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P1 interneurons promote a persistent internal state that enhances inter-male aggression in Drosophila

  1. Eric D Hoopfer
  2. Yonil Jung
  3. Hidehiko K Inagaki
  4. Gerald M Rubin
  5. David J Anderson  Is a corresponding author
  1. Janelia Research Campus, Howard Hughes Medical Institute, United States
  2. California Institute of Technology, United States
  3. Howard Hughes Medical Institute, California Institute of Technology, United States
Research Article
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Cite this article as: eLife 2015;4:e11346 doi: 10.7554/eLife.11346

Abstract

How brains are hardwired to produce aggressive behavior, and how aggression circuits are related to those that mediate courtship, is not well understood. A large-scale screen for aggression-promoting neurons in Drosophila identified several independent hits that enhanced both inter-male aggression and courtship. Genetic intersections revealed that P1 interneurons, previously thought to exclusively control male courtship, were responsible for both phenotypes. The aggression phenotype was fly-intrinsic, and required male-specific chemosensory cues on the opponent. Optogenetic experiments indicated that P1 activation promoted aggression vs. wing extension at low vs. high thresholds, respectively. High frequency photostimulation promoted wing extension and aggression in an inverse manner, during light ON and OFF, respectively. P1 activation enhanced aggression by promoting a persistent internal state, which could endure for minutes prior to social contact. Thus P1 neurons promote an internal state that facilitates both aggression and courtship, and can control these social behaviors in a threshold-dependent manner.

Article and author information

Author details

  1. Eric D Hoopfer

    Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, United States
    Competing interests
    The authors declare that no competing interests exist.
  2. Yonil Jung

    Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, United States
    Competing interests
    The authors declare that no competing interests exist.
  3. Hidehiko K Inagaki

    Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, United States
    Competing interests
    The authors declare that no competing interests exist.
  4. Gerald M Rubin

    Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, United States
    Competing interests
    The authors declare that no competing interests exist.
  5. David J Anderson

    Division of Biology and Biological Engineering, Howard Hughes Medical Institute, California Institute of Technology, Pasadena, United States
    For correspondence
    wuwei@caltech.edu
    Competing interests
    The authors declare that no competing interests exist.

Reviewing Editor

  1. Mani Ramaswami, Trinity College Dublin, Ireland

Publication history

  1. Received: September 3, 2015
  2. Accepted: December 15, 2015
  3. Accepted Manuscript published: December 29, 2015 (version 1)
  4. Version of Record published: January 29, 2016 (version 2)

Copyright

© 2015, Hoopfer et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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