PMID- 23006775
OWN - NLM
STAT- MEDLINE
DCOM- 20130722
LR  - 20191014
IS  - 1095-9327 (Electronic)
IS  - 1044-7431 (Linking)
VI  - 52
DP  - 2013 Jan
TI  - beta3GnT2 null mice exhibit defective accessory olfactory bulb innervation.
PG  - 73-86
LID - S1044-7431(12)00179-0 [pii]
LID - 10.1016/j.mcn.2012.09.003 [doi]
AB  - 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.
CI  - Published by Elsevier Inc.
FAU - Henion, Timothy R
AU  - Henion TR
AD  - Department of Cell Biology, University of Massachusetts Medical School, 55 Lake 
      Avenue North, Worcester, MA 01655, USA. timothy.henion@umassmed.edu
FAU - Madany, Pasil A
AU  - Madany PA
FAU - Faden, Ashley A
AU  - Faden AA
FAU - Schwarting, Gerald A
AU  - Schwarting GA
LA  - eng
GR  - DC00953/DC/NIDCD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20120921
PL  - United States
TA  - Mol Cell Neurosci
JT  - Molecular and cellular neurosciences
JID - 9100095
RN  - 0 (Cell Adhesion Molecules)
RN  - EC 2.4.1.- (N-Acetylglucosaminyltransferases)
RN  - EC 2.4.1.149 (B3GNT2 protein, human)
SB  - IM
MH  - Animals
MH  - Axons/*metabolism
MH  - Cell Adhesion Molecules/*metabolism
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Mice
MH  - Mice, Knockout
MH  - N-Acetylglucosaminyltransferases/*metabolism
MH  - Olfactory Bulb/*metabolism
MH  - Vomeronasal Organ/*innervation/metabolism
EDAT- 2012/09/26 06:00
MHDA- 2013/07/23 06:00
CRDT- 2012/09/26 06:00
PHST- 2012/01/26 00:00 [received]
PHST- 2012/08/14 00:00 [revised]
PHST- 2012/09/14 00:00 [accepted]
PHST- 2012/09/26 06:00 [entrez]
PHST- 2012/09/26 06:00 [pubmed]
PHST- 2013/07/23 06:00 [medline]
AID - S1044-7431(12)00179-0 [pii]
AID - 10.1016/j.mcn.2012.09.003 [doi]
PST - ppublish
SO  - Mol Cell Neurosci. 2013 Jan;52:73-86. doi: 10.1016/j.mcn.2012.09.003. Epub 2012 
      Sep 21.