ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Chondrolectin mediates growth cone interactions of motor axons with an intermediate target.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
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- iPSC-derived models of PACS1 syndrome reveal transcriptional and functional deficits in neuron activity.Nature communications · 2024Article
- Transcriptional consequences of trisomy 21 on neural induction.Frontiers in cellular neuroscience · 2024Article
- Perspective on automatedNeural regeneration research · 2022Article
- Modeling neuromuscular diseases in zebrafish.Frontiers in molecular neuroscience · 2022Review
- Development of a high-throughput tailored imaging method in zebrafish to understand and treat neuromuscular diseases.Frontiers in molecular neuroscience · 2022Article
- Automated in vivo drug screen in zebrafish identifies synapse-stabilising drugs with relevance to spinal muscular atrophy.Disease models & mechanisms · 2021Article
- Nusinersen ameliorates motor function and prevents motoneuron Cajal body disassembly and abnormal poly(A) RNA distribution in a SMA mouse model.Scientific reports · 2020Article
- Interaction between alpha-COP and SMN ameliorates disease phenotype in a mouse model of spinal muscular atrophy.Biochemical and biophysical research communications · 2019Article
- Molecular and electrophysiological properties of mouse motoneuron and motor unit subtypes.Current opinion in physiology · 2019Article
- Article
- Expression of CHODL in hepatocellular carcinoma affects invasion and migration of liver cancer cells.Oncology letters · 2017Article
- Cell-type-specific miR-431 dysregulation in a motor neuron model of spinal muscular atrophy.Human molecular genetics · 2016Article
- Gene expression changes in spinal motoneurons of the SOD1(G93A) transgenic model for ALS after treatment with G-CSF.Frontiers in cellular neuroscience · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
Abstract
The C-type lectin chondrolectin (chodl) represents one of the major gene products dysregulated in spinal muscular atrophy models in mice. However, to date, no function has been determined for the gene. We have identified chodl and other novel genes potentially involved in motor axon differentiation, by expression profiling of transgenically labeled motor neurons in embryonic zebrafish. To enrich the profile for genes involved in differentiation of peripheral motor axons, we inhibited the function of LIM-HDs (LIM homeodomain factors) by overexpression of a dominant-negative cofactor, thereby rendering labeled axons unable to grow out of the spinal cord. Importantly, labeled cells still exhibited axon growth and most cells retained markers of motor neuron identity. Functional tests of chodl, by overexpression and knockdown, confirm crucial functions of this gene for motor axon growth in vivo. Indeed, knockdown of chodl induces arrest or stalling of motor axon growth at the horizontal myoseptum, an intermediate target and navigational choice point, and reduced muscle innervation at later developmental stages. This phenotype is rescued by chodl overexpression, suggesting that correct expression levels of chodl are important for interactions of growth cones of motor axons with the horizontal myoseptum. Combined, these results identify upstream regulators and downstream functions of chodl during motor axon growth.
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