Event Title

RNAi As a Potential Mechanism of Antiviral Immunity in Neurons

Presenter Information

Yuxiao Tan, Ohio Wesleyan University

Presentation Type

Presentation

Location

Schimmel/Conrades Science Center 180

Start Date

20-4-2016 4:55 PM

End Date

20-4-2016 5:10 PM

Disciplines

Genetics | Immunology of Infectious Disease

Abstract

Innate immunity has been demonstrated as a way to protect against bacterial and fungal infections through Toll signaling and immune deficiency (Imd) pathways. RNA interference (RNAi) was more recently demonstrated as a mechanism to protect against viral infection; however it is uncertain which cell types can employ RNAi as an immune mechanism against viruses. To test if neurons can use RNAi to counter virus infection, we used neuronal cells from Drosophila melanogaster (fruit fly) lines that have specific loss-of-function mutations in genes that control RNAi activity – Dicer-2 and Argonaute-2. Mutations in Dicer-2 or Argonaute-2 were predicted to increase neuronal susceptibility to infection by the neurotropic virus, Sigma Virus (SV). In addition, multiple cross between different mutant flies were designed to test the effect of crossing on RNAi activity, and determined using qPCR. Baby hamster kidney (BHK) cells were used to generate SV stock and quantification of SV stock was performed via plaque assay with Vero cells. This study will better define immune properties of neurons and the nervous system, which may lead to improved therapies for neuronal disorders and infections.

Faculty Mentor

Suren Ambegaokar

 
Apr 20th, 4:55 PM Apr 20th, 5:10 PM

RNAi As a Potential Mechanism of Antiviral Immunity in Neurons

Schimmel/Conrades Science Center 180

Innate immunity has been demonstrated as a way to protect against bacterial and fungal infections through Toll signaling and immune deficiency (Imd) pathways. RNA interference (RNAi) was more recently demonstrated as a mechanism to protect against viral infection; however it is uncertain which cell types can employ RNAi as an immune mechanism against viruses. To test if neurons can use RNAi to counter virus infection, we used neuronal cells from Drosophila melanogaster (fruit fly) lines that have specific loss-of-function mutations in genes that control RNAi activity – Dicer-2 and Argonaute-2. Mutations in Dicer-2 or Argonaute-2 were predicted to increase neuronal susceptibility to infection by the neurotropic virus, Sigma Virus (SV). In addition, multiple cross between different mutant flies were designed to test the effect of crossing on RNAi activity, and determined using qPCR. Baby hamster kidney (BHK) cells were used to generate SV stock and quantification of SV stock was performed via plaque assay with Vero cells. This study will better define immune properties of neurons and the nervous system, which may lead to improved therapies for neuronal disorders and infections.