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Fxr1 regulates sleep and synaptic homeostasis.
Jivan Khlghatyan1,2, Alesya Evstratova1, Lusine Bozoyan1
1Department of Pharmacology & Toxicology, University of Toronto, Toronto, ON, Canada.
The EMBO Journal
|September 7, 2020
Summary
Fragile X autosomal homolog 1 (Fxr1) downregulation is crucial for synaptic scaling and sleep. This protein acts as a key signaling hub, impacting brain function and potentially neuropsychiatric disorders.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Homeostatic regulation of synaptic strength is vital for brain function, involving sleep and cell-autonomous processes.
- The fragile X autosomal homolog 1 (Fxr1) gene is linked to schizophrenia and insomnia, and regulated by lithium.
Purpose of the Study:
- To investigate the role of Fxr1 in cell-autonomous homeostatic synaptic scaling.
- To examine Fxr1's contribution to neuronal responses during sleep deprivation.
Main Methods:
- Utilized gene overexpression and CRISPR/Cas9-mediated somatic knockouts to modulate Fxr1 expression.
- Analyzed changes in AMPA receptor expression and synaptic strength.
- Recorded EEG signatures and sequenced neuronal translatomes.
Main Results:
- Fxr1 is downregulated during synaptic scaling and sleep deprivation through a GSK3β-dependent pathway.
- Fxr1 downregulation is essential for modulating surface AMPA receptors and synaptic strength.
- Preventing Fxr1 downregulation during sleep loss altered EEG patterns and neuronal translatomes.
Conclusions:
- Fxr1 acts as a shared signaling hub connecting homeostatic plasticity and sleep.
- Fxr1's role has implications for understanding and treating neuropsychiatric disorders.
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