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Elife. 2016 Sep 9;5. pii: e15693. doi: 10.7554/eLife.15693.

Regulation of starvation-induced hyperactivity by insulin and glucagon signaling in adult Drosophila.

Yu Y1,2, Huang R1,2, Ye J1,2, Zhang V3, Wu C1,2, Cheng G1,2, Jia J1,2, Wang L1,2.

Author information

1
Life Sciences Institute, Zhejiang University, Hangzhou, China.
2
Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
3
Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.

Abstract

Starvation induces sustained increase in locomotion, which facilitates food localization and acquisition and hence composes an important aspect of food-seeking behavior. We investigated how nutritional states modulated starvation-induced hyperactivity in adult Drosophila. The receptor of the adipokinetic hormone (AKHR), the insect analog of glucagon, was required for starvation-induced hyperactivity. AKHR was expressed in a small group of octopaminergic neurons in the brain. Silencing AKHR+ neurons and blocking octopamine signaling in these neurons eliminated starvation-induced hyperactivity, whereas activation of these neurons accelerated the onset of hyperactivity upon starvation. Neither AKHR nor AKHR+ neurons were involved in increased food consumption upon starvation, suggesting that starvation-induced hyperactivity and food consumption are independently regulated. Single cell analysis of AKHR+ neurons identified the co-expression of Drosophila insulin-like receptor (dInR), which imposed suppressive effect on starvation-induced hyperactivity. Therefore, insulin and glucagon signaling exert opposite effects on starvation-induced hyperactivity via a common neural target in Drosophila.

KEYWORDS:

AKHR; D. melanogaster; Drosophila; dInR; food seeking; neuroscience; octopamine

Conflict of interest statement

The authors declare that no competing interests exist.

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