Conditional genetic labeling of mitral cells of the mouse accessory olfactory bulb to visualize the organization of their apical dendritic tufts.

Chemical information captured through the vomeronasal sensory neurons is transmitted to mitral cells in the accessory olfactory bulb (AOB). Morphological characterization of AOB mitral cells is crucial to reveal the mechanisms underlying pheromone and other chemical information processing. Here, we developed a conditional genetic approach to visualize single AOB mitral cells in mice and analyzed the distribution of their apical dendritic tufts and cell bodies. We found that there is a subpopulation of superficial AOB mitral cells with small cell bodies and simple dendritic arborization. We also showed that segregation of the anterior and posterior AOB appears incomplete at the level of the mitral cell positions. Furthermore, we demonstrated that significant population of the anterior AOB mitral cells has multiple apical dendritic tufts organized in a quite small range along the dorsal-ventral axis. These findings have important implications in how various chemical signals may be processed in the AOB.

Lim kinase regulates the development of olfactory and neuromuscular synapses.

Lim Kinase (Limk) belongs to a phylogenetically conserved family of serine/threonine kinases, which have been shown to be potent regulators of the actin cytoskeleton. Despite accumulating evidence of its biochemical actions, its in vivo function has remained poorly understood. The association of the Limk1 gene with Williams Syndrome indicates that proteins of this family play a role in the nervous system. To unravel the cellular and molecular functions of Limk, we have either knocked out or activated the Limk gene in Drosophila. At the neuromuscular junction, loss of Limk leads to enlarged terminals, while increasing the activity of Limk leads to stunted terminals with fewer synaptic boutons. In the antennal lobe, loss of Limk abolishes the ability of p21-activated kinase (Pak) to alter glomerular development. In contrast, increase in Limk function leads to ectopic glomeruli, a phenotype suppressible by the coexpression of a hyperactive Cofilin gene. These results establish Limk as a critical regulator of Cofilin function and synapse development, and a downstream effector of Pak in vivo.