A Ca2+ channel differentially regulates Clathrin-mediated and activity-dependent bulk endocytosis
Clathrin-mediated endocytosis (CME) and activity-dependent bulk endocytosis (ADBE) are two predominant forms of synaptic vesicle (SV) endocytosis, elicited by moderate and strong stimuli, respectively. They are tightly coupled with exocytosis for sustained neurotransmission. However, the underlying...
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| description | Clathrin-mediated endocytosis (CME) and activity-dependent bulk endocytosis (ADBE) are two predominant forms of synaptic vesicle (SV) endocytosis, elicited by moderate and strong stimuli, respectively. They are tightly coupled with exocytosis for sustained neurotransmission. However, the underlying mechanisms are ill defined. We previously reported that the Flower (Fwe) Ca2+ channel present in SVs is incorporated into the periactive zone upon SV fusion, where it triggers CME, thus coupling exocytosis to CME. Here, we show that Fwe also promotes ADBE. Intriguingly, the effects of Fwe on CME and ADBE depend on the strength of the stimulus. Upon mild stimulation, Fwe controls CME independently of Ca2+ channeling. However, upon strong stimulation, Fwe triggers a Ca2+ influx that initiates ADBE. Moreover, knockout of rodent fwe in cultured rat hippocampal neurons impairs but does not completely abolish CME, similar to the loss of Drosophila fwe at the neuromuscular junction, suggesting that Fwe plays a regulatory role in regulating CME across species. In addition, the function of Fwe in ADBE is conserved at mammalian central synapses. Hence, Fwe exerts different effects in response to different stimulus strengths to control two major modes of endocytosis. |
| doi_str_mv | 10.1371/journal.pbio.2000931 |
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They are tightly coupled with exocytosis for sustained neurotransmission. However, the underlying mechanisms are ill defined. We previously reported that the Flower (Fwe) Ca2+ channel present in SVs is incorporated into the periactive zone upon SV fusion, where it triggers CME, thus coupling exocytosis to CME. Here, we show that Fwe also promotes ADBE. Intriguingly, the effects of Fwe on CME and ADBE depend on the strength of the stimulus. Upon mild stimulation, Fwe controls CME independently of Ca2+ channeling. However, upon strong stimulation, Fwe triggers a Ca2+ influx that initiates ADBE. Moreover, knockout of rodent fwe in cultured rat hippocampal neurons impairs but does not completely abolish CME, similar to the loss of Drosophila fwe at the neuromuscular junction, suggesting that Fwe plays a regulatory role in regulating CME across species. In addition, the function of Fwe in ADBE is conserved at mammalian central synapses. Hence, Fwe exerts different effects in response to different stimulus strengths to control two major modes of endocytosis.</description><identifier>ISSN: 1545-7885</identifier><identifier>ISSN: 1544-9173</identifier><identifier>EISSN: 1545-7885</identifier><identifier>DOI: 10.1371/journal.pbio.2000931</identifier><identifier>PMID: 28414717</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Animals, Genetically Modified ; Biology and Life Sciences ; Calcium - metabolism ; Calcium - pharmacology ; Calcium channels ; Calcium Channels - genetics ; Calcium Channels - metabolism ; Calcium ions ; Cell Line ; Channeling ; Chemistry ; Clathrin - metabolism ; Data collection ; Drosophila ; Drosophila Proteins - genetics ; Drosophila Proteins - metabolism ; Endocytosis ; Endocytosis - drug effects ; Endocytosis - physiology ; Exocytosis - physiology ; Funding ; Gene Knockdown Techniques ; Hippocampus ; Insects ; Lanthanum - pharmacology ; Medicine and Health Sciences ; Mice ; Mutation ; Neurons ; Neurons - metabolism ; Physical Sciences ; Physiology ; Protein Isoforms ; Proteins ; Rats ; Roles ; Software ; Stimulation ; Synapses ; Synapses - metabolism ; Synaptic vesicles ; Synaptic Vesicles - metabolism</subject><ispartof>PLoS biology, 2017-04, Vol.15 (4), p.e2000931-e2000931</ispartof><rights>2017 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: channel differentially regulates Clathrin-mediated and activity-dependent bulk endocytosis. PLoS Biol 15(4): e2000931. https://doi.org/10.1371/journal.pbio.2000931</rights><rights>2017 Yao et al 2017 Yao et al</rights><rights>2017 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: channel differentially regulates Clathrin-mediated and activity-dependent bulk endocytosis. PLoS Biol 15(4): e2000931. https://doi.org/10.1371/journal.pbio.2000931</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-19cb5e39d86437188d786d7c69f4e3be1b1307ac0978ab22fc278c213e3c5cdd3</citedby><cites>FETCH-LOGICAL-c456t-19cb5e39d86437188d786d7c69f4e3be1b1307ac0978ab22fc278c213e3c5cdd3</cites><orcidid>0000-0003-0977-4347</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5393565/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5393565/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28414717$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Schmid, Sandra</contributor><creatorcontrib>Yao, Chi-Kuang</creatorcontrib><creatorcontrib>Liu, Yu-Tzu</creatorcontrib><creatorcontrib>Lee, I-Chi</creatorcontrib><creatorcontrib>Wang, You-Tung</creatorcontrib><creatorcontrib>Wu, Ping-Yen</creatorcontrib><title>A Ca2+ channel differentially regulates Clathrin-mediated and activity-dependent bulk endocytosis</title><title>PLoS biology</title><addtitle>PLoS Biol</addtitle><description>Clathrin-mediated endocytosis (CME) and activity-dependent bulk endocytosis (ADBE) are two predominant forms of synaptic vesicle (SV) endocytosis, elicited by moderate and strong stimuli, respectively. They are tightly coupled with exocytosis for sustained neurotransmission. However, the underlying mechanisms are ill defined. We previously reported that the Flower (Fwe) Ca2+ channel present in SVs is incorporated into the periactive zone upon SV fusion, where it triggers CME, thus coupling exocytosis to CME. Here, we show that Fwe also promotes ADBE. Intriguingly, the effects of Fwe on CME and ADBE depend on the strength of the stimulus. Upon mild stimulation, Fwe controls CME independently of Ca2+ channeling. However, upon strong stimulation, Fwe triggers a Ca2+ influx that initiates ADBE. Moreover, knockout of rodent fwe in cultured rat hippocampal neurons impairs but does not completely abolish CME, similar to the loss of Drosophila fwe at the neuromuscular junction, suggesting that Fwe plays a regulatory role in regulating CME across species. In addition, the function of Fwe in ADBE is conserved at mammalian central synapses. Hence, Fwe exerts different effects in response to different stimulus strengths to control two major modes of endocytosis.</description><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Biology and Life Sciences</subject><subject>Calcium - metabolism</subject><subject>Calcium - pharmacology</subject><subject>Calcium channels</subject><subject>Calcium Channels - genetics</subject><subject>Calcium Channels - metabolism</subject><subject>Calcium ions</subject><subject>Cell Line</subject><subject>Channeling</subject><subject>Chemistry</subject><subject>Clathrin - metabolism</subject><subject>Data collection</subject><subject>Drosophila</subject><subject>Drosophila Proteins - genetics</subject><subject>Drosophila Proteins - metabolism</subject><subject>Endocytosis</subject><subject>Endocytosis - drug effects</subject><subject>Endocytosis - physiology</subject><subject>Exocytosis - physiology</subject><subject>Funding</subject><subject>Gene Knockdown Techniques</subject><subject>Hippocampus</subject><subject>Insects</subject><subject>Lanthanum - pharmacology</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mutation</subject><subject>Neurons</subject><subject>Neurons - metabolism</subject><subject>Physical Sciences</subject><subject>Physiology</subject><subject>Protein Isoforms</subject><subject>Proteins</subject><subject>Rats</subject><subject>Roles</subject><subject>Software</subject><subject>Stimulation</subject><subject>Synapses</subject><subject>Synapses - metabolism</subject><subject>Synaptic vesicles</subject><subject>Synaptic Vesicles - metabolism</subject><issn>1545-7885</issn><issn>1544-9173</issn><issn>1545-7885</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNptUsuKFDEULURxHvoHogVuBqTaPCvJRhgaHwMDbnQd8rjVnTZdaZOqgf5703bPMCMuwg0355zcczlN8wajBaYCf9ykOY8mLnY2pAVBCCmKnzXnmDPeCSn580f3s-ailA1ChCgiXzZnRDLMBBbnjblul4Z8aN3ajCPE1odhgAzjFEyM-zbDao5mgtIua1nnMHZb8KF2fGvGetwU7sK07zzsYPSV19o5_mrrPbn9lEoor5oXg4kFXp_qZfPzy-cfy2_d7fevN8vr284x3k8dVs5yoMrLnlV7Unohey9crwYG1AK2mCJhHFJCGkvI4IiQjmAK1HHnPb1s3h11dzEVfdpO0VgqRYnsqayImyPCJ7PRuxy2Ju91MkH_baS80iZPwUXQgjugyHtLhGDSSsMU7i1ilnvsBoeq1qfTb7OtG3HVeTbxiejTlzGs9SrdaU4V5T2vAlcngZx-z1AmvQ3FQYxmhDQf5paKSiaxqtD3_0D_744dUS6nUjIMD8NgpA-JuWfpQ2L0KTGV9vaxkQfSfUToH1F_wEY</recordid><startdate>20170401</startdate><enddate>20170401</enddate><creator>Yao, Chi-Kuang</creator><creator>Liu, Yu-Tzu</creator><creator>Lee, I-Chi</creator><creator>Wang, You-Tung</creator><creator>Wu, Ping-Yen</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PATMY</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><scope>CZG</scope><orcidid>https://orcid.org/0000-0003-0977-4347</orcidid></search><sort><creationdate>20170401</creationdate><title>A Ca2+ channel differentially regulates Clathrin-mediated and activity-dependent bulk endocytosis</title><author>Yao, Chi-Kuang ; Liu, Yu-Tzu ; Lee, I-Chi ; Wang, You-Tung ; Wu, Ping-Yen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-19cb5e39d86437188d786d7c69f4e3be1b1307ac0978ab22fc278c213e3c5cdd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>Biology and Life Sciences</topic><topic>Calcium - 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metabolism</topic><topic>Synaptic vesicles</topic><topic>Synaptic Vesicles - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yao, Chi-Kuang</creatorcontrib><creatorcontrib>Liu, Yu-Tzu</creatorcontrib><creatorcontrib>Lee, I-Chi</creatorcontrib><creatorcontrib>Wang, You-Tung</creatorcontrib><creatorcontrib>Wu, Ping-Yen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><collection>PLoS Biology</collection><jtitle>PLoS biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yao, Chi-Kuang</au><au>Liu, Yu-Tzu</au><au>Lee, I-Chi</au><au>Wang, You-Tung</au><au>Wu, Ping-Yen</au><au>Schmid, Sandra</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Ca2+ channel differentially regulates Clathrin-mediated and activity-dependent bulk endocytosis</atitle><jtitle>PLoS biology</jtitle><addtitle>PLoS Biol</addtitle><date>2017-04-01</date><risdate>2017</risdate><volume>15</volume><issue>4</issue><spage>e2000931</spage><epage>e2000931</epage><pages>e2000931-e2000931</pages><issn>1545-7885</issn><issn>1544-9173</issn><eissn>1545-7885</eissn><abstract>Clathrin-mediated endocytosis (CME) and activity-dependent bulk endocytosis (ADBE) are two predominant forms of synaptic vesicle (SV) endocytosis, elicited by moderate and strong stimuli, respectively. They are tightly coupled with exocytosis for sustained neurotransmission. However, the underlying mechanisms are ill defined. We previously reported that the Flower (Fwe) Ca2+ channel present in SVs is incorporated into the periactive zone upon SV fusion, where it triggers CME, thus coupling exocytosis to CME. Here, we show that Fwe also promotes ADBE. Intriguingly, the effects of Fwe on CME and ADBE depend on the strength of the stimulus. Upon mild stimulation, Fwe controls CME independently of Ca2+ channeling. However, upon strong stimulation, Fwe triggers a Ca2+ influx that initiates ADBE. Moreover, knockout of rodent fwe in cultured rat hippocampal neurons impairs but does not completely abolish CME, similar to the loss of Drosophila fwe at the neuromuscular junction, suggesting that Fwe plays a regulatory role in regulating CME across species. In addition, the function of Fwe in ADBE is conserved at mammalian central synapses. Hence, Fwe exerts different effects in response to different stimulus strengths to control two major modes of endocytosis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28414717</pmid><doi>10.1371/journal.pbio.2000931</doi><orcidid>https://orcid.org/0000-0003-0977-4347</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Animals, Genetically Modified Biology and Life Sciences Calcium - metabolism Calcium - pharmacology Calcium channels Calcium Channels - genetics Calcium Channels - metabolism Calcium ions Cell Line Channeling Chemistry Clathrin - metabolism Data collection Drosophila Drosophila Proteins - genetics Drosophila Proteins - metabolism Endocytosis Endocytosis - drug effects Endocytosis - physiology Exocytosis - physiology Funding Gene Knockdown Techniques Hippocampus Insects Lanthanum - pharmacology Medicine and Health Sciences Mice Mutation Neurons Neurons - metabolism Physical Sciences Physiology Protein Isoforms Proteins Rats Roles Software Stimulation Synapses Synapses - metabolism Synaptic vesicles Synaptic Vesicles - metabolism |
| title | A Ca2+ channel differentially regulates Clathrin-mediated and activity-dependent bulk endocytosis |
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