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

Détails

ID Serval
serval:BIB_3D38D556B473
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Neurotrophin receptors TrkA and TrkC cause neuronal death whereas TrkB does not.
Périodique
Nature
Auteur⸱e⸱s
Nikoletopoulou V., Lickert H., Frade J.M., Rencurel C., Giallonardo P., Zhang L., Bibel M., Barde Y.A.
ISSN
1476-4687 (Electronic)
ISSN-L
0028-0836
Statut éditorial
Publié
Date de publication
02/09/2010
Peer-reviewed
Oui
Volume
467
Numéro
7311
Pages
59-63
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
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.
Mots-clé
Animals, Cell Death, Cell Differentiation, Embryonic Stem Cells/cytology, Mice, Neurons/cytology, Neurons/metabolism, Receptor, trkA/metabolism, Receptor, trkB/metabolism, Receptor, trkC/metabolism
Pubmed
Web of science
Création de la notice
27/01/2021 16:55
Dernière modification de la notice
28/01/2021 7:26
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