ArticleJournal of cell science2016
The role of Sema3-Npn-1 signaling during diaphragm innervation and muscle development.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- A unifying mechanism for presynaptic homeostatic plasticity at mammalian peripheral and central synapses.Neuron · 2025Article
- Motor innervation directs the correct development of the mouse sympathetic nervous system.Nature communications · 2024Article
- Netrin-1 as A neural guidance protein in development and reinnervation of the larynx.Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft · 2024Review
- Single-Cell RNA-Sequencing Provides Insight into Skeletal Muscle Evolution during the Selection of Muscle Characteristics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Sema3a-Nrp1 Signaling Mediates Fast-Twitch Myofiber Specificity of Tw2Developmental cell · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 (Npn-1 is also known as NRP1) 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 misguidance of myoblast precursors due to the loss of Sema3A-Npn-1 signaling, we conditionally ablated Npn-1 in somatic motor neurons, which led 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 chemoattractant effect of Slit2 on primary diaphragm myoblasts. Thus, we postulate that factors released by motor neuron growth cones have an influence on the migration properties of myoblasts during establishment of the diaphragm.
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