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    beta3GnT2 null mice exhibit defective accessory olfactory bulb innervation

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    Authors
    Henion, Timothy R.
    Madany, Pasil A.
    Faden, Ashley A.
    Schwarting, Gerald A.
    UMass Chan Affiliations
    Department of Cell and Developmental Biology
    Document Type
    Journal Article
    Publication Date
    2013-01-01
    Keywords
    Olfactory Bulb
    Sensory Receptor Cells
    Vomeronasal Organ
    N-Acetylglucosaminyltransferases
    Cell and Developmental Biology
    Cell Biology
    Neuroscience and Neurobiology
    
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    http://dx.doi.org/10.1016/j.mcn.2012.09.003
    Abstract
    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.
    Source
    Mol Cell Neurosci. 2013 Jan;52:73-86. doi: 10.1016/j.mcn.2012.09.003. Link to article on publisher's site
    DOI
    10.1016/j.mcn.2012.09.003
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/26440
    PubMed ID
    23006775
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.mcn.2012.09.003
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