Journal
ISCIENCE
Volume 25, Issue 2, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.isci.2022.103791
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Funding
- NIH Office of Research Infrastructure Programs [P40 OD010440]
- National Bio-resource Project (Japan)
- European Research Council (ERC) [260807]
- Monash Biomedicine Discovery Fellowship
- NHMRC [GNT1105374]
- NHMRC Senior Research Fellowship [GNT1137645]
- Victorian Endowment for Science, Knowledge and Innovation Fellowship [VIF23]
- European Research Council (ERC) [260807] Funding Source: European Research Council (ERC)
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Coordinated expression of cell adhesion and signaling molecules is crucial for brain development. This study found that SMA-6 acts independently of DAF-4 to control neuronal guidance by limiting the expression of NLR-1.
Coordinated expression of cell adhesion and signaling molecules is crucial for brain development. Here, we report that the Caenorhabditis elegans transforming growth factor beta (TGF-beta) type I receptor SMA-6 (small-6) acts independently of its cognate TGF-beta 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-beta 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-beta-mediated regulatory mechanism to ensure correct neuronal development.
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