Biology subjects

Tomita, J.

Publications and source records attributed to Tomita, J..

3 recordsLinked to original sources

bioRxiv2022

Interneurons of fan-shaped body promote arousal in Drosophila

Sleep is required to maintain physiological functions and is widely conserved across species. To understand the sleep-regulatory mechanisms, sleep-regulating genes and neuronal circuits are studied in various animal species. In the sleep-regulatory neuronal circuits in Drosophila melanogaster, the dorsal fan-shaped body (dFB) is a major sleep-promoting region. However, other sleep-regulating neuronal circuits were not well identified. We recently found a novel sleep-regulatory circuit consisting of arousal-promoting T1 dopamine neurons and protocerebral bridge (PB) neurons innervating the ventral part of the FB, which we named "the PB-FB pathway". However, the post-synaptic target of the PB-FB pathway was still unknown. To identify it, we performed anterograde tracing, immunohistochemistry, and Ca2+ imaging analysis and found that the PB-FB pathway projects to FB interneurons, also known as pontine neurons. Besides, we found that cholinergic pontine neurons promote arousal. Moreover, we indicated that pontine neurons form an anatomical connection with sleep-promoting dFB neurons. Together, we showed that pontine neurons receive excitatory signals from the PB-FB pathway and cholinergic pontine neurons promote arousal. These results completed one of the output pathways from the PB-FB pathway.

neuroscience↗

bioRxiv2022

The regulation of circadian rhythm by insulin signaling in Drosophila

Circadian rhythm is well conserved across species and relates to numerous biological functions. Circadian misalignment impairs metabolic function. Insulin signaling is a key modulator of metabolism in the fruit fly as well as mammals and its defects cause metabolic disease. Daily diet timing affects both circadian rhythmicities of behavior and metabolism. However, the relationship between circadian clock and insulin signaling is still elusive. Here, we report that insulin signaling regulates circadian rhythm in Drosophila melanogaster. We found the insulin receptor substrate mutant, chico1, showed a shorter free-running circadian period. The knockdown of insulin receptor (InR), or another signaling molecule downstream of InR, dp110, or the expression of a dominant-negative form of InR resulted in the shortening of the circadian period and diminished its amplitude. The impairment of insulin signaling both in all neurons and restricted circadian clock neurons altered circadian period length, indicating the insulin signaling plays a role in the regulation of circadian rhythm in clock cells. Among 3 insulin-like ligands expressed in the brain, dilp5 showed the largest effect on circadian phenotype when deleted. These results suggested that insulin signaling contributes to the robustness of the circadian oscillation and coordinates metabolism and behavior. HighlightsO_LIInsulin receptor substrate mutant, chico1, displayed circadian rhythm phenotype. C_LIO_LIPan-neuronal inhibition of insulin receptor signaling shortened circadian cycle. C_LIO_LIInhibition of insulin signaling only in clock neurons altered circadian cycle. C_LIO_LIDilp5 is a major insulin receptor ligand for circadian effects. C_LI

animal behavior and cognition↗

bioRxiv2020

Protocerebral bridge neurons that regulate sleep in Drosophila melanogaster

The central complex is one of the major brain regions that control sleep in Drosophila, but the circuitry details of sleep regulation have yet to be elucidated. Here, we show a novel sleep-regulating neuronal circuit in the protocerebral bridge (PB) of the central complex. Activation of the PB interneurons labeled by the R59E08-Gal4 and the PB columnar neurons in the R52B10-Gal4 promoted sleep and wakefulness, respectively. A targeted GFP reconstitution across synaptic partners (t-GRASP) analysis demonstrated synaptic contacts between these two groups of sleep-regulating PB neurons. Furthermore, we found that activation of a pair of dopaminergic (DA) neurons projecting to the PB (T1 DA neurons) decreased sleep. The wake-promoting T1 DA neurons and the sleep-promoting PB interneurons formed close associations. Dopamine 2-like receptor (Dop2R) knockdown in the sleep-promoting PB interneurons increased sleep. These results indicated that the neuronal circuit in the PB regulated by dopamine signaling mediates sleep-wakefulness.

neuroscience↗