Dlk1 Promotes a Fast Motor Neuron Biophysical Signature Required for Peak Force Execution

A publication (journal article) of the University of Göttingen

Jump to: Cite & Linked | Documents & Media | Details | Version history

Cite this publication

​Dlk1 Promotes a Fast Motor Neuron Biophysical Signature Required for Peak Force Execution​
Mueller, D.; Cherukuri, P.; Henningfeld, K. A.; Poh, C. H.; Wittler, L.; Grote, P. & Schlüter, O. M.  et al.​ (2014) 
Science343(6176) pp. 1264​-1266​.​

Documents & Media

Autorenversion / Postprint6.52 MBAdobe PDF

License

Author's Version

Special user license Goescholar License

Details

Authors
Mueller, Daniel; Cherukuri, Pitchaiah; Henningfeld, Kristine A.; Poh, Chor Hoon; Wittler, Lars; Grote, Phillip; Schlüter, Oliver M. ; Schmidt, Jennifer; Laborda, Jorge; Bauer, Steven R.; Brownstone, Robert M.; Marquardt, Till 
Abstract
Motor neurons, which relay neural commands to drive skeletal muscle movements, encompass types ranging from "slow" to "fast," whose biophysical properties govern the timing, gradation, and amplitude of muscle force. Here we identify the noncanonical Notch ligand Delta-like homolog 1 (Dlk1) as a determinant of motor neuron functional diversification. Dlk1, expressed by similar to 30% of motor neurons, is necessary and sufficient to promote a fast biophysical signature in the mouse and chick. Dlk1 suppresses Notch signaling and activates expression of the K+ channel subunit Kcng4 to modulate delayed-rectifier currents. Dlk1 inactivation comprehensively shifts motor neurons toward slow biophysical and transcriptome signatures, while abolishing peak force outputs. Our findings provide insights into the development of motor neuron functional diversity and its contribution to the execution of movements.
Issue Date
2014
Publisher
Amer Assoc Advancement Science
Journal
Science 
ISSN
1095-9203; 0036-8075

Reference

Citations


Social Media