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The Ret receptor regulates sensory neuron dendrite growth and integrin mediated adhesion

  1. Peter Soba  Is a corresponding author
  2. Chun Han
  3. Yi Zheng
  4. Daniel Perea
  5. Irene Miguel-Aliaga
  6. Lily Yeh Jan
  7. Yuh Nung Jan
  1. University of Hamburg, Germany
  2. Cornell University, United States
  3. Howard Hughes Medical Institute, University of California, San Francisco, United States
  4. Imperial College London, United Kingdom
Research Article
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Cite this article as: eLife 2015;4:e05491 doi: 10.7554/eLife.05491

Abstract

Neurons develop highly stereotyped receptive fields by coordinated growth of their dendrites. Although cell surface cues play a major role in this process, few dendrite specific signals have been identified to date. We conducted an in vivo RNAi screen in Drosophila class IV dendritic arborization (C4da) neurons and identified the conserved Ret receptor, known to play a role in axon guidance, as an important regulator of dendrite development. The loss of Ret results in severe dendrite defects due to loss of extracellular matrix adhesion, thus impairing growth within a 2D plane. We provide evidence that Ret interacts with integrins to regulate dendrite adhesion via rac1. In addition, Ret is required for dendrite stability and normal F-actin distribution suggesting it has an essential role in dendrite maintenance. We propose novel functions for Ret as a regulator in dendrite patterning and adhesion distinct from its role in axon guidance.

Article and author information

Author details

  1. Peter Soba

    Center for Molecular Neurobiology, University Medical Campus, University of Hamburg, Hamburg, Germany
    For correspondence
    peter.soba@zmnh.uni-hamburg.de
    Competing interests
    The authors declare that no competing interests exist.
  2. Chun Han

    Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, United States
    Competing interests
    The authors declare that no competing interests exist.
  3. Yi Zheng

    Department of Physiology, Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, United States
    Competing interests
    The authors declare that no competing interests exist.
  4. Daniel Perea

    Gut Signalling and Metabolism Group, MRC Clinical Sciences Centre, Imperial College London, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  5. Irene Miguel-Aliaga

    Gut Signalling and Metabolism Group, MRC Clinical Sciences Centre, Imperial College London, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  6. Lily Yeh Jan

    Department of Physiology, Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, United States
    Competing interests
    The authors declare that no competing interests exist.
  7. Yuh Nung Jan

    Department of Physiology, Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, United States
    Competing interests
    The authors declare that no competing interests exist.

Reviewing Editor

  1. Christine E Holt, University of Cambridge, United Kingdom

Publication history

  1. Received: November 5, 2014
  2. Accepted: March 11, 2015
  3. Accepted Manuscript published: March 12, 2015 (version 1)
  4. Version of Record published: April 9, 2015 (version 2)

Copyright

© 2015, Soba 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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