The role of Diaphanous in the reactivation of quiescent neural stem cells
Authors: Kun-Yang Lin 1; Wei Yung Ding 1; Hongyan Wang 1,2
Affiliations: 1) Neuroscience & Behavioral Disorders Programme, Duke-NUS Medical School, Singapore, ; 2) Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
Keywords: c. neural stem cells; a. cytoskeleton
The switch between quiescence and proliferation of stem cells is critical for tissue development and homeostasis. The failure of neural stem cell reactivation is associated with neurodevelopmental disorders, such as microcephaly. Drosophila neural stem cells (NSCs) have emerged as an ideal in vivo model for studying quiescence and reactivation. Previously, we discovered that the primary protrusion, a hallmark of quiescent NSCs, is enriched for the actin cytoskeleton. However, the role of the actin cytoskeleton and its regulators have not been established in quiescent NSCs. Here, we report that Diaphanous (Dia), an actin regulator promoting actin polymerization, regulates F-actin polymerization and reactivation of quiescent NSCs. dia mutants show delayed NSC reactivation and small brain phenotype. Depletion of dia via RNA interference in the quiescent NSCs causes a reactivation delay and the reduction of Filamentous actin. Moreover, overexpression of constitutively active form of Dia leads to the delay of NSC reactivation and larval growth, while overexpressing wild-type form of Dia does not affect NSC reactivation. Together, our results suggest that Dia regulates actin polymerization and is a novel regulator for the reactivation in quiescence NSC.