ArticleMolecular brain2015
Fstl1 is involved in the regulation of radial glial scaffold development.
Article in Molecular brain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- The Adipose-Sympathetic Nerve Crosstalk: FSTL1 as an Adipocyte-Derived Neurotrophic Factor for WAT Browning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Comparative Multiomics Analysis of Cerebral Organoid-Derived Exosomes during Organoid Maturation.Nano letters · 2026Article
- Post-symptomatic administration of hMSCs exerts therapeutic effects in SCA2 mice.Stem cell research & therapy · 2024Article
- Radial glia progenitor polarity in health and disease.Frontiers in cell and developmental biology · 2024Review
- PDK1 Regulates the Maintenance of Cell Body and the Development of Dendrites of Purkinje Cells by pS6 and PKCγ.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Extracellular Control of Radial Glia Proliferation and Scaffolding During Cortical Development and Pathology.Frontiers in cell and developmental biology · 2020Review
- Expression of the RNA methyltransferase Nsun5 is essential for developing cerebral cortex.Molecular brain · 2019Article
- Follistatin-like 1 in development and human diseases.Cellular and molecular life sciences : CMLS · 2018Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRadial 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.
resultsHere, 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.
conclusionsIn 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.
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