LGI1–ADAM22–MAGUK configures transsynaptic nanoalignment for synaptic transmission and epilepsy prevention
Physiological functioning and homeostasis of the brain rely on finely tuned synaptic transmission, which involves nanoscale alignment between presynaptic neurotransmitter-release machinery and postsynaptic receptors. However, the molecular identity and physiological significance of transsynaptic nan...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2021-01, Vol.118 (3), p.1-12 |
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| creator | Fukata, Yuko Chen, Xiumin Chiken, Satomi Hirano, Yoko Yamagata, Atsushi Inahashi, Hiroki Sanbo, Makoto Sano, Hiromi Goto, Teppei Hirabayashi, Masumi Kornau, Hans-Christian Prüss, Harald Nambu, Atsushi Fukai, Shuya Nicoll, Roger A. Fukata, Masaki |
| description | Physiological functioning and homeostasis of the brain rely on finely tuned synaptic transmission, which involves nanoscale alignment between presynaptic neurotransmitter-release machinery and postsynaptic receptors. However, the molecular identity and physiological significance of transsynaptic nanoalignment remain incompletely understood. Here, we report that epilepsy gene products, a secreted protein LGI1 and its receptor ADAM22, govern transsynaptic nanoalignment to prevent epilepsy. We found that LGI1–ADAM22 instructs PSD-95 family membrane-associated guanylate kinases (MAGUKs) to organize transsynaptic protein networks, including NMDA/AMPA receptors, Kv₁ channels, and LRRTM4–Neurexin adhesion molecules. Adam22ΔC5/ΔC5
knock-in mice devoid of the ADAM22–MAGUK interaction display lethal epilepsy of hippocampal origin, representing the mouse model for ADAM22-related epileptic encephalopathy. This model shows less-condensed PSD-95 nanodomains, disordered transsynaptic nanoalignment, and decreased excitatory synaptic transmission in the hippocampus. Strikingly, without ADAM22 binding, PSD-95 cannot potentiate AMPA receptor-mediated synaptic transmission. Furthermore, forced coexpression of ADAM22 and PSD-95 reconstitutes nano-condensates in nonneuronal cells. Collectively, this study reveals LGI1–ADAM22–MAGUK as an essential component of transsynaptic nanoarchitecture for precise synaptic transmission and epilepsy prevention. |
| doi_str_mv | 10.1073/pnas.2022580118 |
| format | Article |
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knock-in mice devoid of the ADAM22–MAGUK interaction display lethal epilepsy of hippocampal origin, representing the mouse model for ADAM22-related epileptic encephalopathy. This model shows less-condensed PSD-95 nanodomains, disordered transsynaptic nanoalignment, and decreased excitatory synaptic transmission in the hippocampus. Strikingly, without ADAM22 binding, PSD-95 cannot potentiate AMPA receptor-mediated synaptic transmission. Furthermore, forced coexpression of ADAM22 and PSD-95 reconstitutes nano-condensates in nonneuronal cells. Collectively, this study reveals LGI1–ADAM22–MAGUK as an essential component of transsynaptic nanoarchitecture for precise synaptic transmission and epilepsy prevention.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.2022580118</identifier><identifier>PMID: 33397806</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Biological Sciences ; Encephalopathy ; Epilepsy ; Glutamic acid receptors (ionotropic) ; Hippocampus ; Homeostasis ; Kinases ; LGI1 protein ; N-Methyl-D-aspartic acid receptors ; Neurotransmitters ; Physiology ; Postsynaptic density proteins ; Prevention ; Proteins ; Receptors ; Synaptic transmission ; α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid ; α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2021-01, Vol.118 (3), p.1-12</ispartof><rights>Copyright © 2021 the Author(s). Published by PNAS.</rights><rights>Copyright National Academy of Sciences Jan 19, 2021</rights><rights>Copyright © 2021 the Author(s). Published by PNAS. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c553t-c7479e60252acafc0e4c4eefbfbe4c45b366de1a781d129b6d004ad25d1d054b3</citedby><cites>FETCH-LOGICAL-c553t-c7479e60252acafc0e4c4eefbfbe4c45b366de1a781d129b6d004ad25d1d054b3</cites><orcidid>0000-0001-8806-1745 ; 0000-0003-4187-7549 ; 0000-0001-7347-8150 ; 0000-0002-0081-3357 ; 0000-0001-7724-8643 ; 0000-0002-8283-7976 ; 0000-0003-2153-5445 ; 0000-0001-5200-9806 ; 0000-0002-1241-1443 ; 0000-0002-1059-5883</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/27012240$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/27012240$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27924,27925,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33397806$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fukata, Yuko</creatorcontrib><creatorcontrib>Chen, Xiumin</creatorcontrib><creatorcontrib>Chiken, Satomi</creatorcontrib><creatorcontrib>Hirano, Yoko</creatorcontrib><creatorcontrib>Yamagata, Atsushi</creatorcontrib><creatorcontrib>Inahashi, Hiroki</creatorcontrib><creatorcontrib>Sanbo, Makoto</creatorcontrib><creatorcontrib>Sano, Hiromi</creatorcontrib><creatorcontrib>Goto, Teppei</creatorcontrib><creatorcontrib>Hirabayashi, Masumi</creatorcontrib><creatorcontrib>Kornau, Hans-Christian</creatorcontrib><creatorcontrib>Prüss, Harald</creatorcontrib><creatorcontrib>Nambu, Atsushi</creatorcontrib><creatorcontrib>Fukai, Shuya</creatorcontrib><creatorcontrib>Nicoll, Roger A.</creatorcontrib><creatorcontrib>Fukata, Masaki</creatorcontrib><title>LGI1–ADAM22–MAGUK configures transsynaptic nanoalignment for synaptic transmission and epilepsy prevention</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Physiological functioning and homeostasis of the brain rely on finely tuned synaptic transmission, which involves nanoscale alignment between presynaptic neurotransmitter-release machinery and postsynaptic receptors. However, the molecular identity and physiological significance of transsynaptic nanoalignment remain incompletely understood. Here, we report that epilepsy gene products, a secreted protein LGI1 and its receptor ADAM22, govern transsynaptic nanoalignment to prevent epilepsy. We found that LGI1–ADAM22 instructs PSD-95 family membrane-associated guanylate kinases (MAGUKs) to organize transsynaptic protein networks, including NMDA/AMPA receptors, Kv₁ channels, and LRRTM4–Neurexin adhesion molecules. Adam22ΔC5/ΔC5
knock-in mice devoid of the ADAM22–MAGUK interaction display lethal epilepsy of hippocampal origin, representing the mouse model for ADAM22-related epileptic encephalopathy. This model shows less-condensed PSD-95 nanodomains, disordered transsynaptic nanoalignment, and decreased excitatory synaptic transmission in the hippocampus. Strikingly, without ADAM22 binding, PSD-95 cannot potentiate AMPA receptor-mediated synaptic transmission. Furthermore, forced coexpression of ADAM22 and PSD-95 reconstitutes nano-condensates in nonneuronal cells. Collectively, this study reveals LGI1–ADAM22–MAGUK as an essential component of transsynaptic nanoarchitecture for precise synaptic transmission and epilepsy prevention.</description><subject>Biological Sciences</subject><subject>Encephalopathy</subject><subject>Epilepsy</subject><subject>Glutamic acid receptors (ionotropic)</subject><subject>Hippocampus</subject><subject>Homeostasis</subject><subject>Kinases</subject><subject>LGI1 protein</subject><subject>N-Methyl-D-aspartic acid receptors</subject><subject>Neurotransmitters</subject><subject>Physiology</subject><subject>Postsynaptic density proteins</subject><subject>Prevention</subject><subject>Proteins</subject><subject>Receptors</subject><subject>Synaptic transmission</subject><subject>α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid</subject><subject>α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNpdkc1u1DAUha2qiA6FdVegSGzYpL3-i-NNpVEpQ8VU3dC15TjO4FHGDnZSaXa8A2_YJ8HDlAG68pXP53N9dBA6w3COQdCLwet0ToAQXgPG9RGaYZC4rJiEYzQDIKKsGWEn6FVKawCQmXuJTiilUtRQzZBfLm7w44-f84_zW0LycDtf3H8pTPCdW03RpmKM2qe09XoYnSm89kH3buU31o9FF2JxkH6DG5eSC77Qvi3s4Ho7pG0xRPuQ8Xz_Gr3odJ_sm6fzFN1_uv569blc3i1urubL0nBOx9IIJqStgHCije4MWGaYtV3TNbuJN7SqWou1qHGLiWyqFoDplvAWt8BZQ0_R5d53mJqNbU3eHnWvhug2Om5V0E79r3j3Ta3CgxI1qaik2eDDk0EM3yebRpWTGdv32tswJUWY4FRKCXVG3z9D12GKPsfbURXnjFGRqYs9ZWJIKdru8BkMatel2nWp_naZX7z7N8OB_1NeBt7ugXUaQzzoRAAmhAH9BRDZqOw</recordid><startdate>20210119</startdate><enddate>20210119</enddate><creator>Fukata, Yuko</creator><creator>Chen, Xiumin</creator><creator>Chiken, Satomi</creator><creator>Hirano, Yoko</creator><creator>Yamagata, Atsushi</creator><creator>Inahashi, Hiroki</creator><creator>Sanbo, Makoto</creator><creator>Sano, Hiromi</creator><creator>Goto, Teppei</creator><creator>Hirabayashi, Masumi</creator><creator>Kornau, Hans-Christian</creator><creator>Prüss, Harald</creator><creator>Nambu, Atsushi</creator><creator>Fukai, Shuya</creator><creator>Nicoll, Roger A.</creator><creator>Fukata, Masaki</creator><general>National Academy of Sciences</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8806-1745</orcidid><orcidid>https://orcid.org/0000-0003-4187-7549</orcidid><orcidid>https://orcid.org/0000-0001-7347-8150</orcidid><orcidid>https://orcid.org/0000-0002-0081-3357</orcidid><orcidid>https://orcid.org/0000-0001-7724-8643</orcidid><orcidid>https://orcid.org/0000-0002-8283-7976</orcidid><orcidid>https://orcid.org/0000-0003-2153-5445</orcidid><orcidid>https://orcid.org/0000-0001-5200-9806</orcidid><orcidid>https://orcid.org/0000-0002-1241-1443</orcidid><orcidid>https://orcid.org/0000-0002-1059-5883</orcidid></search><sort><creationdate>20210119</creationdate><title>LGI1–ADAM22–MAGUK configures transsynaptic nanoalignment for synaptic transmission and epilepsy prevention</title><author>Fukata, Yuko ; Chen, Xiumin ; Chiken, Satomi ; Hirano, Yoko ; Yamagata, Atsushi ; Inahashi, Hiroki ; Sanbo, Makoto ; Sano, Hiromi ; Goto, Teppei ; Hirabayashi, Masumi ; Kornau, Hans-Christian ; Prüss, Harald ; Nambu, Atsushi ; Fukai, Shuya ; Nicoll, Roger A. ; Fukata, Masaki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c553t-c7479e60252acafc0e4c4eefbfbe4c45b366de1a781d129b6d004ad25d1d054b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Biological Sciences</topic><topic>Encephalopathy</topic><topic>Epilepsy</topic><topic>Glutamic acid receptors (ionotropic)</topic><topic>Hippocampus</topic><topic>Homeostasis</topic><topic>Kinases</topic><topic>LGI1 protein</topic><topic>N-Methyl-D-aspartic acid receptors</topic><topic>Neurotransmitters</topic><topic>Physiology</topic><topic>Postsynaptic density proteins</topic><topic>Prevention</topic><topic>Proteins</topic><topic>Receptors</topic><topic>Synaptic transmission</topic><topic>α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid</topic><topic>α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fukata, Yuko</creatorcontrib><creatorcontrib>Chen, Xiumin</creatorcontrib><creatorcontrib>Chiken, Satomi</creatorcontrib><creatorcontrib>Hirano, Yoko</creatorcontrib><creatorcontrib>Yamagata, Atsushi</creatorcontrib><creatorcontrib>Inahashi, Hiroki</creatorcontrib><creatorcontrib>Sanbo, Makoto</creatorcontrib><creatorcontrib>Sano, Hiromi</creatorcontrib><creatorcontrib>Goto, Teppei</creatorcontrib><creatorcontrib>Hirabayashi, Masumi</creatorcontrib><creatorcontrib>Kornau, Hans-Christian</creatorcontrib><creatorcontrib>Prüss, Harald</creatorcontrib><creatorcontrib>Nambu, Atsushi</creatorcontrib><creatorcontrib>Fukai, Shuya</creatorcontrib><creatorcontrib>Nicoll, Roger A.</creatorcontrib><creatorcontrib>Fukata, Masaki</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</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>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fukata, Yuko</au><au>Chen, Xiumin</au><au>Chiken, Satomi</au><au>Hirano, Yoko</au><au>Yamagata, Atsushi</au><au>Inahashi, Hiroki</au><au>Sanbo, Makoto</au><au>Sano, Hiromi</au><au>Goto, Teppei</au><au>Hirabayashi, Masumi</au><au>Kornau, Hans-Christian</au><au>Prüss, Harald</au><au>Nambu, Atsushi</au><au>Fukai, Shuya</au><au>Nicoll, Roger A.</au><au>Fukata, Masaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LGI1–ADAM22–MAGUK configures transsynaptic nanoalignment for synaptic transmission and epilepsy prevention</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2021-01-19</date><risdate>2021</risdate><volume>118</volume><issue>3</issue><spage>1</spage><epage>12</epage><pages>1-12</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Physiological functioning and homeostasis of the brain rely on finely tuned synaptic transmission, which involves nanoscale alignment between presynaptic neurotransmitter-release machinery and postsynaptic receptors. However, the molecular identity and physiological significance of transsynaptic nanoalignment remain incompletely understood. Here, we report that epilepsy gene products, a secreted protein LGI1 and its receptor ADAM22, govern transsynaptic nanoalignment to prevent epilepsy. We found that LGI1–ADAM22 instructs PSD-95 family membrane-associated guanylate kinases (MAGUKs) to organize transsynaptic protein networks, including NMDA/AMPA receptors, Kv₁ channels, and LRRTM4–Neurexin adhesion molecules. Adam22ΔC5/ΔC5
knock-in mice devoid of the ADAM22–MAGUK interaction display lethal epilepsy of hippocampal origin, representing the mouse model for ADAM22-related epileptic encephalopathy. This model shows less-condensed PSD-95 nanodomains, disordered transsynaptic nanoalignment, and decreased excitatory synaptic transmission in the hippocampus. Strikingly, without ADAM22 binding, PSD-95 cannot potentiate AMPA receptor-mediated synaptic transmission. Furthermore, forced coexpression of ADAM22 and PSD-95 reconstitutes nano-condensates in nonneuronal cells. Collectively, this study reveals LGI1–ADAM22–MAGUK as an essential component of transsynaptic nanoarchitecture for precise synaptic transmission and epilepsy prevention.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>33397806</pmid><doi>10.1073/pnas.2022580118</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-8806-1745</orcidid><orcidid>https://orcid.org/0000-0003-4187-7549</orcidid><orcidid>https://orcid.org/0000-0001-7347-8150</orcidid><orcidid>https://orcid.org/0000-0002-0081-3357</orcidid><orcidid>https://orcid.org/0000-0001-7724-8643</orcidid><orcidid>https://orcid.org/0000-0002-8283-7976</orcidid><orcidid>https://orcid.org/0000-0003-2153-5445</orcidid><orcidid>https://orcid.org/0000-0001-5200-9806</orcidid><orcidid>https://orcid.org/0000-0002-1241-1443</orcidid><orcidid>https://orcid.org/0000-0002-1059-5883</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Biological Sciences Encephalopathy Epilepsy Glutamic acid receptors (ionotropic) Hippocampus Homeostasis Kinases LGI1 protein N-Methyl-D-aspartic acid receptors Neurotransmitters Physiology Postsynaptic density proteins Prevention Proteins Receptors Synaptic transmission α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors |
| title | LGI1–ADAM22–MAGUK configures transsynaptic nanoalignment for synaptic transmission and epilepsy prevention |
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