Circadian Rhythms in Rho1 Activity Regulate Neuronal Plasticity and Network Hierarchy

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


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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Axons / metabolism
  • Biological Clocks
  • Circadian Rhythm*
  • Drosophila Proteins / metabolism*
  • Drosophila melanogaster / physiology*
  • Guanine Nucleotide Exchange Factors / metabolism
  • Myosins / metabolism
  • Neuronal Plasticity
  • Phosphorylation
  • Seasons
  • Signal Transduction
  • Spectrin / metabolism
  • Synapses / metabolism
  • rho GTP-Binding Proteins / metabolism*


  • Drosophila Proteins
  • Guanine Nucleotide Exchange Factors
  • Pura protein, Drosophila
  • Spectrin
  • Myosins
  • Rho1 protein, Drosophila
  • rho GTP-Binding Proteins