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Adar3 Is Involved in Learning and Memory in Mice
Dessislava Mladenova1,2, Guy Barry1,2, Lyndsey M Konen1,3,4
1Garvan Institute of Medical Research, Sydney, NSW, Australia.
Frontiers in Neuroscience
|May 3, 2018
Summary
ADAR3, a brain-expressed protein, is crucial for cognitive evolution. Mice lacking ADAR3 show anxiety and memory deficits, highlighting its role in mammalian brain function and RNA editing regulation.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- RNA editing, specifically adenosine to inosine (A-I) deamination, increases with developmental complexity.
- ADAR proteins, including the vertebrate-specific ADAR3, are involved in A-I RNA editing.
- ADAR3 is highly expressed in the brain, but its function remains largely unknown.
Purpose of the Study:
- To investigate the functional significance of ADAR3 in mammalian cognitive processes.
- To explore the role of ADAR3 in regulating A-I RNA editing and synaptic function.
Main Methods:
- Meta-analysis of mouse Adar3 expression patterns.
- Generation and analysis of Adar3-deficient mice (lacking exon 3).
- Behavioral testing (anxiety, hippocampus-dependent memory).
- RNA sequencing of hippocampal tissue.
- Cellular studies on ADAR3 translocation.
Main Results:
- Adar3 expression is highest in brain regions associated with cognition (hippocampus, thalamus, amygdala, olfactory region).
- Adar3-deficient mice exhibit increased anxiety and impaired hippocampus-dependent memory.
- RNA sequencing reveals dysregulation of synaptic function genes in Adar3-deficient mice.
- ADAR3 translocates to the nucleus upon activation in neuronal cells.
Conclusions:
- ADAR3 plays a significant role in cognitive processes, including memory formation and anxiety regulation.
- ADAR3 deficiency leads to synaptic gene dysregulation in the hippocampus.
- These findings suggest ADAR3 is a key contributor to mammalian brain function and cognitive evolution.
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