Loss of RhoA in neural progenitor cells causes the disruption of adherens junctions and hyperproliferation

• DOI: 10.1073/pnas.1101347108
• Publication Date: 2011-04-19T04:19:39Z
• Authors: Kei-ichi Katayama; Jaime Melendez; Jessica M. Baumann; Jennifer R. Leslie; Bharesh K. Chauhan; Niza Nemkul; Richard A. Lang; Chia-Yi Kuan; Yi Zheng; Yutaka Yoshida
• Keywords: Adherens junction; Neuroepithelial cell; Neural Development; Beta-catenin

The organization of neural progenitors in the developing mammalian neuroepithelium is marked by cadherin-based adherens junctions. Whereas RhoA, a founding member small Rho GTPase family, has been shown to play important roles epithelial junctions, its physiological development remain uncertain due lack specific loss-of-function studies. Here, we show that RhoA protein accumulates at junctions mouse brain and colocalizes cadherin–catenin complex. Conditional deletion midbrain forebrain using Wnt1-Cre Foxg1-Cre mice, respectively, disrupts apical causes massive dysplasia brain. Furthermore, -deficient progenitor cells exhibit accelerated proliferation, reduction cell- cycle exit, increased expression downstream target genes hedgehog pathway. Consequently, both lines conditional embryos expansion exencephaly-like protrusions. These results demonstrate critical role maintenance regulation proliferation