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The semaphorin 4D-plexin-B signalling complex regulates dendritic and axonal complexity in developing neurons via
Peter Vodrazka1, Alexander Korostylev, Alexandra Hirschberg
1Institute of Pharmacology, University of Heidelberg, Heidelberg, Germany.
The European Journal of Neuroscience
|October 1, 2009
Summary
Semaphorin 4D (Sema4D) signaling through Plexin-B1 promotes neuronal branching and complexity in developing hippocampal neurons, revealing novel roles in later neurite development.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Signaling
Background:
- Semaphorins and plexins are crucial for neuronal development.
- Plexin-B family functions in developing neurons are poorly understood.
- Sema4D-Plexin-B1 interaction acutely collapses growth cones early in neurite outgrowth.
Purpose of the Study:
- To investigate the role of Sema4D-Plexin-B1 interactions in later stages of neuronal development, differentiation, and maturation.
- To elucidate the signaling pathways involved in Sema4D-mediated neuronal morphogenesis.
Main Methods:
- Morphogenetic assays on developing rat hippocampal neurons.
- Time-lapse imaging.
- Analysis of downstream signaling pathways including receptor tyrosine kinases, Rho kinase, PI3K, ERK1/2, mTOR, and GSK-3β.
Main Results:
- Sema4D treatment over hours promotes hippocampal neuron branching and complexity via Plexin-B1 activation.
- Sema4D differentially regulates axonal and dendritic morphogenesis by activating receptor tyrosine kinases and Rho kinase.
- Phosphoinositide-3-kinase (PI3K) and mammalian target of rapamycin (mTOR) are critical for Sema4D-induced dendritic branching, while ERK1/2 and GSK-3β are not involved.
Conclusions:
- Sema4D-Plexin-B1 interactions modulate dendritic and axonal arborization in developing neurons.
- These effects are mediated by coordinated activation of diverse signaling pathways, including PI3K/mTOR.
- This study reveals a novel role for Sema4D-Plexin-B1 in promoting neuronal complexity during later developmental stages.
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