UNC-80 and the NCA Ion Channels Contribute to Endocytosis Defects in Synaptojanin Mutants
Synaptojanin is a lipid phosphatase required to degrade phosphatidylinositol 4,5 bisphosphate (PIP2) at cell membranes during synaptic vesicle recycling [1, 2]. Synaptojanin mutants in C. elegans are severely uncoordinated and are depleted of synaptic vesicles, possibly because of accumulation of PI...
Gespeichert in:
| Veröffentlicht in: | Current biology 2007-09, Vol.17 (18), p.1595-1600 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1600 |
|---|---|
| container_issue | 18 |
| container_start_page | 1595 |
| container_title | Current biology |
| container_volume | 17 |
| creator | Jospin, Maelle Watanabe, Shigeki Joshi, Deepa Young, Sean Hamming, Kevin Thacker, Colin Snutch, Terrance P. Jorgensen, Erik M. Schuske, Kim |
| description | Synaptojanin is a lipid phosphatase required to degrade phosphatidylinositol 4,5 bisphosphate (PIP2) at cell membranes during synaptic vesicle recycling [1, 2]. Synaptojanin mutants in C. elegans are severely uncoordinated and are depleted of synaptic vesicles, possibly because of accumulation of PIP2[2]. To identify proteins that act downstream of PIP2 during endocytosis, we screened for suppressors of synaptojanin mutants in the nematode C. elegans. A class of uncoordinated mutants called “fainters” partially suppress the locomotory, vesicle depletion, and electrophysiological defects in synaptojanin mutants. These suppressor loci include the genes for the NCA ion channels [3], which are homologs of the vertebrate cation leak channel NALCN [4], and a novel gene called unc-80. We demonstrate that unc-80 encodes a novel, but highly conserved, neuronal protein required for the proper localization of the NCA-1 and NCA-2 ion channel subunits. These data suggest that activation of the NCA ion channel in synaptojanin mutants leads to defects in recycling of synaptic vesicles. |
| doi_str_mv | 10.1016/j.cub.2007.08.036 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_68289917</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0960982207018532</els_id><sourcerecordid>20546209</sourcerecordid><originalsourceid>FETCH-LOGICAL-c491t-e2c056b51ac3090dcba6bd122e356e97f1cacfb475fcae88a7f8a0eda41fff6f3</originalsourceid><addsrcrecordid>eNqFkEFrFDEYhoNY7Fr7A7xITt5m_JKdZBI8lWnVQm0P2kNPIZP5QrPsJuskI-y_N2UXvOnp44XnfeF7CHnPoGXA5KdN65ax5QB9C6qFtXxFVkz1uoGuE6_JCrSERivOz8nbnDcAjCst35Bz1isuhNAr8vR4PzQKqI0TLc9I74crepsiHZ5tjLjNdEixzGFcCtKS6E2ckjuUlEOm1-jRlUxDpD8O0e5L2thYw_el2FjyO3Lm7Tbj5elekMcvNz-Hb83dw9fb4equcZ1mpUHuQMhRMOvWoGFyo5XjxDjHtZCoe8-cdX7seuGdRaVs75UFnGzHvPfSry_Ix-Pufk6_FszF7EJ2uN3aiGnJRqr6tGb9f0EOopMcdAXZEXRzynlGb_Zz2Nn5YBiYF_FmY6p48yLegDJVfO18OI0v4w6nv42T6Qp8PgJVKv4OOJvsAkaHU5irRjOl8I_5P0cYk98</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>20546209</pqid></control><display><type>article</type><title>UNC-80 and the NCA Ion Channels Contribute to Endocytosis Defects in Synaptojanin Mutants</title><source>MEDLINE</source><source>Cell Press Free Archives</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Access via ScienceDirect (Elsevier)</source><creator>Jospin, Maelle ; Watanabe, Shigeki ; Joshi, Deepa ; Young, Sean ; Hamming, Kevin ; Thacker, Colin ; Snutch, Terrance P. ; Jorgensen, Erik M. ; Schuske, Kim</creator><creatorcontrib>Jospin, Maelle ; Watanabe, Shigeki ; Joshi, Deepa ; Young, Sean ; Hamming, Kevin ; Thacker, Colin ; Snutch, Terrance P. ; Jorgensen, Erik M. ; Schuske, Kim</creatorcontrib><description>Synaptojanin is a lipid phosphatase required to degrade phosphatidylinositol 4,5 bisphosphate (PIP2) at cell membranes during synaptic vesicle recycling [1, 2]. Synaptojanin mutants in C. elegans are severely uncoordinated and are depleted of synaptic vesicles, possibly because of accumulation of PIP2[2]. To identify proteins that act downstream of PIP2 during endocytosis, we screened for suppressors of synaptojanin mutants in the nematode C. elegans. A class of uncoordinated mutants called “fainters” partially suppress the locomotory, vesicle depletion, and electrophysiological defects in synaptojanin mutants. These suppressor loci include the genes for the NCA ion channels [3], which are homologs of the vertebrate cation leak channel NALCN [4], and a novel gene called unc-80. We demonstrate that unc-80 encodes a novel, but highly conserved, neuronal protein required for the proper localization of the NCA-1 and NCA-2 ion channel subunits. These data suggest that activation of the NCA ion channel in synaptojanin mutants leads to defects in recycling of synaptic vesicles.</description><identifier>ISSN: 0960-9822</identifier><identifier>EISSN: 1879-0445</identifier><identifier>DOI: 10.1016/j.cub.2007.08.036</identifier><identifier>PMID: 17825559</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>Animals ; Axons - metabolism ; Caenorhabditis elegans ; Caenorhabditis elegans - genetics ; Caenorhabditis elegans - metabolism ; Caenorhabditis elegans - physiology ; Caenorhabditis elegans Proteins - analysis ; Caenorhabditis elegans Proteins - genetics ; Caenorhabditis elegans Proteins - metabolism ; Caenorhabditis elegans Proteins - physiology ; CELLBIO ; Endocytosis - genetics ; Endocytosis - physiology ; Green Fluorescent Proteins - analysis ; Ion Channels - analysis ; Ion Channels - metabolism ; Models, Genetic ; MOLNEURO ; Mutation ; Nematoda ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Nerve Tissue Proteins - physiology ; Neurons - metabolism ; Phosphoric Monoester Hydrolases - genetics ; Synaptic Transmission - genetics ; Synaptic Vesicles - metabolism</subject><ispartof>Current biology, 2007-09, Vol.17 (18), p.1595-1600</ispartof><rights>2007 Elsevier Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c491t-e2c056b51ac3090dcba6bd122e356e97f1cacfb475fcae88a7f8a0eda41fff6f3</citedby><cites>FETCH-LOGICAL-c491t-e2c056b51ac3090dcba6bd122e356e97f1cacfb475fcae88a7f8a0eda41fff6f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.cub.2007.08.036$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>315,782,786,3554,27933,27934,46004</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17825559$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jospin, Maelle</creatorcontrib><creatorcontrib>Watanabe, Shigeki</creatorcontrib><creatorcontrib>Joshi, Deepa</creatorcontrib><creatorcontrib>Young, Sean</creatorcontrib><creatorcontrib>Hamming, Kevin</creatorcontrib><creatorcontrib>Thacker, Colin</creatorcontrib><creatorcontrib>Snutch, Terrance P.</creatorcontrib><creatorcontrib>Jorgensen, Erik M.</creatorcontrib><creatorcontrib>Schuske, Kim</creatorcontrib><title>UNC-80 and the NCA Ion Channels Contribute to Endocytosis Defects in Synaptojanin Mutants</title><title>Current biology</title><addtitle>Curr Biol</addtitle><description>Synaptojanin is a lipid phosphatase required to degrade phosphatidylinositol 4,5 bisphosphate (PIP2) at cell membranes during synaptic vesicle recycling [1, 2]. Synaptojanin mutants in C. elegans are severely uncoordinated and are depleted of synaptic vesicles, possibly because of accumulation of PIP2[2]. To identify proteins that act downstream of PIP2 during endocytosis, we screened for suppressors of synaptojanin mutants in the nematode C. elegans. A class of uncoordinated mutants called “fainters” partially suppress the locomotory, vesicle depletion, and electrophysiological defects in synaptojanin mutants. These suppressor loci include the genes for the NCA ion channels [3], which are homologs of the vertebrate cation leak channel NALCN [4], and a novel gene called unc-80. We demonstrate that unc-80 encodes a novel, but highly conserved, neuronal protein required for the proper localization of the NCA-1 and NCA-2 ion channel subunits. These data suggest that activation of the NCA ion channel in synaptojanin mutants leads to defects in recycling of synaptic vesicles.</description><subject>Animals</subject><subject>Axons - metabolism</subject><subject>Caenorhabditis elegans</subject><subject>Caenorhabditis elegans - genetics</subject><subject>Caenorhabditis elegans - metabolism</subject><subject>Caenorhabditis elegans - physiology</subject><subject>Caenorhabditis elegans Proteins - analysis</subject><subject>Caenorhabditis elegans Proteins - genetics</subject><subject>Caenorhabditis elegans Proteins - metabolism</subject><subject>Caenorhabditis elegans Proteins - physiology</subject><subject>CELLBIO</subject><subject>Endocytosis - genetics</subject><subject>Endocytosis - physiology</subject><subject>Green Fluorescent Proteins - analysis</subject><subject>Ion Channels - analysis</subject><subject>Ion Channels - metabolism</subject><subject>Models, Genetic</subject><subject>MOLNEURO</subject><subject>Mutation</subject><subject>Nematoda</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Nerve Tissue Proteins - physiology</subject><subject>Neurons - metabolism</subject><subject>Phosphoric Monoester Hydrolases - genetics</subject><subject>Synaptic Transmission - genetics</subject><subject>Synaptic Vesicles - metabolism</subject><issn>0960-9822</issn><issn>1879-0445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEFrFDEYhoNY7Fr7A7xITt5m_JKdZBI8lWnVQm0P2kNPIZP5QrPsJuskI-y_N2UXvOnp44XnfeF7CHnPoGXA5KdN65ax5QB9C6qFtXxFVkz1uoGuE6_JCrSERivOz8nbnDcAjCst35Bz1isuhNAr8vR4PzQKqI0TLc9I74crepsiHZ5tjLjNdEixzGFcCtKS6E2ckjuUlEOm1-jRlUxDpD8O0e5L2thYw_el2FjyO3Lm7Tbj5elekMcvNz-Hb83dw9fb4equcZ1mpUHuQMhRMOvWoGFyo5XjxDjHtZCoe8-cdX7seuGdRaVs75UFnGzHvPfSry_Ix-Pufk6_FszF7EJ2uN3aiGnJRqr6tGb9f0EOopMcdAXZEXRzynlGb_Zz2Nn5YBiYF_FmY6p48yLegDJVfO18OI0v4w6nv42T6Qp8PgJVKv4OOJvsAkaHU5irRjOl8I_5P0cYk98</recordid><startdate>20070918</startdate><enddate>20070918</enddate><creator>Jospin, Maelle</creator><creator>Watanabe, Shigeki</creator><creator>Joshi, Deepa</creator><creator>Young, Sean</creator><creator>Hamming, Kevin</creator><creator>Thacker, Colin</creator><creator>Snutch, Terrance P.</creator><creator>Jorgensen, Erik M.</creator><creator>Schuske, Kim</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20070918</creationdate><title>UNC-80 and the NCA Ion Channels Contribute to Endocytosis Defects in Synaptojanin Mutants</title><author>Jospin, Maelle ; Watanabe, Shigeki ; Joshi, Deepa ; Young, Sean ; Hamming, Kevin ; Thacker, Colin ; Snutch, Terrance P. ; Jorgensen, Erik M. ; Schuske, Kim</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c491t-e2c056b51ac3090dcba6bd122e356e97f1cacfb475fcae88a7f8a0eda41fff6f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Axons - metabolism</topic><topic>Caenorhabditis elegans</topic><topic>Caenorhabditis elegans - genetics</topic><topic>Caenorhabditis elegans - metabolism</topic><topic>Caenorhabditis elegans - physiology</topic><topic>Caenorhabditis elegans Proteins - analysis</topic><topic>Caenorhabditis elegans Proteins - genetics</topic><topic>Caenorhabditis elegans Proteins - metabolism</topic><topic>Caenorhabditis elegans Proteins - physiology</topic><topic>CELLBIO</topic><topic>Endocytosis - genetics</topic><topic>Endocytosis - physiology</topic><topic>Green Fluorescent Proteins - analysis</topic><topic>Ion Channels - analysis</topic><topic>Ion Channels - metabolism</topic><topic>Models, Genetic</topic><topic>MOLNEURO</topic><topic>Mutation</topic><topic>Nematoda</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Nerve Tissue Proteins - physiology</topic><topic>Neurons - metabolism</topic><topic>Phosphoric Monoester Hydrolases - genetics</topic><topic>Synaptic Transmission - genetics</topic><topic>Synaptic Vesicles - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jospin, Maelle</creatorcontrib><creatorcontrib>Watanabe, Shigeki</creatorcontrib><creatorcontrib>Joshi, Deepa</creatorcontrib><creatorcontrib>Young, Sean</creatorcontrib><creatorcontrib>Hamming, Kevin</creatorcontrib><creatorcontrib>Thacker, Colin</creatorcontrib><creatorcontrib>Snutch, Terrance P.</creatorcontrib><creatorcontrib>Jorgensen, Erik M.</creatorcontrib><creatorcontrib>Schuske, Kim</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Current biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jospin, Maelle</au><au>Watanabe, Shigeki</au><au>Joshi, Deepa</au><au>Young, Sean</au><au>Hamming, Kevin</au><au>Thacker, Colin</au><au>Snutch, Terrance P.</au><au>Jorgensen, Erik M.</au><au>Schuske, Kim</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>UNC-80 and the NCA Ion Channels Contribute to Endocytosis Defects in Synaptojanin Mutants</atitle><jtitle>Current biology</jtitle><addtitle>Curr Biol</addtitle><date>2007-09-18</date><risdate>2007</risdate><volume>17</volume><issue>18</issue><spage>1595</spage><epage>1600</epage><pages>1595-1600</pages><issn>0960-9822</issn><eissn>1879-0445</eissn><abstract>Synaptojanin is a lipid phosphatase required to degrade phosphatidylinositol 4,5 bisphosphate (PIP2) at cell membranes during synaptic vesicle recycling [1, 2]. Synaptojanin mutants in C. elegans are severely uncoordinated and are depleted of synaptic vesicles, possibly because of accumulation of PIP2[2]. To identify proteins that act downstream of PIP2 during endocytosis, we screened for suppressors of synaptojanin mutants in the nematode C. elegans. A class of uncoordinated mutants called “fainters” partially suppress the locomotory, vesicle depletion, and electrophysiological defects in synaptojanin mutants. These suppressor loci include the genes for the NCA ion channels [3], which are homologs of the vertebrate cation leak channel NALCN [4], and a novel gene called unc-80. We demonstrate that unc-80 encodes a novel, but highly conserved, neuronal protein required for the proper localization of the NCA-1 and NCA-2 ion channel subunits. These data suggest that activation of the NCA ion channel in synaptojanin mutants leads to defects in recycling of synaptic vesicles.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>17825559</pmid><doi>10.1016/j.cub.2007.08.036</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0960-9822 |
| ispartof | Current biology, 2007-09, Vol.17 (18), p.1595-1600 |
| issn | 0960-9822 1879-0445 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_68289917 |
| source | MEDLINE; Cell Press Free Archives; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Access via ScienceDirect (Elsevier) |
| subjects | Animals Axons - metabolism Caenorhabditis elegans Caenorhabditis elegans - genetics Caenorhabditis elegans - metabolism Caenorhabditis elegans - physiology Caenorhabditis elegans Proteins - analysis Caenorhabditis elegans Proteins - genetics Caenorhabditis elegans Proteins - metabolism Caenorhabditis elegans Proteins - physiology CELLBIO Endocytosis - genetics Endocytosis - physiology Green Fluorescent Proteins - analysis Ion Channels - analysis Ion Channels - metabolism Models, Genetic MOLNEURO Mutation Nematoda Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Nerve Tissue Proteins - physiology Neurons - metabolism Phosphoric Monoester Hydrolases - genetics Synaptic Transmission - genetics Synaptic Vesicles - metabolism |
| title | UNC-80 and the NCA Ion Channels Contribute to Endocytosis Defects in Synaptojanin Mutants |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-02T07%3A05%3A31IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=UNC-80%20and%20the%20NCA%20Ion%20Channels%20Contribute%20to%20Endocytosis%20Defects%20in%20Synaptojanin%20Mutants&rft.jtitle=Current%20biology&rft.au=Jospin,%20Maelle&rft.date=2007-09-18&rft.volume=17&rft.issue=18&rft.spage=1595&rft.epage=1600&rft.pages=1595-1600&rft.issn=0960-9822&rft.eissn=1879-0445&rft_id=info:doi/10.1016/j.cub.2007.08.036&rft_dat=%3Cproquest_cross%3E20546209%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=20546209&rft_id=info:pmid/17825559&rft_els_id=S0960982207018532&rfr_iscdi=true |