Cell Reports
Volume 15, Issue 6, 10 May 2016, Pages 1329-1344
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Article
Myosin Va and Endoplasmic Reticulum Calcium Channel Complex Regulates Membrane Export during Axon Guidance

https://doi.org/10.1016/j.celrep.2016.04.021Get rights and content
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Highlights

  • Myosin Va binds to ryanodine receptors and tethers membrane vesicles to the ER

  • Myosin Va acts as a Ca2+ sensor near the ER to regulate targeted membrane export

  • Photo-induced membrane export from the ER drives attractive growth cone turning

  • The pathway dependent on myosin Va is likely to control axon guidance in vivo

Summary

During axon guidance, growth cones navigate toward attractive cues by inserting new membrane on the cue side. This process depends on Ca2+ release from endoplasmic reticulum (ER) Ca2+ channels, but the Ca2+ sensor and effector governing this asymmetric vesicle export remain unknown. We identified a protein complex that controls asymmetric ER Ca2+-dependent membrane vesicle export. The Ca2+-dependent motor protein myosin Va (MyoVa) tethers membrane vesicles to the ER via a common binding site on the two major ER Ca2+ channels, inositol 1,4,5-trisphosphate and ryanodine receptors. In response to attractive cues, micromolar Ca2+ from ER channels triggers MyoVa-channel dissociation and the movement of freed vesicles to the cue side, enabling growth cone turning. MyoVa-Ca2+ channel interactions are required for proper long-range axon growth in developing spinal cord in vivo. These findings reveal a peri-ER membrane export pathway for Ca2+-dependent attraction in axon guidance.

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