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

Details

Serval ID
serval:BIB_3D38D556B473
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Neurotrophin receptors TrkA and TrkC cause neuronal death whereas TrkB does not.
Journal
Nature
Author(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
Publication state
Published
Issued date
02/09/2010
Peer-reviewed
Oui
Volume
467
Number
7311
Pages
59-63
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
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.
Keywords
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
Create date
27/01/2021 16:55
Last modification date
28/01/2021 7:26
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