Home
Deutsch
Advanced Search
Browse by ...
Publication overview
Contact persons
Help
Publ. Version/Full Text
Postprint
DOI
PMC
 |
Open Access Green |
as soon as is submitted to ZB.
The role of Sema3-Npn-1 signaling during diaphragm innervation and muscle development.
J. Cell Sci. 129, 3295-3308 (2016)
Correct innervation of the main respiratory muscle in mammals, namely the thoracic diaphragm, is a crucial pre-requisite for the functionality of this muscle and the viability of the entire organism. Systemic impairment of Sema3A-Npn-1 signaling causes excessive branching of phrenic nerves in the diaphragm and into the central tendon region, where the majority of misguided axons innervate ectopic musculature. To elucidate whether these ectopic muscles are a result of misguided myoblast precursors due to the loss of Sema3A-Npn-1 signaling, we conditionally ablated Npn-1 in somatic motor neurons which leads to a similar phenotype of phrenic nerve defasciculation and, intriguingly, also formation of innervated ectopic muscles. We therefore hypothesize that ectopic myocyte fusion is caused by additional factors released by misprojecting growth cones. Slit2 and its Robo receptors are expressed by phrenic motor axons and migrating myoblasts, respectively, during innervation of the diaphragm. In vitro analyses revealed a chemo-attractive effect of Slit2 on primary diaphragm myoblasts. Thus, we postulate an influence of factors released by motor neuron growth cones on the migration properties of myoblasts during establishment of the diaphragm.
Altmetric
Additional Metrics?
Edit extra informations
Login
Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Axon Pathfinding ; Diaphragm ; Muscle Development ; Npn-1 ; Phrenic Nerve ; Sema3a; Motor Axon Guidance; Neuromuscular Synapses; Skeletal-muscles; Satellite Cells; Nervous-system; Migration; Neurons; Mice; Expression; Semaphorin
ISSN (print) / ISBN
0021-9533
e-ISSN
1477-9137
Journal
Journal of Cell Science
Quellenangaben
Volume: 129,
Issue: 17,
Pages: 3295-3308
Publisher
Company of Biologists
Publishing Place
Cambridge
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Developmental Genetics (IDG)