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Cell. 2015 Aug 13;162(4):823-35. doi: 10.1016/j.cell.2015.07.010. Epub 2015 Jul 30.

Circadian Rhythms in Rho1 Activity Regulate Neuronal Plasticity and Network Hierarchy.

Author information

1
Department of Biology, New York University, 100 Washington Square East, New York, NY 10003, USA.
2
Courant Institute for Applied Mathematics, New York University, New York, NY 10003, USA; Department of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
3
Department of Biology, New York University, 100 Washington Square East, New York, NY 10003, USA; Center for Genomics & Systems Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates; Program in Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates. Electronic address: justin.blau@nyu.edu.

Abstract

Neuronal plasticity helps animals learn from their environment. However, it is challenging to link specific changes in defined neurons to altered behavior. Here, we focus on circadian rhythms in the structure of the principal s-LNv clock neurons in Drosophila. By quantifying neuronal architecture, we observed that s-LNv structural plasticity changes the amount of axonal material in addition to cycles of fasciculation and defasciculation. We found that this is controlled by rhythmic Rho1 activity that retracts s-LNv axonal termini by increasing myosin phosphorylation and simultaneously changes the balance of pre-synaptic and dendritic markers. This plasticity is required to change clock network hierarchy and allow seasonal adaptation. Rhythms in Rho1 activity are controlled by clock-regulated transcription of Puratrophin-1-like (Pura), a Rho1 GEF. Since spinocerebellar ataxia is associated with mutations in human Puratrophin-1, our data support the idea that defective actin-related plasticity underlies this ataxia.

PMID:
26234154
PMCID:
PMC4537806
DOI:
10.1016/j.cell.2015.07.010
[Indexed for MEDLINE]
Free PMC Article

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