Interaction of axonal Chondrolectin with Collagen XIXa1 is necessary for precise neuromuscular junction formation

Ana Oprisoreanu, Hannah Smith, Sukrat Ayra, Richard Webster, Zhen Zhong, Charlotte Eaton-Hart, Daniel Wehner, Marcos J Cardozo, Thomas Becker, Kevin Talbot, Catherina G Becker

Research output: Contribution to journalArticlepeer-review

Abstract

Chondrolectin (Chodl) is needed for motor axon extension in zebrafish and is dysregulated in mouse models of spinal muscular atrophy (SMA). However, the mechanistic basis of Chodl function is not known. Here, we use Chodl-deficient zebrafish and mouse mutants to show that the absence of Chodl leads to anatomical and functional defects of the neuromuscular synapse. In zebrafish, the growth of an identified motor axon beyond an “en passant” synapse and later axon branching from synaptic points are impaired, leading to functional deficits. Mechanistically, motor-neuron-autonomous Chodl function depends on its intracellular domain and on binding muscle-derived collagen XIXa1 by its extracellular C-type lectin domain. Our data support evolutionarily conserved roles of Chodl in synaptogenesis and provide evidence for a “synapse-first” scenario of motor axon growth in zebrafish.
Original languageEnglish
Pages (from-to)1082-1098.e10
Number of pages17
JournalCell Reports
Volume29
Issue number5
DOIs
Publication statusPublished - 29 Oct 2019

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