Atypical TGF-β signaling controls neuronal guidance in Caenorhabditis elegans

iScience

Wei Cao¹  Mikael Egebjerg Pedersen²  Goda Snieckute³  Matilda Haas³  Oguzhan Baltaci³  Tessa Sherry³  Ava Handley³  Stuart Archer³  Roger Pocock⁴ 

[1] Biotech Research and Innovation Centre, University of Copenhagen, Ole Maaløes Vej 5, Copenhagen, Denmark;Biotech Research and Innovation Centre, University of Copenhagen, Ole Maaløes Vej 5, Copenhagen, Denmark;Development and Stem Cells Program, Monash Biomedicine Discovery Institute and Department of Anatomy and Developmental Biology, Monash University, Melbourne, VIC 3800, Australia;Monash Bioinformatics Platform, Monash University, Melbourne, VIC 3800, Australia;

关键词: Biological sciences;    Molecular neuroscience;    Developmental neuroscience;   

DOI  :  

来源: DOAJ

【 摘 要 】

Summary: Coordinated expression of cell adhesion and signaling molecules is crucial for brain development. Here, we report that the Caenorhabditis elegans transforming 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.

【 授权许可】

Unknown