title: Fstl1 is involved in the regulation of radial glial scaffold development.
abstract: BACKGROUND
  Radial glial cells (RGCs), the instructive scaffolds for neuronal migration, are well characterized by their unique morphology and polarization; these cells extend elongated basal processes to the pial basement membrane (BM) and parallel to one another. However, little is known about the mechanisms that underlie the developmental regulation and maintenance of this unique morphology.
  
  
  RESULTS
  Here, by crossing Fstl1 (fl/fl) mice with an EIIa-Cre line, we identified a new role for the secreted glycoprotein Follistatin like-1 (FSTL1). The ablation of Fstl1 in both of its cortical expression domains, the ventricular zone (VZ) and the pia mater, resulted in RGC morphologic disruption; basal processes were not parallel to each other, and endfeet exhibited greater density and branching. However, Fstl1 deletion in only the VZ in the Emx1 (IREScre); Fstl1 (fl/fl) line did not affect RGC morphology, indicating that FSTL1 derived from the pia mater might be more important for RGC morphology. In addition, upper-layer projection neurons, not deeper-layer projection neurons, failed to reach their appropriate positions. We also found that BMP, AKT/PKB, Cdc42, GSK3β, integrin and reelin signals, which have previously been reported to regulate RGC development, were unchanged, indicating that Fstl1 may function through a unique mechanism.
  
  
  CONCLUSIONS
  In the present study, we identified a new role for FSTL1 in the development of radial glial scaffolds and the neuronal migration of upper-layer projection neurons. Our findings will improve understanding of the regulation of RGC development and neuronal migration.
authors.affiliation: Key Laboratory of Developmental Genes and Human Diseases, MOE, Department of Anatomy and Neuroscience, Medical School, Southeast University, Nanjing, 210009, China. ruiliu_1986@sina.com.
authors.forename: Rui
authors.initials: R
authors.lastname: Liu
authors.affiliation: Key Laboratory of Developmental Genes and Human Diseases, MOE, Department of Anatomy and Neuroscience, Medical School, Southeast University, Nanjing, 210009, China. ate5455@163.com.
authors.forename: Yang
authors.initials: Y
authors.lastname: Yang
authors.affiliation: Key Laboratory of Developmental Genes and Human Diseases, MOE, Department of Anatomy and Neuroscience, Medical School, Southeast University, Nanjing, 210009, China. 961240280@qq.com.
authors.forename: Junhui
authors.initials: J
authors.lastname: Shen
authors.affiliation: Key Laboratory of Developmental Genes and Human Diseases, MOE, Department of Anatomy and Neuroscience, Medical School, Southeast University, Nanjing, 210009, China. m15850656172@163.com.
authors.forename: He
authors.initials: H
authors.lastname: Chen
authors.affiliation: Key Laboratory of Developmental Genes and Human Diseases, MOE, Department of Anatomy and Neuroscience, Medical School, Southeast University, Nanjing, 210009, China. 1558579563@qq.com.
authors.forename: Qianqian
authors.initials: Q
authors.lastname: Zhang
authors.affiliation: Key Laboratory of Developmental Genes and Human Diseases, MOE, Department of Anatomy and Neuroscience, Medical School, Southeast University, Nanjing, 210009, China. 1093802727@qq.com.
authors.forename: Ru
authors.initials: R
authors.lastname: Ba
authors.affiliation: Key Laboratory of Developmental Genes and Human Diseases, MOE, Department of Anatomy and Neuroscience, Medical School, Southeast University, Nanjing, 210009, China. i1206j@qq.com.
authors.forename: Yongjie
authors.initials: Y
authors.lastname: Wei
authors.affiliation: Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China. kaichengl@yahoo.com.
authors.forename: Kai-Cheng
authors.initials: KC
authors.lastname: Li
authors.affiliation: Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China. xu.zhang@ion.ac.cn.
authors.forename: Xu
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Key Laboratory of Developmental Genes and Human Diseases, MOE, Department of Anatomy and Neuroscience, Medical School, Southeast University, Nanjing, 210009, China. zhaocj@seu.edu.cn.|Center of Depression, Beijing Institute for Brain Disorders, Beijing, 100069, China. zhaocj@seu.edu.cn.
authors.forename: Chunjie
authors.initials: C
authors.lastname: Zhao
mesh_terms: D000818:Animals; D001485:Basement Membrane / Q000378:metabolism; D016764:Cell Polarity; D048430:Cell Shape; D002540:Cerebral Cortex / Q000166:cytology / Q000378:metabolism; D002552:Cerebral Ventricles / Q000166:cytology / Q000378:metabolism; D038702:Follistatin-Related Proteins / Q000172:deficiency / Q000378:metabolism*; D017353:Gene Deletion; D051379:Mice; D009457:Neuroglia / Q000166:cytology / Q000378:metabolism*; D010841:Pia Mater / Q000378:metabolism; D000091042:Reelin Protein
chemical_list: D038702:Follistatin-Related Proteins; C448720:Fstl1 protein, mouse; D000091042:Reelin Protein; C000717127:RELN protein, human; C000717128:Reln protein, mouse