Semaphorin3A accelerates neuronal polarity in vitro and in its absence the orientation of DRG neuronal polarity in vivo is distorted

Omer Lerman, Ayal Ben-Zvi, Zohar Yagil, Oded Behar*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

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 GSK3β 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 GSK3β polarization. Taken together, our findings suggest that Semaphorin3A plays a role in the formation of neuronal polarity, in addition to its classic repellent role.

Original languageAmerican English
Pages (from-to)222-234
Number of pages13
JournalMolecular and Cellular Neuroscience
Volume36
Issue number2
DOIs
StatePublished - Oct 2007

Bibliographical note

Funding Information:
We are grateful to Dr. Norman Grover (Department of Experimental Medicine, the Hebrew University) for helpful advice regarding the statistical analyses. This work was supported by a grant from the Israel Science Foundation (grant number 573/04).

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