Drosophila melanogaster is a common model used to study circadian rhythms in 
behavior and circadian clocks. However, numerous circadian rhythms have also 
been detected in non-clock neurons, especially in the first optic neuropil 
(lamina) of the fly's visual system. Such rhythms have been observed in the 
number of synapses and in the structure of interneurons, which exhibit changes 
in size and shape in a circadian manner. Although the patterns of these changes 
are known, the mechanism remains unclear. In the present study, we investigated 
the role of the TOR signaling pathway and autophagy in regulating circadian 
rhythms based on the behavior and structural plasticity of the lamina L2 
monopolar cell dendritic trees. In addition, we examined the cyclic expression 
of the TOR signaling pathway (Tor, Pi3K class 1, Akt1) and autophagy (Atg5 and 
Atg7) genes in the fly's brain. We observed that Tor, Atg5 and Atg7 exhibit 
rhythmic expressions in the brain of wild-type flies in day/night conditions (LD 
12:12) that are abolished in per01 clock mutants. The silencing of Tor in per 
expressing cells shortens a period of the locomotor activity rhythm of flies. In 
addition, silencing of the Tor and Atg5 genes in L2 cells disrupts the circadian 
plasticity of the L2 cell dendritic trees measured in the distal lamina. In 
turn, silencing of the Atg7 gene in L2 cells changes the pattern of this rhythm. 
Our results indicate that the TOR signaling pathway and autophagy are involved 
in the regulation of circadian rhythms in the behavior and plasticity of neurons 
in the brain of adult flies.