Semaphorin3A accelerates neuronal polarity in vitro and in its absence the orientation of DRG neuronal polarity in vivo is distorted
Autor: | Omer Lerman, Oded Behar, Ayal Ben-Zvi, Zohar Yagil |
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Rok vydání: | 2007 |
Předmět: |
Male
MAPK/ERK pathway Time Factors Motility RAC1 In Vitro Techniques Biology Catechin Glycogen Synthase Kinase 3 Mice Cellular and Molecular Neuroscience Semaphorin Cell Movement Pregnancy Tubulin Ganglia Spinal Cell polarity Animals Enzyme Inhibitors Growth cone Molecular Biology GSK3B Cells Cultured Mice Knockout Neurons Mice Inbred ICR Chi-Square Distribution Glycogen Synthase Kinase 3 beta Dose-Response Relationship Drug Cell Polarity Semaphorin-3A Dendrites Cell Biology Embryo Mammalian Axons nervous system Female Axon guidance Neuroscience |
Zdroj: | Molecular and Cellular Neuroscience. 36:222-234 |
ISSN: | 1044-7431 |
DOI: | 10.1016/j.mcn.2007.07.003 |
Popis: | Axon guidance cues are critical for neuronal circuitry formation. Guidance molecules may repel or attract axons directly by effecting growth cone motility, or by impinging on neuronal polarity. In Semaphorin3A null mice, many axonal errors are detected, most prominently in DRG neurons. It has been generally assumed the repellent properties of Semaphorin3A are the cause of these erroneous axonal projections. Here we show that, in semaphorin3A-null mice, the initial trajectory of neurons in the DRG is abnormal, suggesting that Semaphorin3A may instruct neuronal polarity. In corroboration, in vitro Semaphorin3A dramatically increases neuronal polarization, as indicated by GSK3beta and Rac1 sub-cellular localization in DRG neurons. Polarization effects of Semaphorin3A are regulated by activated MAPK, as indicated by p-MAPK 42/44 polarization and the need for its activity for Rac1 and GSK3beta polarization. Taken together, our findings suggest that Semaphorin3A plays a role in the formation of neuronal polarity, in addition to its classic repellent role. |
Databáze: | OpenAIRE |
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