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ADAMTS2 promotes radial migration by activating TGF-β signaling in the developing neocortex
Noe Kaneko1,2, Kumiko Hirai1, Minori Oshima1,2
1Developmental Neuroscience Project, Department of Brain & Neurosciences, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
EMBO Reports
|June 13, 2024
Summary
A disintegrin and metalloproteinase with thrombospondin motif 2 (ADAMTS2) is crucial for neuron migration in the mammalian neocortex. ADAMTS2 activates transforming growth factor beta (TGF-β) signaling, facilitating neuron transition and radial migration.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- Neocortical development relies on radial migration of excitatory neurons.
- Neurons transition from multipolar to bipolar shapes at the subplate (SP) layer, rich in extracellular matrix (ECM).
Purpose of the Study:
- To investigate the role of ECM components in the SP layer during neuronal migration.
- To elucidate the function of ADAMTS2 in the multipolar-to-bipolar transition of migrating neurons.
Main Methods:
- Gene knockdown and knockout of Adamts2 in mice.
- Time-lapse luminescence imaging to track TGF-β signaling.
- Overexpression of TGF-β2 in migrating neurons.
Main Results:
- Adamts2 deficiency disrupted neuronal multipolar-to-bipolar transition and radial migration.
- ADAMTS2 activates TGF-β signaling in migrating neurons at the SP layer.
- Overexpressing TGF-β2 partially rescued migration defects in Adamts2 knockout mice.
Conclusions:
- ADAMTS2, secreted by migrating neurons, remodels the SP layer's ECM.
- This remodeling activates TGF-β signaling, driving the multipolar-to-bipolar transition essential for neocortical development.
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