Circadian Rhythms in Rho1 Activity Regulate Neuronal Plasticity and Network Hierarchy

Area of Science:

• Neuroscience
• Chronobiology
• Cell Biology

Background:

• Neuronal plasticity enables animals to learn from environmental cues.
• Linking specific neuronal structural changes to behavioral alterations remains a challenge.
• Circadian rhythms in clock neurons are crucial for temporal regulation.

Purpose of the Study:

• To investigate the structural plasticity of s-LNv clock neurons in Drosophila.
• To understand the molecular mechanisms controlling neuronal architecture changes in response to circadian rhythms.
• To explore the functional significance of this plasticity in seasonal adaptation and its potential link to human neurological disorders.

Main Methods:

• Quantification of neuronal architecture in Drosophila s-LNv neurons.
• Analysis of Rho1 activity and its downstream effects, including myosin phosphorylation.
• Assessment of pre-synaptic and dendritic markers.
• Investigation of clock-regulated gene transcription, specifically Puratrophin-1-like (Pura).

Main Results:

• Observed structural plasticity in s-LNv neurons involving axonal material changes and fasciculation/defasciculation cycles.
• Identified rhythmic Rho1 activity as the controller of s-LNv axonal termini retraction via myosin phosphorylation.
• Demonstrated that this plasticity is essential for altering clock network hierarchy and enabling seasonal adaptation.
• Found that clock-regulated transcription of Pura, a Rho1 GEF, controls Rho1 activity rhythms.

Conclusions:

• Structural plasticity of s-LNv clock neurons is regulated by rhythmic Rho1 activity, crucial for seasonal adaptation in Drosophila.
• The findings link actin-related plasticity to spinocerebellar ataxia, suggesting defective plasticity underlies the human condition.