, 2008 and Shitamukai et al., 2011). Moreover, a novel type of self-renewing progenitor cells that have no contact with the ventricular surface, termed outer radial glial cells (oRGs), has recently been described in the cerebral cortex in several mammalian species, including mice, in which they are rare, and ferrets and humans, in which they are abundant (Fietz and Huttner, 2011 and Lui et al., 2011). oRGs retain a basal process

that may be important for the reception of signals maintaining the progenitor state, such as Notch signal. However, they are devoid PD0332991 of an apical process and apically located polarity molecules such as CD133, Par3, or aPKC (Fietz and Huttner, 2011 and Lui et al., 2011). So, why do NPCs that express Foxp4 and lose their apical process attachment (but presumably retain a basal process) differentiate rather than continue to self renew? One possibility is that a neuronal fate determinant tethered to apical junctions in neuroepithelial NPCs is released by the disruption of adherens SKI-606 concentration junctions and thus becomes free

to promote differentiation (Bultje et al., 2009). Consistent with this model, Rousso et al. (2012) show that the Notch pathway inhibitor Numb is released into the cytoplasm when Foxp4 is overexpressed or N-cadherin activity is antagonized. They suggest that the resulting inhibition of Notch signaling might contribute to the initiation of neuronal differentiation that follows adherens junction disruption. In contrast, a change of plane of division, such as that occurring in LGN mutant mice (Konno et al., 2008), might segregate the daughter cell losing the apical domain away from the apically localized neuronal

fate determinant and thus Olopatadine allow this cell to remain proliferative. Further investigation should provide fascinating insights on how Foxp genes control the fate of neuroepithelial NPCs and contribute to the generation of other types of progenitors found in mammalian cortices. “
“Although most cells are measured in microns, neurons, especially peripheral neurons, can be a meter long and therefore make extreme demands on our molecular motors. Small wonder that mutations in ubiquitous motor proteins give rise to specifically neurological diseases. Two such diseases, Perry syndrome and the distal hereditary motor neuropathy 7B (HMN7B), are examples of that phenomenon and their cell biological basis has been examined by two papers in this issue of Neuron ( Moughamian and Holzbaur, 2012 and Lloyd et al., 2012). Although their symptoms are quite different, both diseases are caused by mutations in the same domain of the dynactin subunit p150Glued. By approaching the function of this domain in Drosophila neurons and mouse dorsal root ganglion (DRG) neurons, the present studies illuminate the function of p150Glued in axonal transport. Axonal microtubules are uniformly polarized with their plus ends away from the soma.