We clarified projection pathways from the central ommatidia of the compound eye, which are the photoreceptor for photoperiodism, to the brain and the cells in the cephalic ganglia expressing a clock protein.
It was unsuccessful to measure the juvenile hormone titer as an index of photoperiodism. Clock genes were involved in the photoperiodic response of lipid accumulation, which is independent of juvenile hormone. Therefore, these genes do not seem to play a role in the endocrine effector system but in the center of photoperiodism. Genes of which the expression levels are related to the photoperiod were identified.
Because we succeeded in culture of the head and RNAi in vitro, now it is possible to examine the molecular basis of the photoperiodism in the central nervous system apart from the other parts of the body.
