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Mol Cell Neurosci

Title:		beta3GnT2 null mice exhibit defective accessory olfactory bulb innervation
Author(s):		Henion TR; Madany PA; Faden AA; Schwarting GA;
Address:		"Department of Cell Biology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. timothy.henion@umassmed.edu"
Journal Title:		Mol Cell Neurosci
Year:		2013
Volume:		20120921
Issue:
Page Number:		73 - 86
DOI:		10.1016/j.mcn.2012.09.003
ISSN/ISBN:		1095-9327 (Electronic) 1044-7431 (Linking)
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"
Keywords:		"Animals Axons/*metabolism Cell Adhesion Molecules/*metabolism Immunohistochemistry In Situ Hybridization Mice Mice, Knockout N-Acetylglucosaminyltransferases/*metabolism Olfactory Bulb/*metabolism Vomeronasal Organ/*innervation/metabolism;"
Notes:		"MedlineHenion, Timothy R Madany, Pasil A Faden, Ashley A Schwarting, Gerald A eng DC00953/DC/NIDCD NIH HHS/ Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't 2012/09/26 Mol Cell Neurosci. 2013 Jan; 52:73-86. doi: 10.1016/j.mcn.2012.09.003. Epub 2012 Sep 21"