Abstract

Starvation caused by adverse feeding stresses or food shortages has been reported to result in sleep loss in animals. However, how the starvation signal interacts with the central nervous system is still unknown. Here, the adipokinetic hormone (AKH)—Fork head Box-O (FOXO) pathway is shown to respond to energy change and adjust the sleep of Drosophila through remodeling of the s-LNv (small ventral lateral neurons) dorsal projections. Our results show that starvation prevents flies from going to sleep after the first light-dark transition. The LNvs are required for starvation-induced sleep loss through extension of the pigment dispersing factor (PDF)-containing s-LNv dorsal projections. Further studies reveal that loss of AKH or AKHR (akh receptor) function blocks starvation-induced extension of s-LNv dorsal projections and rescues sleep suppression during food deprivation. FOXO, which has been reported to regulate synapse plasticity of neurons, acts as starvation response factor downstream of AKH, and down regulation of FOXO level considerably alleviates the influence of starvation on s-LNv dorsal projections and sleep. Taking together, our results outline the transduction pathways between starvation signal and sleep, and reveal a novel functional site for sleep regulation.

Highlights

  • Starvation, a frequent result of feeding stresses or food shortages for animals, is a passively endured experience, and a trigger for a reorganization of metabolism and behavior [1, 2]

  • Sleep of Drosophila is regulated by circadian rhythm and homeostasis on the normal condition, in the presence of cellular stress or injury, the central nervous system neurons adjust sleep on the basis of impulse, which is transmitted by neuropeptides generated by cytokines from either peripheral tissues or nervous system cells

  • In this study we find the starvation prevent flies going to sleep, pigment dispersing factor (PDF)/PDFR and LNvs are required for starvation induced sleep loss, during starvation flies show more expanded s-LNvs dorsal projection compared to flies on the normal

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Summary

Introduction

Starvation, a frequent result of feeding stresses or food shortages for animals, is a passively endured experience, and a trigger for a reorganization of metabolism and behavior [1, 2]. In response to energy deficiency, the organisms metabolize stored energy to meet the needs and drive a complex behavioral program to forage and ingest food. DILPs cause class IIa deacetylase (HDAC4) to be phosphorylated and detained in the cytoplasm by upregulating the activity of Ser/Thr kinase 3 (SIK3), which prevents FOXO deacetylation and suppresses catabolic gene expression [3]. The AKH/ AKHR pathway cause a SIK3 phosphorylation decrease, which leads to the dephosphorylation and nuclear translocation of HDAC4 and FOXO deacetylation, and induces the expression of brummer to break down stored lipids for energy [5]

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