IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v467y2010i7311d10.1038_nature09336.html
   My bibliography  Save this article

Neurotrophin receptors TrkA and TrkC cause neuronal death whereas TrkB does not

Author

Listed:
  • Vassiliki Nikoletopoulou

    (Biozentrum, University of Basel)

  • Heiko Lickert

    (Helmholtz Zentrum München, Institute of Stem Cell Research, Ingolstädter Landstrasse 1, D-85764 Neuherberg, Germany)

  • José Maria Frade

    (Instituto Cajal, CSIC)

  • Chantal Rencurel

    (Biozentrum, University of Basel)

  • Patrizia Giallonardo

    (Helmholtz Zentrum München, Institute of Stem Cell Research, Ingolstädter Landstrasse 1, D-85764 Neuherberg, Germany)

  • Lixin Zhang

    (Biozentrum, University of Basel
    Present address: Novartis Pharma AG, Department of Neuroscience/Ophthalmics, Clinical Development & Medical Affairs, CH-4051 Basel, Switzerland.)

  • Miriam Bibel

    (Neuroscience Research, Novartis Institutes for BioMedical Research)

  • Yves-Alain Barde

    (Biozentrum, University of Basel)

Abstract

Neurons of the peripheral nervous system have long been known to require survival factors to prevent their death during development. But why they selectively become dependent on secretory molecules has remained a mystery, as is the observation that in the central nervous system, most neurons do not show this dependency. Using engineered embryonic stem cells, we show here that the neurotrophin receptors TrkA and TrkC (tropomyosin receptor kinase A and C, also known as Ntrk1 and Ntrk3, respectively) instruct developing neurons to die, both in vitro and in vivo. By contrast, TrkB (also known as Ntrk2), a closely related receptor primarily expressed in the central nervous system, does not. These results indicate that TrkA and TrkC behave as dependence receptors, explaining why developing sympathetic and sensory neurons become trophic-factor-dependent for survival. We suggest that the expansion of the Trk gene family that accompanied the segregation of the peripheral from the central nervous system generated a novel mechanism of cell number control.

Suggested Citation

  • Vassiliki Nikoletopoulou & Heiko Lickert & José Maria Frade & Chantal Rencurel & Patrizia Giallonardo & Lixin Zhang & Miriam Bibel & Yves-Alain Barde, 2010. "Neurotrophin receptors TrkA and TrkC cause neuronal death whereas TrkB does not," Nature, Nature, vol. 467(7311), pages 59-63, September.
    • Handle: RePEc:nat:nature:v:467:y:2010:i:7311:d:10.1038_nature09336
    DOI: 10.1038/nature09336
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature09336
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.
    File URL: https://libkey.io/10.1038/nature09336?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Erik F. Kot & Sergey A. Goncharuk & María Luisa Franco & Daniel M. McKenzie & Alexander S. Arseniev & Andrea Benito-Martínez & Mario Costa & Antonino Cattaneo & Kalina Hristova & Marçal Vilar & Konsta, 2024. "Structural basis for the transmembrane signaling and antidepressant-induced activation of the receptor tyrosine kinase TrkB," Nature Communications, Nature, vol. 15(1), pages 1-16, December.
    2. Hirofumi Nagao & Ashok Kumar Jayavelu & Weikang Cai & Hui Pan & Jonathan M. Dreyfuss & Thiago M. Batista & Bruna B. Brandão & Matthias Mann & C. Ronald Kahn, 2023. "Unique ligand and kinase-independent roles of the insulin receptor in regulation of cell cycle, senescence and apoptosis," Nature Communications, Nature, vol. 14(1), pages 1-18, December.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:nature:v:467:y:2010:i:7311:d:10.1038_nature09336. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.