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dc.contributor.authorHenion, Timothy R.
dc.contributor.authorMadany, Pasil A.
dc.contributor.authorFaden, Ashley A.
dc.contributor.authorSchwarting, Gerald A.
dc.date2022-08-11T08:08:03.000
dc.date.accessioned2022-08-23T15:40:37Z
dc.date.available2022-08-23T15:40:37Z
dc.date.issued2013-01-01
dc.date.submitted2013-03-22
dc.identifier.citationMol Cell Neurosci. 2013 Jan;52:73-86. doi: 10.1016/j.mcn.2012.09.003. <a href="http://dx.doi.org/10.1016/j.mcn.2012.09.003">Link to article on publisher's site</a>
dc.identifier.issn1044-7431 (Linking)
dc.identifier.doi10.1016/j.mcn.2012.09.003
dc.identifier.pmid23006775
dc.identifier.urihttp://hdl.handle.net/20.500.14038/26440
dc.description.abstractVomeronasal sensory neurons (VSNs) extend axons to the accessory olfactory bulb (AOB) where they form synaptic connections that relay pheromone signals to the brain. The projections of apical and basal VSNs segregate in the AOB into anterior (aAOB) and posterior (pAOB) compartments. Although some aspects of this organization exhibit fundamental similarities with the main olfactory system, the mechanisms that regulate mammalian vomeronasal targeting are not as well understood. In the olfactory epithelium (OE), the glycosyltransferase beta3GnT2 maintains expression of axon guidance cues required for proper glomerular positioning and neuronal survival. We show here that beta3GnT2 also regulates guidance and adhesion molecule expression in the vomeronasal system in ways that are partially distinct from the OE. In wildtype mice, ephrinA5(+) axons project to stereotypic subdomains in both the aAOB and pAOB compartments. This pattern is dramatically altered in beta3GnT2(-/-) mice, where ephrinA5 is upregulated exclusively on aAOB axons. Despite this, apical and basal VSN projections remain strictly segregated in the null AOB, although some V2r1b axons that normally project to the pAOB inappropriately innervate the anterior compartment. These fibers appear to arise from ectopic expression of V2r1b receptors in a subset of apical VSNs. The homotypic adhesion molecules Kirrel2 and OCAM that facilitate axon segregation and glomerular compartmentalization in the main olfactory bulb are ablated in the beta3GnT2(-/-) aAOB. This loss is accompanied by a two-fold increase in the total number of V2r1b glomeruli and a failure to form morphologically distinct glomeruli in the anterior compartment. These results identify a novel function for beta3GnT2 glycosylation in maintaining expression of layer-specific vomeronasal receptors, as well as adhesion molecules required for proper AOB glomerular formation.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=23006775&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.mcn.2012.09.003
dc.subjectOlfactory Bulb
dc.subjectSensory Receptor Cells
dc.subjectVomeronasal Organ
dc.subjectN-Acetylglucosaminyltransferases
dc.subjectCell and Developmental Biology
dc.subjectCell Biology
dc.subjectNeuroscience and Neurobiology
dc.titlebeta3GnT2 null mice exhibit defective accessory olfactory bulb innervation
dc.typeJournal Article
dc.source.journaltitleMolecular and cellular neurosciences
dc.source.volume52
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/cellbiology_pp/122
dc.identifier.contextkey3943383
html.description.abstract<p>Vomeronasal sensory neurons (VSNs) extend axons to the accessory olfactory bulb (AOB) where they form synaptic connections that relay pheromone signals to the brain. The projections of apical and basal VSNs segregate in the AOB into anterior (aAOB) and posterior (pAOB) compartments. Although some aspects of this organization exhibit fundamental similarities with the main olfactory system, the mechanisms that regulate mammalian vomeronasal targeting are not as well understood. In the olfactory epithelium (OE), the glycosyltransferase beta3GnT2 maintains expression of axon guidance cues required for proper glomerular positioning and neuronal survival. We show here that beta3GnT2 also regulates guidance and adhesion molecule expression in the vomeronasal system in ways that are partially distinct from the OE. In wildtype mice, ephrinA5(+) axons project to stereotypic subdomains in both the aAOB and pAOB compartments. This pattern is dramatically altered in beta3GnT2(-/-) mice, where ephrinA5 is upregulated exclusively on aAOB axons. Despite this, apical and basal VSN projections remain strictly segregated in the null AOB, although some V2r1b axons that normally project to the pAOB inappropriately innervate the anterior compartment. These fibers appear to arise from ectopic expression of V2r1b receptors in a subset of apical VSNs. The homotypic adhesion molecules Kirrel2 and OCAM that facilitate axon segregation and glomerular compartmentalization in the main olfactory bulb are ablated in the beta3GnT2(-/-) aAOB. This loss is accompanied by a two-fold increase in the total number of V2r1b glomeruli and a failure to form morphologically distinct glomeruli in the anterior compartment. These results identify a novel function for beta3GnT2 glycosylation in maintaining expression of layer-specific vomeronasal receptors, as well as adhesion molecules required for proper AOB glomerular formation.</p>
dc.identifier.submissionpathcellbiology_pp/122
dc.contributor.departmentDepartment of Cell and Developmental Biology
dc.source.pages73-86


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