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Interactions between Dpr11 and DIP-γ control selection of amacrine neurons in Drosophila color vision circuits

  1. Kaushiki P Menon  Is a corresponding author
  2. Vivek Kulkarni
  3. Shin-ya Takemura
  4. Michael Anaya
  5. Kai Zinn  Is a corresponding author
  1. California Institute of Technology, United States
  2. Janelia Research Campus, Howard Hughes Medical Institute, United States
Research Article
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Cite this article as: eLife 2019;8:e48935 doi: 10.7554/eLife.48935

Abstract

Drosophila R7 UV photoreceptors (PRs) are divided into yellow (y) and pale (p) subtypes. yR7 PRs express the Dpr11 cell surface protein and are presynaptic to Dm8 amacrine neurons (yDm8) that express Dpr11's binding partner DIP-g, while pR7 PRs synapse onto DIP-g-negative pDm8. Dpr11 and DIP-g expression patterns define 'yellow' and 'pale' color vision circuits. We examined Dm8 neurons in these circuits by electron microscopic reconstruction and expansion microscopy. DIP-g and dpr11 mutations affect the morphologies of yDm8 distal ('home column') dendrites. yDm8 neurons are generated in excess during development and compete for presynaptic yR7 PRs, and interactions between Dpr11 and DIP-g are required for yDm8 survival. These interactions also allow yDm8 neurons to select yR7 PRs as their appropriate home column partners. yDm8 and pDm8 neurons do not normally compete for survival signals or R7 partners, but can be forced to do so by manipulation of R7 subtype fate.

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All data generated or analysed during this study are included in the manuscript and supporting files.

Article and author information

Author details

  1. Kaushiki P Menon

    Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, United States
    For correspondence
    menonk@caltech.edu
    Competing interests
    The authors declare that no competing interests exist.
  2. Vivek Kulkarni

    Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, United States
    Competing interests
    The authors declare that no competing interests exist.
  3. Shin-ya Takemura

    Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-2400-6426
  4. Michael Anaya

    Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, United States
    Competing interests
    The authors declare that no competing interests exist.
  5. Kai Zinn

    Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, United States
    For correspondence
    zinnk@caltech.edu
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-6706-5605

Funding

National Institutes of Health (R37 NS28182)

  • Kai Zinn

National Institutes of Health (RO1 EY028116)

  • Kai Zinn

Howard Hughes Medical Institute

  • Shin-ya Takemura

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Hugo J Bellen, Baylor College of Medicine, United States

Publication history

  1. Received: May 31, 2019
  2. Accepted: November 5, 2019
  3. Accepted Manuscript published: November 6, 2019 (version 1)
  4. Version of Record published: November 26, 2019 (version 2)

Copyright

© 2019, Menon 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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