β3GnT2 null mice exhibit defective accessory olfactory bulb innervation

Area of Science:

• Neuroscience
• Molecular Biology
• Developmental Biology

Background:

• Vomeronasal sensory neurons (VSNs) project to the accessory olfactory bulb (AOB), segregating into anterior (aAOB) and posterior (pAOB) compartments to relay pheromone signals.
• The glycosyltransferase β3GnT2 in the olfactory epithelium (OE) is known to regulate axon guidance cues for proper neuronal organization.
• Mechanisms governing mammalian vomeronasal targeting and AOB organization are not fully understood.

Purpose of the Study:

• To investigate the role of β3GnT2 in vomeronasal system axon guidance and AOB organization.
• To determine how β3GnT2 influences the expression of guidance and adhesion molecules in the vomeronasal system.
• To elucidate the impact of β3GnT2 deficiency on VSN projection patterns and glomerular formation in the AOB.

Main Methods:

• Analysis of β3GnT2 knockout mice (β3GnT2(-/-)) and wildtype littermates.
• Immunohistochemical staining to examine the expression patterns of ephrinA5, V2r1b, Kirrel2, and OCAM.
• Microscopic analysis of AOB structure, including glomerular morphology and compartmentalization.

Main Results:

• β3GnT2 deficiency alters ephrinA5 expression, leading to its upregulation on aAOB axons.
• Despite altered ephrinA5, apical and basal VSN projections remain segregated, but V2r1b axons inappropriately innervate the aAOB due to ectopic receptor expression.
• Loss of Kirrel2 and OCAM in β3GnT2(-/-) aAOB results in increased V2r1b glomeruli and failed formation of distinct anterior glomeruli.

Conclusions:

• β3GnT2 plays a distinct role in the vomeronasal system, regulating guidance and adhesion molecules essential for AOB organization.
• β3GnT2 glycosylation is vital for maintaining expression of layer-specific vomeronasal receptors and adhesion molecules.
• Proper AOB glomerular formation and vomeronasal sensory processing depend on β3GnT2-mediated regulation of molecular expression.