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Adar3 is involved in learning and memory in mice
Mladenova, Dessislava Barry, Guy Konen, Lyndsey M. Pineda, Sandy S. Guennewig, Boris Avesson, Lotta Zinn, Raphael Schonrock, Nicole Bitar, Maina Jonkhout, Nicky
Mladenova, Dessislava
Barry, Guy
Konen, Lyndsey M.
Pineda, Sandy S.
Guennewig, Boris
Avesson, Lotta
Zinn, Raphael
Schonrock, Nicole
Bitar, Maina
Jonkhout, Nicky
Author
Abstract
The amount of regulatory RNA encoded in the genome and the extent of RNA editing by the post-transcriptional deamination of adenosine to inosine (A-I) have increased with developmental complexity and may be an important factor in the cognitive evolution of animals. The newest member of the A-I editing family of ADAR proteins, the vertebrate-specific ADAR3, is highly expressed in the brain, but its functional significance is unknown. In vitro studies have suggested that ADAR3 acts as a negative regulator of A-I RNA editing but the scope and underlying mechanisms are also unknown. Meta-analysis of published data indicates that mouse Adar3 expression is highest in the hippocampus, thalamus, amygdala, and olfactory region. Consistent with this, we show that mice lacking exon 3 of Adar3 (which encodes two double stranded RNA binding domains) have increased levels of anxiety and deficits in hippocampus-dependent short- and long-term memory formation. RNA sequencing revealed a dysregulation of genes involved in synaptic function in the hippocampi of Adar3-deficient mice. We also show that ADAR3 transiently translocates from the cytoplasm to the nucleus upon KCl-mediated activation in SH-SY5Y cells. These results indicate that ADAR3 contributes to cognitive processes in mammals.
Keywords
ADAR3, Adar3exon3 mouse model, RNA editing, learning and memory, Adarb2
Date
2018
Type
Journal article
Journal
Frontiers in Neuroscience
Book
Volume
12
Issue
Page Range
1-17
Article Number
ACU Department
Mary MacKillop Institute for Health Research
Faculty of Health Sciences
Faculty of Health Sciences
Collections
Relation URI
Source URL
Event URL
Open Access Status
Open access
License
CC BY-NC 3.0
File Access
Open