Synaptotagmin I functions as a calcium regulator of release probability
In all synapses, Ca 2+ triggers neurotransmitter release to initiate signal transmission. Ca 2+ presumably acts by activating synaptic Ca 2+ sensors, but the nature of these sensors—which are the gatekeepers to neurotransmission—remains unclear. One of the candidate Ca 2+ sensors in release is the s...
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| Veröffentlicht in: | Nature (London) 2001-03, Vol.410 (6824), p.41-49 |
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| creator | Fernández-Chacón, Rafael Königstorfer, Andreas Gerber, Stefan H. García, Jesús Matos, Maria F. Stevens, Charles F. Brose, Nils Rizo, Josep Rosenmund, Christian Südhof, Thomas C. |
| description | In all synapses, Ca
2+
triggers neurotransmitter release to initiate signal transmission. Ca
2+
presumably acts by activating synaptic Ca
2+
sensors, but the nature of these sensors—which are the gatekeepers to neurotransmission—remains unclear. One of the candidate Ca
2+
sensors in release is the synaptic Ca
2+
-binding protein synaptotagmin I. Here we have studied a point mutation in synaptotagmin I that causes a twofold decrease in overall Ca
2+
affinity without inducing structural or conformational changes. When introduced by homologous recombination into the endogenous
synaptotagmin I
gene in mice, this point mutation decreases the Ca
2+
sensitivity of neurotransmitter release twofold, but does not alter spontaneous release or the size of the readily releasable pool of neurotransmitters. Therefore, Ca
2+
binding to synaptotagmin I participates in triggering neurotransmitter release at the synapse. |
| doi_str_mv | 10.1038/35065004 |
| format | Article |
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2+
triggers neurotransmitter release to initiate signal transmission. Ca
2+
presumably acts by activating synaptic Ca
2+
sensors, but the nature of these sensors—which are the gatekeepers to neurotransmission—remains unclear. One of the candidate Ca
2+
sensors in release is the synaptic Ca
2+
-binding protein synaptotagmin I. Here we have studied a point mutation in synaptotagmin I that causes a twofold decrease in overall Ca
2+
affinity without inducing structural or conformational changes. When introduced by homologous recombination into the endogenous
synaptotagmin I
gene in mice, this point mutation decreases the Ca
2+
sensitivity of neurotransmitter release twofold, but does not alter spontaneous release or the size of the readily releasable pool of neurotransmitters. Therefore, Ca
2+
binding to synaptotagmin I participates in triggering neurotransmitter release at the synapse.</description><identifier>ISSN: 0028-0836</identifier><identifier>EISSN: 1476-4687</identifier><identifier>DOI: 10.1038/35065004</identifier><identifier>PMID: 11242035</identifier><identifier>CODEN: NATUAS</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Biological and medical sciences ; Calcium ; Calcium - metabolism ; Calcium-Binding Proteins - genetics ; Calcium-Binding Proteins - metabolism ; Calcium-Binding Proteins - physiology ; Cell physiology ; Cells, Cultured ; Fundamental and applied biological sciences. Psychology ; Genes ; Humanities and Social Sciences ; Membrane Glycoproteins - chemistry ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - metabolism ; Membrane Glycoproteins - physiology ; Mice ; Molecular and cellular biology ; multidisciplinary ; Mutagenesis, Site-Directed ; Mutation ; Nerve Tissue Proteins - chemistry ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Nerve Tissue Proteins - physiology ; Neurology ; Neurons - metabolism ; Neurotransmission ; Neurotransmitter Agents - chemistry ; Neurotransmitter Agents - genetics ; Neurotransmitter Agents - metabolism ; Neurotransmitter Agents - physiology ; Point Mutation ; Protein Binding ; Protein Conformation ; Proteins ; Rodents ; Science ; Science (multidisciplinary) ; Sensors ; Synapses - physiology ; Synaptic Vesicles - metabolism ; Synaptotagmin I ; Synaptotagmins</subject><ispartof>Nature (London), 2001-03, Vol.410 (6824), p.41-49</ispartof><rights>Macmillan Magazines Ltd. 2001</rights><rights>2001 INIST-CNRS</rights><rights>COPYRIGHT 2001 Nature Publishing Group</rights><rights>Copyright Macmillan Journals Ltd. Mar 1, 2001</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c671t-cbb5ecbd012ca64675552a899b35162dde7f5e37ab7dfdb536f93af2303296533</citedby><cites>FETCH-LOGICAL-c671t-cbb5ecbd012ca64675552a899b35162dde7f5e37ab7dfdb536f93af2303296533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/35065004$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/35065004$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=883658$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11242035$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fernández-Chacón, Rafael</creatorcontrib><creatorcontrib>Königstorfer, Andreas</creatorcontrib><creatorcontrib>Gerber, Stefan H.</creatorcontrib><creatorcontrib>García, Jesús</creatorcontrib><creatorcontrib>Matos, Maria F.</creatorcontrib><creatorcontrib>Stevens, Charles F.</creatorcontrib><creatorcontrib>Brose, Nils</creatorcontrib><creatorcontrib>Rizo, Josep</creatorcontrib><creatorcontrib>Rosenmund, Christian</creatorcontrib><creatorcontrib>Südhof, Thomas C.</creatorcontrib><title>Synaptotagmin I functions as a calcium regulator of release probability</title><title>Nature (London)</title><addtitle>Nature</addtitle><addtitle>Nature</addtitle><description>In all synapses, Ca
2+
triggers neurotransmitter release to initiate signal transmission. Ca
2+
presumably acts by activating synaptic Ca
2+
sensors, but the nature of these sensors—which are the gatekeepers to neurotransmission—remains unclear. One of the candidate Ca
2+
sensors in release is the synaptic Ca
2+
-binding protein synaptotagmin I. Here we have studied a point mutation in synaptotagmin I that causes a twofold decrease in overall Ca
2+
affinity without inducing structural or conformational changes. When introduced by homologous recombination into the endogenous
synaptotagmin I
gene in mice, this point mutation decreases the Ca
2+
sensitivity of neurotransmitter release twofold, but does not alter spontaneous release or the size of the readily releasable pool of neurotransmitters. Therefore, Ca
2+
binding to synaptotagmin I participates in triggering neurotransmitter release at the synapse.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium</subject><subject>Calcium - metabolism</subject><subject>Calcium-Binding Proteins - genetics</subject><subject>Calcium-Binding Proteins - metabolism</subject><subject>Calcium-Binding Proteins - physiology</subject><subject>Cell physiology</subject><subject>Cells, Cultured</subject><subject>Fundamental and applied biological sciences. 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2+
triggers neurotransmitter release to initiate signal transmission. Ca
2+
presumably acts by activating synaptic Ca
2+
sensors, but the nature of these sensors—which are the gatekeepers to neurotransmission—remains unclear. One of the candidate Ca
2+
sensors in release is the synaptic Ca
2+
-binding protein synaptotagmin I. Here we have studied a point mutation in synaptotagmin I that causes a twofold decrease in overall Ca
2+
affinity without inducing structural or conformational changes. When introduced by homologous recombination into the endogenous
synaptotagmin I
gene in mice, this point mutation decreases the Ca
2+
sensitivity of neurotransmitter release twofold, but does not alter spontaneous release or the size of the readily releasable pool of neurotransmitters. Therefore, Ca
2+
binding to synaptotagmin I participates in triggering neurotransmitter release at the synapse.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>11242035</pmid><doi>10.1038/35065004</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0028-0836 |
| ispartof | Nature (London), 2001-03, Vol.410 (6824), p.41-49 |
| issn | 0028-0836 1476-4687 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_743494974 |
| source | Nature_系列刊; MEDLINE; Springer Online Journals |
| subjects | Animals Biological and medical sciences Calcium Calcium - metabolism Calcium-Binding Proteins - genetics Calcium-Binding Proteins - metabolism Calcium-Binding Proteins - physiology Cell physiology Cells, Cultured Fundamental and applied biological sciences. Psychology Genes Humanities and Social Sciences Membrane Glycoproteins - chemistry Membrane Glycoproteins - genetics Membrane Glycoproteins - metabolism Membrane Glycoproteins - physiology Mice Molecular and cellular biology multidisciplinary Mutagenesis, Site-Directed Mutation Nerve Tissue Proteins - chemistry Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Nerve Tissue Proteins - physiology Neurology Neurons - metabolism Neurotransmission Neurotransmitter Agents - chemistry Neurotransmitter Agents - genetics Neurotransmitter Agents - metabolism Neurotransmitter Agents - physiology Point Mutation Protein Binding Protein Conformation Proteins Rodents Science Science (multidisciplinary) Sensors Synapses - physiology Synaptic Vesicles - metabolism Synaptotagmin I Synaptotagmins |
| title | Synaptotagmin I functions as a calcium regulator of release probability |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-14T15%3A44%3A42IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Synaptotagmin%20I%20functions%20as%20a%20calcium%20regulator%20of%20release%20probability&rft.jtitle=Nature%20(London)&rft.au=Fern%C3%A1ndez-Chac%C3%B3n,%20Rafael&rft.date=2001-03-01&rft.volume=410&rft.issue=6824&rft.spage=41&rft.epage=49&rft.pages=41-49&rft.issn=0028-0836&rft.eissn=1476-4687&rft.coden=NATUAS&rft_id=info:doi/10.1038/35065004&rft_dat=%3Cgale_proqu%3EA188007413%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=204494992&rft_id=info:pmid/11242035&rft_galeid=A188007413&rfr_iscdi=true |