Novel genetic interactions with the double-stranded RNA-induced autoimmunity pathways
This project aims to dissect genetic interactions with a form of RNA modification termed, Adenosine-to-Inosine (A-to-I) editing. A-to-I editing results in a change to the encoded RNA sequence and its misregulation can have diverse consequences such as the development of the severe autoimmune disease, Aicardi-Goutieres syndrome, where the editing enzyme ADAR1 is mutated. Changes in RNA editing have also been implicated in cancer progression, and several neurological conditions such as autism, schizophrenia and epilepsy. The primary function of ADAR1 is do edit self double-stranded RNA (dsRNA) and mask it from our own immune system. We use mouse models, cell culture and molecular and biochemical techniques to model loss of editing by ADAR1 to better understand how cells deal with their own dsRNA. This project would characterize new players in this pathway identified in a genome-wide CRISPR/Cas9 screen.
Techniques – RNA biology, mouse genetics, cell culture assays, molecular biology/biochem, CRISPR/Cas9, bioinformatics
Prof Carl Walkley
Dr Jacki Heraud-Farlow
Cancer & RNA biology
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