Tachykinin-expressing neurons control male-specific aggressive arousal in Drosophila.
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.
Howard Hughes Medical Institute, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA; Division of Biology, 156-29, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA.
Kenta
K
Asahina
Howard Hughes Medical Institute, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA; Division of Biology, 156-29, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA.
Kiichi
K
Watanabe
Howard Hughes Medical Institute, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA; Division of Biology, 156-29, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA.
Brian J
BJ
Duistermars
Howard Hughes Medical Institute, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA; Division of Biology, 156-29, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA; Janelia Farm Research Campus, HHMI, 19700 Helix Drive, Ashburn, VA 20147, USA.
Eric
E
Hoopfer
Division of Engineering and Applied Science, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA.
Carlos Roberto
CR
González
Division of Engineering and Applied Science, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA.
Eyrún Arna
EA
Eyjólfsdóttir
Division of Engineering and Applied Science, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA.
Pietro
P
Perona
Howard Hughes Medical Institute, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA; Division of Biology, 156-29, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA. Electronic address: wuwei@caltech.edu.
David J
DJ
Anderson
D000374:Aggression; D000818:Animals; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism; D004331:Drosophila melanogaster / Q000502:physiology*; D005260:Female; D008297:Male; D009154:Mutation; D009474:Neurons / Q000378:metabolism*; D018039:Receptors, Tachykinin / Q000235:genetics / Q000378:metabolism; D012727:Sex Characteristics; D015320:Tachykinins / Q000378:metabolism*
D029721:Drosophila Proteins; D018039:Receptors, Tachykinin; D015320:Tachykinins; C072191:TkR86C protein, Drosophila