Cyclin D1 Again Caught in the Act: Dyrk1a Links G1 and Neurogenesis in Down Syndrome

Ian Smith,Federico Calegari

doi:10.1016/j.ebiom.2015.02.003

Abstract

Cyclin D1 Again Caught in the Act: Dyrk1a Links G1 and Neurogenesis in Down Syndrome

Highlights

During mammalian corticogenesis, radial glial (RG) cells primarily divide to either expand their own population or produce intermediate progenitors (IPs)
Changes in cell cycle regulation and cell fate change of neural progenitors were already reported in trisomic mouse models of Down syndrome (DS) (Haydar and Reeves, 2012) and it was known that Dyrk1a could somehow influence both cell cycle progression and neurogenesis in vitro and in vivo (Soppa et al, 2014; Yabut et al, 2010)
Consistent with a decrease in the levels of cyclin D1, the authors found that an increase in the Dyrk1a gene dosage caused a lengthening of both G1 and S phases

Summary

Introduction

Radial glial (RG) cells primarily divide to either expand their own population or produce intermediate progenitors (IPs). Changes in cell cycle regulation and cell fate change of neural progenitors were already reported in trisomic mouse models of DS (Haydar and Reeves, 2012) and it was known that Dyrk1a could somehow influence both cell cycle progression and neurogenesis in vitro and in vivo (Soppa et al, 2014; Yabut et al, 2010). Najas and colleagues generated a number of mouse lines in which either three or one allele of Dyrk1a was present.

Results

Conclusion