Abstract
We previously showed that endocytosis and/or vesicle recycling mechanisms are essential in adult Drosophila glial cells for the neuronal control of circadian locomotor activity. In this study, our goal was to identify specific glial vesicle trafficking, recycling, or release factors that are required for rhythmic behavior. From a glia-specific, RNAi-based genetic screen, we identified eight glial factors that are required for normally robust circadian rhythms in either a light-dark cycle or in constant dark conditions. In particular, we show that conditional knockdown of the ROP vesicle release factor in adult glial cells results in arrhythmic behavior. Immunostaining for ROP reveals reduced protein in glial cell processes and an accumulation of the Par Domain Protein 1ε (PDP1ε) clock output protein in the small lateral clock neurons. These results suggest that glia modulate rhythmic circadian behavior by secretion of factors that act on clock neurons to regulate a clock output factor.
Highlights
During the past decade, it has become apparent that glial cells of vertebrates and invertebrates are active modulators of neuronal development, synaptogenesis, and excitability, in addition to having metabolic support roles
Our studies demonstrate that perturbation of glial vesicle release results in altered neuronal Par Domain Protein 1ε (PDP1ε) abundance, indicating a role for glia-neuron signaling in clock output
Glial Vesicle Trafficking and/or Secretion Mechanisms are Important for Viability and Rhythmic Behavior We previously showed that glia of the adult Drosophila nervous system, in particular astrocytes, are essential for regulation of circadian behavior (Ng et al, 2011): conditional, glia-specific manipulations of several different cellular processes, including vesicle release/recycling, were associated with arrhythmic circadian locomotor activity
Summary
It has become apparent that glial cells of vertebrates and invertebrates are active modulators of neuronal development, synaptogenesis, and excitability, in addition to having metabolic support roles (reviewed in Allen, 2014; Jones and Bouvier, 2014; Freeman, 2015). In addition to secreted proteins, previous studies have suggested that glia release their own transmitters (“gliotransmitters”) including D-serine, glutamate, and ATP, via SNARE-dependent mechanisms, to modulate neuronal excitability and plasticity (reviewed by Araque et al, 2014; Covelo and Araque, 2015; Haydon and Nedergaard, 2015; Zorec et al, 2015). Proteins involved in exocytosis have been best characterized in neurons, some may have similar functions in glial
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