title: Sox9 is critical for suppression of neurogenesis but not initiation of gliogenesis in the cerebellum.
abstract: BACKGROUND
  The high mobility group (HMG) family transcription factor Sox9 is critical for induction and maintenance of neural stem cell pool in the central nervous system (CNS). In the spinal cord and retina, Sox9 is also the master regulator that defines glial fate choice by mediating the neurogenic-to-gliogenic fate switch. On the other hand, the genetic repertoire governing the maintenance and fate decision of neural progenitor pool in the cerebellum has remained elusive.
  
  
  RESULTS
  By employing the Cre/loxP strategy, we specifically inactivated Sox9 in the mouse cerebellum. Unexpectedly, the self-renewal capacity and multipotency of neural progenitors at the cerebellar ventricular zone (VZ) were not perturbed upon Sox9 ablation. Instead, the mutants exhibited an increased number of VZ-derived neurons including Purkinje cells and GABAergic interneurons. Simultaneously, we observed continuous neurogenesis from Sox9-null VZ at late gestation, when normally neurogenesis ceases to occur and gives way for gliogenesis. Surprisingly, glial cell specification was not affected upon Sox9 ablation.
  
  
  CONCLUSIONS
  Our findings suggest Sox9 may mediate the neurogenic-to-gliogenic fate switch in mouse cerebellum by modulating the termination of neurogenesis, and therefore indicate a functional discrepancy of Sox9 between the development of cerebellum and other major neural tissues.
authors.affiliation: School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, P.R. China. kiv1417@gmail.com.
authors.forename: Keng Ioi
authors.initials: KI
authors.lastname: Vong
authors.affiliation: School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, P.R. China. crystal.127@gmail.com.
authors.forename: Crystal Kit Ying
authors.initials: CK
authors.lastname: Leung
authors.affiliation: Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA. rrb@mdanderson.org.
authors.forename: Richard R
authors.initials: RR
authors.lastname: Behringer
authors.affiliation: School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, P.R. China. kmkwan@cuhk.edu.hk.|RGC-AoE Centre for Organelle Biogenesis and Function, The Chinese University of Hong Kong, Hong Kong, P.R. China. kmkwan@cuhk.edu.hk.|Partner State Key Laboratory of Agrobiotechnology (CUHK), The Chinese University of Hong Kong, Hong Kong, P.R. China. kmkwan@cuhk.edu.hk.
authors.forename: Kin Ming
authors.initials: KM
authors.lastname: Kwan
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D019070:Cell Lineage; D049109:Cell Proliferation; D002531:Cerebellum / Q000166:cytology*; D005260:Female; D005455:Fluorescent Antibody Technique; D019426:Integrases / Q000378:metabolism; D018345:Mice, Knockout; D039902:Multipotent Stem Cells / Q000166:cytology / Q000378:metabolism; D058953:Neural Stem Cells / Q000166:cytology / Q000378:metabolism; D055495:Neurogenesis; D009457:Neuroglia / Q000166:cytology / Q000378:metabolism*; D012165:Retinal Ganglion Cells / Q000166:cytology / Q000378:metabolism; D055758:SOX9 Transcription Factor / Q000378:metabolism*
chemical_list: D055758:SOX9 Transcription Factor; C045073:Cre recombinase; D019426:Integrases