Clock genes period and timeless control synaptogenesis in Drosophila motor terminals
Some neurons undergo rhythmic morphological changes that persist in constant darkness and require the expression of clock genes. Flight motoneuron MN5, one of the best studied neurons of Drosophila melanogaster exhibits several examples of this type of circadian structural plasticity. During the morning, when the fly is active, synaptic boutons are larger than during the night when the fly is resting though more synaptic boutons and synapses are observed. Here, by comparing bouton numbers at different timepoints in normal flies and in flies carrying loss-of-function mutations in clock genes timeless (tim) or period (per), we investigate whether the rhythmic changes in numbers of boutons and synapses require the expression of these genes. Absence of tim expression abolished the rhythm in bouton number whereas absence of per expression appeared to increase the rhythm's amplitude. This indicates that in normal flies TIM protein is necessary to drive the normal rhythm of bouton number and PER probably has a damping effect on it. In addition, it appears that tim and per expression normally act as inhibitor of synaptogenesis because their loss-of-function mutations caused over-proliferation of synapses. Unexpectedly, TIM and PER were expressed in different cells. TIM was found in the glial sheath wrapping the motoneuron's axon and PER was predominantly found along the axon, suggesting that the control of the rhythmic change in bouton and synapse numbers requires interactions between different cell types.