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Título: | GAP43 stimulates inositol trisphosphate-mediated calcium release in response to hypotonicity |
Autor: | Caprini, Marco CSIC; Gomis, Ana CSIC ORCID ; Cabedo, Hugo CSIC ORCID; Planells-Cases, Rosa; Belmonte, Carlos CSIC ORCID; Viana, Félix CSIC ORCID ; Ferrer-Montiel, Antonio CSIC ORCID | Fecha de publicación: | 2003 | Editor: | EMBO Press | Citación: | EMBO Journal 22(12): 3004-3014 (2003) | Resumen: | The identification of osmo/mechanosensory proteins in mammalian sensory neurons is still elusive. We have used an expression cloning approach to screen a human dorsal root ganglion cDNA library to look for proteins that respond to hypotonicity by raising the intracellular Ca2+ concentration ([Ca2+]i). We report the unexpected identification of GAP43 (also known as neuromodulin or B50), a membrane-anchored neuronal protein implicated in axonal growth and synaptic plasticity, as an osmosensory protein that augments [Ca2+]i in response to hypotonicity. Palmitoylation of GAP43 plays an important role in the protein osmosensitivity. Depletion of intracellular stores or inhibition of phospholipase C (PLC) activity abrogates hypotonicity-evoked, GAP43-mediated [Ca2+]i elevations. Notably, hypotonicity promoted the selective association of GAP43 with the PLC-δ1 isoform, and a concomitant increase in inositol-1,4,5-trisphosphate (IP3) formation. Collectively, these findings indicate that hypo-osmotic activation of GAP43 induces Ca2+ release from IP3-sensitive intracellular stores. The osmosensitivity of GAP43 furnishes a mechanistic framework that links axon elongation with phospho inositide metabolism, spontaneous triggering of cytosolic Ca2+ transients and the regulation of actin dynamics and motility at the growth cone in response to temporal and local mechanical forces. | Versión del editor: | https://doi.org/10.1093/emboj/cdg294 | URI: | http://hdl.handle.net/10261/308230 | DOI: | 10.1093/emboj/cdg294 | ISSN: | 0261-4189 |
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