CAMSAP2 and CAMSAP3 are differentially distributed in neuronal dendrites and axons, controlling their extension and polarity ( Pongrakhananon et al., 2018 Yau et al., 2014). For example, CAMSAP3 is localized at the apical cortex of intestinal epithelial cells, producing apicobasal arrays of MTs in these cells ( Muroyama et al., 2018 Toya et al., 2016). These proteins specifically bind to the MT minus ends, and are localized at various subcellular sites to which they tether MTs, resulting in formation of MT networks distinct from those organized by the centrosomes. The CAMSAP3 (Nezha)/Patronin family proteins are responsible for assembly of non-centrosomal MTs ( Baines et al., 2009 Goodwin and Vale, 2010 Jiang et al., 2014 Meng et al., 2008 Tanaka et al., 2012). These findings suggest that CAMSAP3 supports mTORC1 signaling required for ependymal cell growth via MT network regulation, and, in turn, shaping of the lateral ventricles. Lysosomes, which mediate mTORC1 activation, tended to be reduced at the apical regions of the mutant cells, along with disorganized apical MT networks at the corresponding sites. mTORC1 was required for ependymal cell growth but its activity was downregulated in mutant cells. This defect was ascribed at least in part to a failure of neocortical ependymal cells to broaden their apical domain, a process necessary for expanding the ventricular cavities. Camsap3-mutated mice showed abnormally narrow lateral ventricles, in which excessive stenosis or fusion was induced, leading to a decrease of neural stem cells at the ventricular and subventricular zones. In differentiating ependymal cells, CAMSAP3 became concentrated at the apical domains, serving to generate MT networks at these sites. Here, we show that CAMSAP3, a non-centrosomal microtubule regulator, is important for shaping the lateral ventricles. Microtubules (MTs) regulate numerous cellular processes, but their roles in brain morphogenesis are not well known.
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