly journals Deep sequencing leads to the identification of eukaryotic translation initiation factor 5A as a key element in Rsv1 -mediated lethal systemic hypersensitive response to Soybean mosaic virus infection in soybean

2016 ◽  
Vol 18 (3) ◽  
pp. 391-404 ◽  
Author(s):  
Hui Chen ◽  
Andrej Adam Arsovski ◽  
Kangfu Yu ◽  
Aiming Wang
Keyword(s):  
Virus Infection ◽  
Deep Sequencing ◽  
Translation Initiation ◽  
Hypersensitive Response ◽  
Soybean Mosaic Virus ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Eukaryotic Translation ◽  
Eukaryotic Translation Initiation ◽  
Mosaic Virus Infection

scholarly journals Resistance to Vesicular Stomatitis Virus Infection Requires a Functional Cross Talk between the Eukaryotic Translation Initiation Factor 2α Kinases PERK and PKR

2004 ◽  
Vol 78 (23) ◽  
pp. 12747-12761 ◽  
Author(s):  
Dionissios Baltzis ◽  
Li-Ke Qu ◽  
Stavroula Papadopoulou ◽  
Jaime D. Blais ◽  
John C. Bell ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Virus Infection ◽  
Vesicular Stomatitis Virus ◽  
Translation Initiation ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Eukaryotic Translation ◽  
Eukaryotic Translation Initiation ◽  
Vesicular Stomatitis ◽  
Eif2α Kinase

ABSTRACT Phosphorylation of the alpha (α) subunit of the eukaryotic translation initiation factor 2 (eIF2) leads to the inhibition of protein synthesis in response to diverse stress conditions, including viral infection. The eIF2α kinase PKR has been shown to play an essential role against vesicular stomatitis virus (VSV) infection. We demonstrate here that another eIF2α kinase, the endoplasmic reticulum-resident protein kinase PERK, contributes to cellular resistance to VSV infection. We demonstrate that mouse embryonic fibroblasts (MEFs) from PERK−/− mice are more susceptible to VSV-mediated apoptosis than PERK+/+ MEFs. The higher replication capacity of VSV in PERK−/− MEFs results from their inability to attenuate viral protein synthesis due to an impaired eIF2α phosphorylation. We also show that VSV-infected PERK−/− MEFs are unable to fully activate PKR, suggesting a cross talk between the two eIF2α kinases in virus-infected cells. These findings further implicate PERK in virus infection, and provide evidence that the antiviral and antiapoptotic roles of PERK are mediated, at least in part, via the activation of PKR.

Sign in / Sign up

Export Citation Format

Share Document