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First published online November 26, 2007
doi: 10.1242/10.1242/dev.008979

Development 134, 4479-4489 (2007)
Published by The Company of Biologists 2007
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Neuronal calcium sensor-1 modulation of optimal calcium level for neurite outgrowth

Kwokyin Hui1, Guang-He Fei1, Bechara J. Saab2,3, Jiang Su1, John C. Roder2,3 and Zhong-Ping Feng1,*

1 Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, M5S 1A8, Canada.
2 Molecular and Medical Genetics, Faculty of Medicine, University of Toronto, Toronto, M5S 1A8, Canada.
3 Mount Sinai Hospital, Toronto, Canada.

* Author for correspondence (e-mail: zp.feng{at}utoronto.ca)

Accepted 13 September 2007

Neurite extension and branching are affected by activity-dependent modulation of intracellular Ca2+, such that an optimal window of [Ca2+] is required for outgrowth. Our understanding of the molecular mechanisms regulating this optimal [Ca2+]i remains unclear. Taking advantage of the large growth cone size of cultured primary neurons from pond snail Lymnaea stagnalis combined with dsRNA knockdown, we show that neuronal calcium sensor-1 (NCS-1) regulates neurite extension and branching, and activity-dependent Ca2+ signals in growth cones. An NCS-1 C-terminal peptide enhances only neurite branching and moderately reduces the Ca2+ signal in growth cones compared with dsRNA knockdown. Our findings suggest that at least two separate structural domains in NCS-1 independently regulate Ca2+ influx and neurite outgrowth, with the C-terminus specifically affecting branching. We describe a model in which NCS-1 regulates cytosolic Ca2+ around the optimal window level to differentially control neurite extension and branching.

Key words: NCS-1, Neurite outgrowth, Activity-dependent calcium signals, fura-2 imaging, Lymnaea stagnalis


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[Abstract] [Full Text] [PDF]


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