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DC Field | Value | Language |
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dc.contributor.author | Cordeiro, Joao Miguel | pt_PT |
dc.contributor.author | Boda, Bernadett | pt_PT |
dc.contributor.author | Gonçalves, Paula P. | pt_PT |
dc.contributor.author | Dunant, Yves | pt_PT |
dc.date.accessioned | 2018-11-06T10:23:35Z | - |
dc.date.available | 2018-11-06T10:23:35Z | - |
dc.date.issued | 2013 | - |
dc.identifier.issn | 0022-3042 | pt_PT |
dc.identifier.uri | http://hdl.handle.net/10773/24564 | - |
dc.description.abstract | A low-affinity Ca(2+) /H(+) -antiport was described in the membrane of mammalian brain synaptic vesicles. Electrophysiological studies showed that this antiport contributes to the extreme brevity of excitation-release coupling in rapid synapses. Synaptotagmin-1, a vesicular protein interacting with membranes upon low-affinity Ca(2+) -binding, plays a major role in excitation-release coupling, by synchronizing calcium entry with fast neurotransmitter release. Here, we report that synaptotagmin-1 is necessary for expression of the vesicular Ca(2+) /H(+) -antiport. We measured Ca(2+) /H(+) -antiport activity in vesicles and granules of pheochromocytoma PC12 cells by three methods: (i) Ca(2+) -induced dissipation of the vesicular H(+) -gradient; (ii) bafilomycin-sensitive calcium accumulation and (iii) pH-jump-induced calcium accumulation. The results were congruent and highly significant: Ca(2+) /H(+) -antiport activity is detectable only in acidic organelles expressing functional synaptotagmin-1. In contrast, synaptotagmin-1-deficient cells - and cells where transgenically encoded synaptotagmin-1 was acutely photo-inactivated - were devoid of any Ca(2+) /H(+) -antiport activity. Therefore, in addition to its previously described functions, synaptotagmin-1 is involved in a rapid vesicular Ca(2+) sequestration through a Ca(2+) /H(+) antiport. | pt_PT |
dc.description.sponsorship | Study supported by a Swiss FNRS grant N°31-057135.99., and the European Commission project Lipidiet (QLK1-CT-2002-00172) to Y.D., and by the Portuguese Foundation for Science and Technology (FCT: SFRH / BD / 6403 / 2001; FSE-POPH-QREN) to J.M.C. We thank Graeme Davis for initial guidance on the FALI technique, Shoji-Kasai and Masami Takahashi for providing G11 and F7 PC12 clones, Dominique Muller and Alain Bloc, for criticism and suggestions, as well as Jean-Pierre Andrivet, Franc oise Loctin, Agostino Massiero and Lorena Jourdain for excellent technical assistance. The authors declare no conflict of interest. | pt_PT |
dc.language.iso | eng | pt_PT |
dc.publisher | Wiley | pt_PT |
dc.rights | restrictedAccess | pt_PT |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | pt_PT |
dc.subject | Ca2+/H+-antiport | pt_PT |
dc.subject | PC12 pheochromocytoma cells | pt_PT |
dc.subject | synaptic vesicles | pt_PT |
dc.subject | synaptotagmin | pt_PT |
dc.title | Synaptotagmin 1 is required for vesicular Ca2+/H +-antiport activity | pt_PT |
dc.type | article | pt_PT |
dc.description.version | published | pt_PT |
dc.peerreviewed | yes | pt_PT |
degois.publication.firstPage | 37 | pt_PT |
degois.publication.issue | 1 | pt_PT |
degois.publication.lastPage | 46 | pt_PT |
degois.publication.title | Journal of Neurochemistry | pt_PT |
degois.publication.volume | 126 | pt_PT |
dc.identifier.doi | 10.1111/jnc.12278 | pt_PT |
dc.identifier.essn | 1471-4159 | pt_PT |
Appears in Collections: | CESAM - Artigos DBio - Artigos |
Files in This Item:
File | Description | Size | Format | |
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Cordeiro et al. - 2013 - Synaptotagmin 1 is required for vesicular Ca2+H+-.pdf | 406.59 kB | Adobe PDF |
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