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  Cis and trans RET signaling control the survival and central projection growth of rapidly adapting mechanoreceptors

Fleming, M. S., Vysochan, A., Paixao, S., Niu, J., Klein, R., Savitt, J. M., et al. (2015). Cis and trans RET signaling control the survival and central projection growth of rapidly adapting mechanoreceptors. eLife, 4: e06828. doi:10.7554/eLife.06828.

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Fleming, Michael S., Author
Vysochan, Anna, Author
Paixao, Sonia1, Author           
Niu, Jingwen, Author
Klein, Rüdiger1, Author           
Savitt, Joseph M., Author
Luo, Wenqin, Author
Affiliations:
1Department: Molecules-Signaling-Development / Klein, MPI of Neurobiology, Max Planck Society, ou_1113546              

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Free keywords: RECEPTOR TYROSINE KINASE; ENTERIC NERVOUS-SYSTEM; NEUROTROPHIC FACTOR; GDNF FAMILY; SPINAL-CORD; NEURONAL SURVIVAL; CELL-ADHESION; NEURTURIN RECEPTOR; DRG NEURONS; LIPID RAFTS
 Abstract: RET can be activated in cis or trans by its co-receptors and ligands in vitro, but the physiological roles of trans signaling are unclear. Rapidly adapting (RA) mechanoreceptors in dorsal root ganglia (DRGs) express Ret and the co-receptor Gfra2 and depend on Ret for survival and central projection growth. Here, we show that Ret and Gfra2 null mice display comparable early central projection deficits, but Gfra2 null RA mechanoreceptors recover later. Loss of Gfra1, the co-receptor implicated in activating RET in trans, causes no significant central projection or cell survival deficit, but Gfra1; Gfra2 double nulls phenocopy Ret nulls. Finally, we demonstrate that GFRa1 produced by neighboring DRG neurons activates RET in RA mechanoreceptors. Taken together, our results suggest that trans and cis RET signaling could function in the same developmental process and that the availability of both forms of activation likely enhances but not diversifies outcomes of RET signaling.

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Language(s): eng - English
 Dates: 2015
 Publication Status: Published in print
 Pages: 67
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: ISI: 000352240400002
DOI: 10.7554/eLife.06828
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Title: eLife
Source Genre: Journal
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Publ. Info: Cambridge : eLife Sciences Publications
Pages: - Volume / Issue: 4 Sequence Number: e06828 Start / End Page: - Identifier: ISSN: 2050-084X
CoNE: https://pure.mpg.de/cone/journals/resource/2050-084X