β-Catenin signals regulate cell growth and the balance between progenitor cell expansion and differentiation in the nervous system

Abstract

beta-Catenin is an essential component of the canonical Wnt signaling system that controls decisive steps in development. We employed here two conditional beta-catenin mutant alleles to alter beta-catenin signaling in the central nervous system of mice: one allele to ablate beta-catenin and the second allele to express a constitutively active beta-catenin. The tissue mass of the spinal cord and brain is reduced after ablation of beta-catenin, and the neuronal precursor population is not maintained. In contrast, the spinal cord and brain of mice that express activated beta-catenin is much enlarged in mass, and the neuronal precursor population is increased in size. beta-Catenin signals are thus essential for the maintenance of proliferation of neuronal progenitors, controlling the size of the progenitor pool, and impinging on the decision of neuronal progenitors to proliferate or to differentiate.

Molecular regulation of kidney development: is the answer blowing in the Wnt?

“…Another possibility is that canonical signaling could be maintaining the cells of the ureteric bud in a precursor/ undifferentiated state, allowing them to continue dividing and/or branching. Such a role has previously been established for canonical signaling in multiple tissues [68][69][70][71].…”

Canonical and noncanonical Wnt signaling in neural stem/progenitor cells

“…Disrupted production of dentate granule neurons and radial glial scaffolding in KO mice [104] Cortical defects in KO mice [74] Increased differentiation into DA neurons in KO mESCs [59] Delayed DA neuron differentiation in KO mice [105] overexpression or activation of β-catenin expands the neuronal progenitor pool in the developing brain [106,107], and expression of constitutively active β-catenin under the control of the GFAP promoter results in enlarged ventricles and an initial expansion of the PAX6-positive ventricular zone that is subsequently lost. Loss of PAX6 expression is not followed by expression of Tbr2, indicating that differentiation is impaired [108].…”

Localization of planarian β-CATENIN-1 reveals multiple roles during anterior-posterior regeneration and organogenesis

“…Our findings thus support three major roles of β-catenin-1 in anterior regeneration: (1) the specification and maintenance of the anterior signaling center, defined by the tiprelated expression of notum (Petersen and Reddien, 2011) and other genes (Chen et al, 2013;Gaviño et al, 2013;Roberts-Galbraith and Newmark, 2013;Scimone et al, 2014;Vásquez-Doorman and Petersen, 2014;Vogg et al, 2014) (Fig. 6A,B); (2) the regeneration of the brain, through the regulation of the brain-related expression of notum (Hill and Petersen, 2015); and (3) the specification of different neuronal cell types, as described in most animal models (Ciani and Salinas, 2005;Hari et al, 2002;Lewis et al, 2004;Machon et al, 2003;Watanabe et al, 2014;Yu and Malenka, 2003;Zechner et al, 2003).…”