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The neuroepithelium gives rise to a great number of neurons and glial cells during mammalian neocortical development.Both neuroepithelial cells and radial glial cells(RGC),which form later,are defined as apical progenitors(APs)because these progenitors are localized at the apical surface of the neuroepithelium.APs exhibit a bipolar shape and share an evolutionarily conserved feature: interkinetic nuclear migration(INM).During the cell cycle,the nuclei of the APs move towards the basal side of the ventricular zone(VZ)during G1 phase,undergo DNA synthesis(S phase),migrate rapidly to the apical surface during G2 phase and then undergo mitosis (Gotz and Huttner,2005; Taverna and Huttner,2010; Willardsen and Link,2011).The nuclei of APs at various positions along the apical-basal axis in the VZ give rise to the remarkable pseudostratification of the mammalian neuroepithelium.This feature is thought to maximize the output of the neuroepithelium(Taverna and Huttner,2010)and to be important for tissue-shape formation(Reiner et al.,2012).Genetic and pharmacological studies have revealed that the cell cycle is required for INM,while INM is dispensable for normal cell cycle progression.Furthermore,nuclear migration remains coordinated with the cell cycle when the cell cycle is modified (Murciano et al.,2002; Schenk et al.,2009; Kosodo et al.,2011).Subsequent studies demonstrated that INM is also highly correlated with neurogenesis(Fietz and Huttner,2011; Willardsen and Link,2011; Kosodo,2012).Additionally,INM is important for regulating proliferation vs.differentiation (Willardsen and Link,2011; Murciano et al.,2002; Buchman and Tsai,2008; Kageyama et al.,2009; Latasa et al.,2009).Forkhead transcription factor M1(FoxM1),a key cell cycle regulator,is a novel candidate that might link proliferation and differentiation(Yokomine et al.,2009; Kalin et al.,2011).Although the functions of FoxM1 in cell cycle progression have been well studied (Krupczak-Hollis et al.,2004; Schuller et al.,2007; Fu et al.,2008; Costa,2005; Laoukili et al.,2007; Radhakrishnan and Gartel,2008),the link between the cell cycle regulator FoxM1 and INM has not yet been examined,and the possible effects of FoxM1 on behavior remain unknown.In the present study,we observed that the conditional disruption of FoxM1 in the telencephalon results in an impairment of INM and abnormal cell cycle progression; these effects are accompanied by a decrease in the number of APs,which may be due to the downregulation of Cyclin B1 and cdc25b.Furthermore,impaired basal-to-apical INM disturbs AP synchronization,resulting in an increased number of BPs in the developing cortex; this leads to a slight reduction in the number of cortical neurons,and the FoxM1 mutants exhibited decreased anxiety-related behavior.Our study demonstrates that the cell cycle regulator FoxM1 is required for INM,and more importantly,deficiency in FoxM1 has effects on adult behavior.