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Mol Brain. 2013 Dec 1;6:51. doi: 10.1186/1756-6606-6-51.

A critical role for STIM1 in filopodial calcium entry and axon guidance.

Author information

1
Departments of Cell Biology and Neurology, Emory University School of Medicine, Atlanta, GA 30078, USA. james.zheng@emory.edu.

Abstract

BACKGROUND:

Stromal interaction molecule 1 (STIM1), a Ca2+ sensor in the endoplasmic reticulum, regulates store-operated Ca2+ entry (SOCE) that is essential for Ca2+ homeostasis in many types of cells. However, if and how STIM1 and SOCE function in nerve growth cones during axon guidance remains to be elucidated.

RESULTS:

We report that STIM1 and transient receptor potential channel 1 (TRPC1)-dependent SOCE operates in Xenopus spinal growth cones to regulate Ca2+ signaling and guidance responses. We found that STIM1 works together with TRPC1 to mediate SOCE within growth cones and filopodia. In particular, STIM1/TRPC1-dependent SOCE was found to mediate oscillatory filopodial Ca2+ transients in the growth cone. Disruption of STIM1 function abolished filopodial Ca2+ transients and impaired Ca2+-dependent attractive responses of Xenopus growth cones to netrin-1. Finally, interference with STIM1 function was found to disrupt midline axon guidance of commissural interneurons in the developing Xenopus spinal cord in vivo.

CONCLUSIONS:

Our data demonstrate that STIM1/TRPC1-dependent SOCE plays an essential role in generating spatiotemporal Ca2+ signals that mediate guidance responses of nerve growth cones.

PMID:
24289807
PMCID:
PMC3907062
DOI:
10.1186/1756-6606-6-51
[Indexed for MEDLINE]
Free PMC Article
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