RRC ID 81491
Author Lin KY, Gujar MR, Lin J, Ding WY, Huang J, Gao Y, Tan YS, Teng X, Christine LSL, Kanchanawong P, Toyama Y, Wang H.
Title Astrocytes control quiescent NSC reactivation via GPCR signaling-mediated F-actin remodeling.
Journal Sci Adv
Abstract The transitioning of neural stem cells (NSCs) between quiescent and proliferative states is fundamental for brain development and homeostasis. Defects in NSC reactivation are associated with neurodevelopmental disorders. Drosophila quiescent NSCs extend an actin-rich primary protrusion toward the neuropil. However, the function of the actin cytoskeleton during NSC reactivation is unknown. Here, we reveal the fine filamentous actin (F-actin) structures in the protrusions of quiescent NSCs by expansion and super-resolution microscopy. We show that F-actin polymerization promotes the nuclear translocation of myocardin-related transcription factor, a microcephaly-associated transcription factor, for NSC reactivation and brain development. F-actin polymerization is regulated by a signaling cascade composed of G protein-coupled receptor Smog, G protein αq subunit, Rho1 guanosine triphosphatase, and Diaphanous (Dia)/Formin during NSC reactivation. Further, astrocytes secrete a Smog ligand folded gastrulation to regulate Gαq-Rho1-Dia-mediated NSC reactivation. Together, we establish that the Smog-Gαq-Rho1 signaling axis derived from astrocytes, an NSC niche, regulates Dia-mediated F-actin dynamics in NSC reactivation.
Volume 10(30)
Pages eadl4694
Published 2024-7-26
DOI 10.1126/sciadv.adl4694
PMID 39047090
PMC PMC11268418
MeSH Actin Cytoskeleton / metabolism Actins* / metabolism Animals Astrocytes* / metabolism Drosophila Proteins* / genetics Drosophila Proteins* / metabolism Drosophila melanogaster / metabolism Neural Stem Cells* / cytology Neural Stem Cells* / metabolism Receptors, G-Protein-Coupled* / metabolism Signal Transduction* rho GTP-Binding Proteins / metabolism
Resource
Drosophila DGRC#105188 DGRC#112853