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  • 标题:Atypical TGF-β signaling controls neuronal guidance in Caenorhabditis elegans
  • 本地全文:下载
  • 作者:Oguzhan Baltaci ; Mikael Egebjerg Pedersen ; Tessa Sherry
  • 期刊名称:iScience
  • 印刷版ISSN:2589-0042
  • 出版年度:2022
  • 卷号:25
  • 期号:2
  • 页码:1-18
  • DOI:10.1016/j.isci.2022.103791
  • 语种:English
  • 出版社:Elsevier
  • 摘要:SummaryCoordinated expression of cell adhesion and signaling molecules is crucial for brain development. Here, we report that theCaenorhabditis eleganstransforming growth factor β (TGF-β) type I receptor SMA-6 (small-6) acts independently of its cognate TGF-β type II receptor DAF-4 (dauer formation-defective-4) to control neuronal guidance. SMA-6 directs neuronal development from the hypodermis through interactions with three, orphan, TGF-β ligands. Intracellular signaling downstream of SMA-6 limits expression of NLR-1, an essential Neurexin-like cell adhesion receptor, to enable neuronal guidance. Together, our data identify an atypical TGF-β-mediated regulatory mechanism to ensure correct neuronal development.Graphical abstractDisplay OmittedHighlights•TheCaenorhabditis elegansTGF-β type I receptor SMA-6 controls neuronal guidance•SMA-6 acts independently of the TGF-β type II receptor to control neuronal guidance•SMA-6 signaling limits expression of the NLR-1 neurexin-like cell adhesion receptor•Epidermal mis-expression of NLR-1 causes neuronal guidance defectsBiological sciences; Molecular neuroscience; Developmental neuroscience
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