Crumbs 2 prevents cortical abnormalities in mouse dorsal telencephalon. (July 2016)

• Record Type: Journal Article
• Authors: Dudok, Jacobus J.; Murtaza, Mariyam; Henrique Alves, C.; Rashbass, Pen; Wijnholds, Jan
• Is Part Of: Neuroscience research. Volume 108(2016:Jul.)
• Page Start: 12
• Page End: 23
• Publication Date: 2016-07
• Subjects: CRB2 -- Cortex -- Apical -- Development -- PALS1 -- Polarity; Neurosciences -- Research -- Periodicals; Neurosciences -- Research -- Japan -- Periodicals; Neurology -- Periodicals; Neurosciences -- Periodicals; Neurosciences -- Recherche -- Périodiques; Neurosciences -- Recherche -- Japon -- Périodiques; Neurosciences -- Research; Japan; Periodicals; 612.8
• DOI: 10.1016/j.neures.2016.01.001
• Languages: English
• ISSNs: 0168-0102

Abstract

Highlights: Loss of CRB2 in the cortex leads to defects in maintenance of the apical complex. Loss of cortical CRB2 leads to premature expression of differentiation proteins. Loss of CRB2 in the cortex results in an increased number of mitotic cells. Abstract: The formation of a functionally integrated nervous system is dependent on a highly organized sequence of events that includes timely division and differentiation of progenitors. Several apical polarity proteins have been shown to play crucial roles during neurogenesis, however, the role of Crumbs 2 (CRB2) in cortical development has not previously been reported. Here, we show that conditional ablation of Crb2 in the murine dorsal telencephalon leads to defects in the maintenance of the apical complex. Furthermore, within the mutant dorsal telencephalon there is premature expression of differentiation proteins. We examined the physiological function of Crb2 on wild type genetic background as well as on background lacking Crb1 . Telencephalon lacking CRB2 resulted in reduced levels of PALS1 and CRB3 from the apical complex, an increased number of mitotic cells and expanded neuronal domain. These defects are transient and therefore only result in rather mild cortical abnormalities. We show that CRB2 is required for maintenance of the apical polarity complex during development of the cortex and regulation of cell division, and that loss of CRB2 results in cortical abnormalities.