Molecular control of spinal accessory motor neuron/axon development in the mouse spinal cord

Allison K Dillon; Shinobu C Fujita; Michael P Matise; Andrew A Jarjour; Timothy E Kennedy; Heike Kollmus; Hans-Henning Arnold; Joshua A Weiner; Joshua R Sanes; Zaven Kaprielian

doi:10.1523/JNEUROSCI.3455-05.2005

Back

Molecular control of spinal accessory motor neuron/axon development in the mouse spinal cord

Journal article

Open access

Peer reviewed

Molecular control of spinal accessory motor neuron/axon development in the mouse spinal cord

Allison K Dillon, Shinobu C Fujita, Michael P Matise, Andrew A Jarjour, Timothy E Kennedy, Heike Kollmus, Hans-Henning Arnold, Joshua A Weiner, Joshua R Sanes and Zaven Kaprielian

The Journal of neuroscience, Vol.25(44), pp.10119-10130

11/02/2005

DOI: 10.1523/JNEUROSCI.3455-05.2005

PMCID: PMC6725793

PMID: 16267219

Files and links (1)

url

https://doi.org/10.1523/JNEUROSCI.3455-05.2005View

Published (Version of record) Open Access

Abstract

Within the developing vertebrate spinal cord, motor neuron subtypes are distinguished by the settling positions of their cell bodies, patterns of gene expression, and the paths their axons follow to exit the CNS. The inclusive set of cues required to guide a given motor axon subtype from cell body to target has yet to be identified, in any species. This is attributable, in part, to the unavailability of markers that demarcate the complete trajectory followed by a specific class of spinal motor axons. Most spinal motor neurons extend axons out of the CNS through ventral exit points. In contrast, spinal accessory motor neurons (SACMNs) project dorsally directed axons through lateral exit points (LEPs), and these axons assemble into the spinal accessory nerve (SAN). Here we show that an antibody against BEN/ALCAM/SC1/DM-GRASP/MuSC selectively labels mouse SACMNs and can be used to trace the pathfinding of SACMN axons. We use this marker, together with a battery of transcription factor-deficient or guidance cue/receptor-deficient mice to identify molecules required for distinct stages of SACMN development. Specifically, we find that Gli2 is required for the initial extension of axons from SACMN cell bodies, and that netrin-1 and its receptor Dcc are required for the proper dorsal migration of these cells and the dorsally directed extension of SACMN axons toward the LEPs. Furthermore, in the absence of the transcription factor Nkx2.9, SACMN axons fail to exit the CNS. Together, these findings suggest molecular mechanisms that are likely to regulate key steps in SACMN development.

Spinal Cord - metabolism

Mice, Inbred C57BL

Axons - metabolism

Male

Mice, Transgenic

Mice, Knockout

Muscle Proteins - biosynthesis

Motor Neurons - metabolism

Pregnancy

Spinal Cord - embryology

Animals

Nuclear Proteins - biosynthesis

Motor Neurons - cytology

Accessory Nerve - metabolism

Female

Mice

Trans-Activators - biosynthesis

Accessory Nerve - cytology

Cell Differentiation - physiology

Accessory Nerve - embryology

Details

Title: Subtitle: Molecular control of spinal accessory motor neuron/axon development in the mouse spinal cord
Creators: Allison K Dillon - Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA
Shinobu C Fujita
Michael P Matise
Andrew A Jarjour
Timothy E Kennedy
Heike Kollmus
Hans-Henning Arnold
Joshua A Weiner
Joshua R Sanes
Zaven Kaprielian
Resource Type: Journal article
Publication Details: The Journal of neuroscience, Vol.25(44), pp.10119-10130
DOI: 10.1523/JNEUROSCI.3455-05.2005
PMID: 16267219
PMCID: PMC6725793
NLM abbreviation: J Neurosci
ISSN: 0270-6474
eISSN: 1529-2401
Publisher: United States
Grant note: F31 NS43852-03 / NINDS NIH HHS
Language: English
Date published: 11/02/2005
Academic Unit: Liberal Arts and Science Admin; Psychiatry; Iowa Neuroscience Institute; Biology
Record Identifier: 9983997436002771

Metrics

21 Record Views

49 Times Cited - Web of Science