Toriyama, M. et al. Shootin1: a protein involved in the organization of an asymmetric signal for neuronal polarization. J. Cell Biol. 175, 147-157

Division of Signal Transduction, Nara Institute of Science and Technology, Ikoma 630-0192, Japan.
The Journal of Cell Biology (Impact Factor: 9.83). 11/2006; 175(1):147-57. DOI: 10.1083/jcb.200604160
Source: PubMed


Neurons have the remarkable ability to polarize even in symmetrical in vitro environments. Although recent studies have shown that asymmetric intracellular signals can induce neuronal polarization, it remains unclear how these polarized signals are organized without asymmetric cues. We describe a novel protein, named shootin1, that became up-regulated during polarization of hippocampal neurons and began fluctuating accumulation among multiple neurites. Eventually, shootin1 accumulated asymmetrically in a single neurite, which led to axon induction for polarization. Disturbing the asymmetric organization of shootin1 by excess shootin1 disrupted polarization, whereas repressing shootin1 expression inhibited polarization. Overexpression and RNA interference data suggest that shootin1 is required for spatially localized phosphoinositide-3-kinase activity. Shootin1 was transported anterogradely to the growth cones and diffused back to the soma; inhibiting this transport prevented its asymmetric accumulation in neurons. We propose that shootin1 is involved in the generation of internal asymmetric signals required for neuronal polarization.

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Available from: Tadayuki Shimada, Aug 27, 2014
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    • "Preparation of the vectors to express shootin1 has been described previously (Toriyama et al., 2006). The vector to express yellow fluorescent protein/cofi- lin-S3A (cofilin dominant active mutant) was prepared as described previously (Endo et al., 2003). "
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