github link
Accession IconSRP098702

RNA editing is the essential function of ADAR1 and, in the absence of MDA5, is dispensable for normal adult homeostasis [RNAseq (Adult Brain)]

Organism Icon Mus musculus
Sample Icon 6 Downloadable Samples
Technology Badge IconNextSeq 500

Submitter Supplied Information

Description
Adenosine-to-Inosine (A-to-I) editing of dsRNA by ADAR proteins is a pervasive feature of the epitranscriptome. There are estimated to be over 100 million potential A-to-I editing sites in humans and A-to-I editing can have varying consequences for gene expression. Whilst editing resulting in protein recoding defines the role of ADAR2, ADAR1 has been proposed to have both editing-dependent and -independent functions. The relative contribution of these putative functions to ADAR1 biology is unclear. We demonstrate that the absence of ADAR1-mediated editing is well tolerated when the cytosolic dsRNA sensor MDA5 is deleted. These mice have normal hematopoiesis, tissue patterning and life span. A direct comparison of the complete deletion of ADAR1 and the specific loss of A-to-I editing activity demonstrates that RNA editing is the only essential function of ADAR1 in adult mice. Therefore, preventing MDA5 substrate formation by endogenous RNA is the essential in vivo function of ADAR1-mediated editing. Overall design: RNAseq of Feotal Brain in a E861A point mutant of ADAR on a MDA5 knockout background generated by deep sequencing, in triplicate using Illumina NextSeq500
PubMed ID
Total Samples
6
Submitter’s Institution
No associated institution

Samples

Show of 0 Total Samples
Filter
Add/Remove
Accession Code
Title
Sex
Age
Specimen part
Cell line
Subject
Processing Information
Additional Metadata
No rows found
Loading...