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dc.contributor.authorZhong, Zhen
dc.contributor.authorOhnmacht, Jochen
dc.contributor.authorReimer, Michell M.
dc.contributor.authorBach, Ingolf
dc.contributor.authorBecker, Thomas C.
dc.contributor.authorBecker, Catherina G.
dc.date2022-08-11T08:10:15.000
dc.date.accessioned2022-08-23T17:01:15Z
dc.date.available2022-08-23T17:01:15Z
dc.date.issued2012-03-28
dc.date.submitted2012-04-24
dc.identifier.citationJ Neurosci. 2012 Mar 28;32(13):4426-39. <a href="http://dx.doi.org/10.1523/JNEUROSCI.5179-11.2012">Link to article on publisher's site</a>
dc.identifier.issn0270-6474 (Linking)
dc.identifier.doi10.1523/JNEUROSCI.5179-11.2012
dc.identifier.pmid22457492
dc.identifier.urihttp://hdl.handle.net/20.500.14038/43967
dc.description.abstractThe 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.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=22457492&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1523/JNEUROSCI.5179-11.2012
dc.subjectMembrane Proteins
dc.subjectLectins, C-Type
dc.subjectAxons
dc.subjectMotor Neurons
dc.subjectCell and Developmental Biology
dc.subjectGenetics and Genomics
dc.titleChondrolectin mediates growth cone interactions of motor axons with an intermediate target
dc.typeJournal Article
dc.source.journaltitleThe Journal of neuroscience : the official journal of the Society for Neuroscience
dc.source.volume32
dc.source.issue13
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/pgfe_pp/179
dc.identifier.contextkey2792616
html.description.abstract<p>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.</p>
dc.identifier.submissionpathpgfe_pp/179
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentProgram in Gene Function and Expression
dc.source.pages4426-39


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