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Published January 16, 2014 | Supplemental Material + Accepted Version
Journal Article Open

Tachykinin-Expressing Neurons Control Male-Specific Aggressive Arousal in Drosophila

Abstract

Males of most species are more aggressive than females, but the neural mechanisms underlying this dimorphism are not clear. Here, we identify a neuron and a gene that control the higher level of aggression characteristic of Drosophila melanogaster males. Males, but not females, contain a small cluster of FruM+ neurons that express the neuropeptide tachykinin (Tk). Activation and silencing of these neurons increased and decreased, respectively, intermale aggression without affecting male-female courtship behavior. Mutations in both Tk and a candidate receptor, Takr86C, suppressed the effect of neuronal activation, whereas overexpression of Tk potentiated it. Tk neuron activation overcame reduced aggressiveness caused by eliminating a variety of sensory or contextual cues, suggesting that it promotes aggressive arousal or motivation. Tachykinin/Substance P has been implicated in aggression in mammals, including humans. Thus, the higher aggressiveness of Drosophila males reflects the sexually dimorphic expression of a neuropeptide that controls agonistic behaviors across phylogeny.

Additional Information

© 2014 Elsevier Inc. Under an Elsevier user license. Received: June 25, 2013; Revised: September 10, 2013; Accepted: November 15, 2013; Published: January 16, 2014. We thank B.J. Dickson, B. Pfeiffer, G.M. Rubin, and D. Nässel for sharing fly strains and antibodies; S. Jeeda and C. Khanbijian for maintenance of fly stocks; G. Mancuso for administrative support; C. Chiu for laboratory management; and B. Pfeiffer, A.M. Wong, and W. Hong for helpful comments on the manuscript. K.A. was a JSPS Postdoctoral Fellow for Research Abroad. K.W. was a Human Frontier Science Program Postdoctoral Fellow. B.J.D. is an Ellison Medical Foundation Fellow of the Life Science Research Foundation. E.H. is supported by an NRSA postdoctoral fellowship. This research was supported in part by NIH grant R01-DA031389 to D.J.A. and a Moore Foundation grant to D.J.A. and P.P. D.J.A. is a Howard Hughes Medical Institute investigator.

Attached Files

Accepted Version - nihms-553077.pdf

Supplemental Material - DocumentS1.pdf

Supplemental Material - MovieS1.mp4

Supplemental Material - MovieS2.mp4

Supplemental Material - MovieS3.mp4

Supplemental Material - TableS1.xlsx

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Created:
August 19, 2023
Modified:
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