Atypical TGF-β signaling controls neuronal guidance in Caenorhabditis elegans

Oguzhan Baltaci; Mikael Egebjerg Pedersen; Tessa Sherry; Ava Handley; Goda Snieckute; Wei Cao; Matilda Haas; Stuart Archer; Roger Pocock

doi:10.1016/j.isci.2022.103791

Atypical TGF-β signaling controls neuronal guidance in Caenorhabditis elegans

iScience. 2022 Jan 18;25(2):103791. doi: 10.1016/j.isci.2022.103791. eCollection 2022 Feb 18.

Authors

Oguzhan Baltaci¹, Mikael Egebjerg Pedersen², Tessa Sherry¹, Ava Handley¹, Goda Snieckute^{1

2}, Wei Cao¹, Matilda Haas¹, Stuart Archer³, Roger Pocock^{1

2}

Affiliations

¹ Development and Stem Cells Program, Monash Biomedicine Discovery Institute and Department of Anatomy and Developmental Biology, Monash University, Melbourne, VIC 3800, Australia.
² Biotech Research and Innovation Centre, University of Copenhagen, Ole Maaløes Vej 5, Copenhagen, Denmark.
³ Monash Bioinformatics Platform, Monash University, Melbourne, VIC 3800, Australia.

Abstract

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.

Keywords: Biological sciences; Developmental neuroscience; Molecular neuroscience.

Grants and funding

P40 OD010440/OD/NIH HHS/United States