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Maintenance of neuronal positions in organized ganglia by SAX-7, a Caenorhabditis elegans homologue of L1
The L1 family of cell adhesion molecules is predominantly expressed in the nervous system. Mutations in human L1 cause neuronal diseases such as HSAS, MASA, and SPG1. Here we show that sax‐7 gene encodes an L1 homologue in Caenorhabditis elegans . In sax‐7 mutants, the organization of ganglia and po...
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Published in: | The EMBO journal 2005-04, Vol.24 (7), p.1477-1488 |
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creator | Sasakura, Hiroyuki Inada, Hitoshi Kuhara, Atsushi Fusaoka, Eri Takemoto, Daisuke Takeuchi, Kosei Mori, Ikue |
description | The L1 family of cell adhesion molecules is predominantly expressed in the nervous system. Mutations in human L1 cause neuronal diseases such as HSAS, MASA, and SPG1. Here we show that
sax‐7
gene encodes an L1 homologue in
Caenorhabditis elegans
. In
sax‐7
mutants, the organization of ganglia and positioning of neurons are abnormal in the adult stage, but these abnormalities are not observed in early larval stage. Misplacement of neurons in
sax‐7
mutants is triggered by mechanical force linked to body movement. Short and long forms of SAX‐7 exhibited strong and weak homophilic adhesion activities in
in vitro
aggregation assay, respectively, which correlated with their different activities
in vivo
. SAX‐7 was localized on plasma membranes of neurons
in vivo
. Expression of SAX‐7 only in a single neuron in
sax‐7
mutants cell‐autonomously restored its normal neuronal position. Expression of SAX‐7 in two different head neurons in
sax‐7
mutants led to the forced attachment of these neurons. We propose that both homophilic and heterophilic interactions of SAX‐7 are essential for maintenance of neuronal positions in organized ganglia. |
doi_str_mv | 10.1038/sj.emboj.7600621 |
format | article |
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sax‐7
gene encodes an L1 homologue in
Caenorhabditis elegans
. In
sax‐7
mutants, the organization of ganglia and positioning of neurons are abnormal in the adult stage, but these abnormalities are not observed in early larval stage. Misplacement of neurons in
sax‐7
mutants is triggered by mechanical force linked to body movement. Short and long forms of SAX‐7 exhibited strong and weak homophilic adhesion activities in
in vitro
aggregation assay, respectively, which correlated with their different activities
in vivo
. SAX‐7 was localized on plasma membranes of neurons
in vivo
. Expression of SAX‐7 only in a single neuron in
sax‐7
mutants cell‐autonomously restored its normal neuronal position. Expression of SAX‐7 in two different head neurons in
sax‐7
mutants led to the forced attachment of these neurons. We propose that both homophilic and heterophilic interactions of SAX‐7 are essential for maintenance of neuronal positions in organized ganglia.</description><identifier>ISSN: 0261-4189</identifier><identifier>EISSN: 1460-2075</identifier><identifier>DOI: 10.1038/sj.emboj.7600621</identifier><identifier>PMID: 15775964</identifier><identifier>CODEN: EMJODG</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Adhesion ; Animals ; Baculoviridae ; Blotting, Western ; Bombyx ; C. elegans ; Caenorhabditis elegans ; Caenorhabditis elegans - metabolism ; Caenorhabditis elegans Proteins - genetics ; Caenorhabditis elegans Proteins - metabolism ; Cell Adhesion - physiology ; Cell Aggregation - genetics ; Cell Aggregation - physiology ; Cells, Cultured ; Cloning, Molecular ; DNA, Complementary - genetics ; EMBO11 ; EMBO27 ; Ganglia, Invertebrate - metabolism ; Gene Components ; Genetic Vectors ; Green Fluorescent Proteins ; L1 family ; Membrane Proteins - metabolism ; Models, Biological ; Mutants ; Mutation ; Mutation - genetics ; Neural Cell Adhesion Molecule L1 - genetics ; Neural Cell Adhesion Molecules - genetics ; Neural Cell Adhesion Molecules - metabolism ; neuronal adhesion ; neuronal placement ; Neurons - metabolism ; organization of ganglia ; Phylogeny</subject><ispartof>The EMBO journal, 2005-04, Vol.24 (7), p.1477-1488</ispartof><rights>European Molecular Biology Organization 2005</rights><rights>Copyright © 2005 European Molecular Biology Organization</rights><rights>Copyright Nature Publishing Group Apr 6, 2005</rights><rights>Copyright © 2005, European Molecular Biology Organization 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6701-38626b7fe7cd93c2a4d2d62d7ec9c88a17c1ccf2b3471be71b659a498a20a8313</citedby><cites>FETCH-LOGICAL-c6701-38626b7fe7cd93c2a4d2d62d7ec9c88a17c1ccf2b3471be71b659a498a20a8313</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142545/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142545/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15775964$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sasakura, Hiroyuki</creatorcontrib><creatorcontrib>Inada, Hitoshi</creatorcontrib><creatorcontrib>Kuhara, Atsushi</creatorcontrib><creatorcontrib>Fusaoka, Eri</creatorcontrib><creatorcontrib>Takemoto, Daisuke</creatorcontrib><creatorcontrib>Takeuchi, Kosei</creatorcontrib><creatorcontrib>Mori, Ikue</creatorcontrib><title>Maintenance of neuronal positions in organized ganglia by SAX-7, a Caenorhabditis elegans homologue of L1</title><title>The EMBO journal</title><addtitle>EMBO J</addtitle><addtitle>EMBO J</addtitle><description>The L1 family of cell adhesion molecules is predominantly expressed in the nervous system. Mutations in human L1 cause neuronal diseases such as HSAS, MASA, and SPG1. Here we show that
sax‐7
gene encodes an L1 homologue in
Caenorhabditis elegans
. In
sax‐7
mutants, the organization of ganglia and positioning of neurons are abnormal in the adult stage, but these abnormalities are not observed in early larval stage. Misplacement of neurons in
sax‐7
mutants is triggered by mechanical force linked to body movement. Short and long forms of SAX‐7 exhibited strong and weak homophilic adhesion activities in
in vitro
aggregation assay, respectively, which correlated with their different activities
in vivo
. SAX‐7 was localized on plasma membranes of neurons
in vivo
. Expression of SAX‐7 only in a single neuron in
sax‐7
mutants cell‐autonomously restored its normal neuronal position. Expression of SAX‐7 in two different head neurons in
sax‐7
mutants led to the forced attachment of these neurons. We propose that both homophilic and heterophilic interactions of SAX‐7 are essential for maintenance of neuronal positions in organized ganglia.</description><subject>Adhesion</subject><subject>Animals</subject><subject>Baculoviridae</subject><subject>Blotting, Western</subject><subject>Bombyx</subject><subject>C. elegans</subject><subject>Caenorhabditis elegans</subject><subject>Caenorhabditis elegans - metabolism</subject><subject>Caenorhabditis elegans Proteins - genetics</subject><subject>Caenorhabditis elegans Proteins - metabolism</subject><subject>Cell Adhesion - physiology</subject><subject>Cell Aggregation - genetics</subject><subject>Cell Aggregation - physiology</subject><subject>Cells, Cultured</subject><subject>Cloning, Molecular</subject><subject>DNA, Complementary - genetics</subject><subject>EMBO11</subject><subject>EMBO27</subject><subject>Ganglia, Invertebrate - metabolism</subject><subject>Gene Components</subject><subject>Genetic Vectors</subject><subject>Green Fluorescent Proteins</subject><subject>L1 family</subject><subject>Membrane Proteins - metabolism</subject><subject>Models, Biological</subject><subject>Mutants</subject><subject>Mutation</subject><subject>Mutation - genetics</subject><subject>Neural Cell Adhesion Molecule L1 - genetics</subject><subject>Neural Cell Adhesion Molecules - genetics</subject><subject>Neural Cell Adhesion Molecules - metabolism</subject><subject>neuronal adhesion</subject><subject>neuronal placement</subject><subject>Neurons - metabolism</subject><subject>organization of ganglia</subject><subject>Phylogeny</subject><issn>0261-4189</issn><issn>1460-2075</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNqFkc2P0zAUxCMEYsvCnQvI4sCJFNtJbOeCtFstXaALh-WjN8txXluXxC52ApS_HtNU7YKE9mC9w_xm_OxJkscEjwnOxMuwHkNbufWYM4wZJXeSEckZTinmxd1khCkjaU5EeZI8CGGNMS4EJ_eTE1JwXpQsHyXmShnbgVVWA3ILZKH3zqoGbVwwnXE2IGOR80tlzS-oUZzLxihUbdH12TzlL5BCEwXW-ZWq6ugICBqIVEAr17rGLftd7ow8TO4tVBPg0X6eJp9eX3ycXKazD9M3k7NZqhnHJM0Eo6ziC-C6LjNNVV7TmtGagy61EIpwTbRe0CrLOakgHlaUKi-FoliJjGSnyashd9NXLdQabOdVIzfetMpvpVNG_q1Ys5JL910SktMiL2LA832Ad996CJ1sTdDQNMqC64NkXGQ8p-JWkPAiY6TMI_jsH3Dteh9_OTJlQVkpdhAeIO1dCB4Wh5UJln_almEtd23LfdvR8vTmU4-Gfb0RKAfgh2lge2ugvLg6f3sMJ4M3RJtdgr-x9P8XejJ4rOp6D4cLj3o66CZ08PMgK_81_mrGC_nl_VTm83fTy_Prz3Ke_QbHkOOA</recordid><startdate>20050406</startdate><enddate>20050406</enddate><creator>Sasakura, Hiroyuki</creator><creator>Inada, Hitoshi</creator><creator>Kuhara, Atsushi</creator><creator>Fusaoka, Eri</creator><creator>Takemoto, Daisuke</creator><creator>Takeuchi, Kosei</creator><creator>Mori, Ikue</creator><general>John Wiley & Sons, Ltd</general><general>Nature Publishing Group UK</general><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PCBAR</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20050406</creationdate><title>Maintenance of neuronal positions in organized ganglia by SAX-7, a Caenorhabditis elegans homologue of L1</title><author>Sasakura, Hiroyuki ; Inada, Hitoshi ; Kuhara, Atsushi ; Fusaoka, Eri ; Takemoto, Daisuke ; Takeuchi, Kosei ; Mori, Ikue</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6701-38626b7fe7cd93c2a4d2d62d7ec9c88a17c1ccf2b3471be71b659a498a20a8313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adhesion</topic><topic>Animals</topic><topic>Baculoviridae</topic><topic>Blotting, Western</topic><topic>Bombyx</topic><topic>C. elegans</topic><topic>Caenorhabditis elegans</topic><topic>Caenorhabditis elegans - metabolism</topic><topic>Caenorhabditis elegans Proteins - genetics</topic><topic>Caenorhabditis elegans Proteins - metabolism</topic><topic>Cell Adhesion - physiology</topic><topic>Cell Aggregation - genetics</topic><topic>Cell Aggregation - physiology</topic><topic>Cells, Cultured</topic><topic>Cloning, Molecular</topic><topic>DNA, Complementary - genetics</topic><topic>EMBO11</topic><topic>EMBO27</topic><topic>Ganglia, Invertebrate - metabolism</topic><topic>Gene Components</topic><topic>Genetic Vectors</topic><topic>Green Fluorescent Proteins</topic><topic>L1 family</topic><topic>Membrane Proteins - metabolism</topic><topic>Models, Biological</topic><topic>Mutants</topic><topic>Mutation</topic><topic>Mutation - genetics</topic><topic>Neural Cell Adhesion Molecule L1 - genetics</topic><topic>Neural Cell Adhesion Molecules - genetics</topic><topic>Neural Cell Adhesion Molecules - metabolism</topic><topic>neuronal adhesion</topic><topic>neuronal placement</topic><topic>Neurons - metabolism</topic><topic>organization of ganglia</topic><topic>Phylogeny</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sasakura, Hiroyuki</creatorcontrib><creatorcontrib>Inada, Hitoshi</creatorcontrib><creatorcontrib>Kuhara, Atsushi</creatorcontrib><creatorcontrib>Fusaoka, Eri</creatorcontrib><creatorcontrib>Takemoto, Daisuke</creatorcontrib><creatorcontrib>Takeuchi, Kosei</creatorcontrib><creatorcontrib>Mori, Ikue</creatorcontrib><collection>Istex</collection><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>Calcium & Calcified Tissue Abstracts</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>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database (Proquest)</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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Earth, Atmospheric & Aquatic Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</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>Research Library Prep</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>PML(ProQuest Medical Library)</collection><collection>ProQuest research library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>ProQuest Biological Science Journals</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Earth, Atmospheric & Aquatic Science 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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The EMBO journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sasakura, Hiroyuki</au><au>Inada, Hitoshi</au><au>Kuhara, Atsushi</au><au>Fusaoka, Eri</au><au>Takemoto, Daisuke</au><au>Takeuchi, Kosei</au><au>Mori, Ikue</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Maintenance of neuronal positions in organized ganglia by SAX-7, a Caenorhabditis elegans homologue of L1</atitle><jtitle>The EMBO journal</jtitle><stitle>EMBO J</stitle><addtitle>EMBO J</addtitle><date>2005-04-06</date><risdate>2005</risdate><volume>24</volume><issue>7</issue><spage>1477</spage><epage>1488</epage><pages>1477-1488</pages><issn>0261-4189</issn><eissn>1460-2075</eissn><coden>EMJODG</coden><abstract>The L1 family of cell adhesion molecules is predominantly expressed in the nervous system. Mutations in human L1 cause neuronal diseases such as HSAS, MASA, and SPG1. Here we show that
sax‐7
gene encodes an L1 homologue in
Caenorhabditis elegans
. In
sax‐7
mutants, the organization of ganglia and positioning of neurons are abnormal in the adult stage, but these abnormalities are not observed in early larval stage. Misplacement of neurons in
sax‐7
mutants is triggered by mechanical force linked to body movement. Short and long forms of SAX‐7 exhibited strong and weak homophilic adhesion activities in
in vitro
aggregation assay, respectively, which correlated with their different activities
in vivo
. SAX‐7 was localized on plasma membranes of neurons
in vivo
. Expression of SAX‐7 only in a single neuron in
sax‐7
mutants cell‐autonomously restored its normal neuronal position. Expression of SAX‐7 in two different head neurons in
sax‐7
mutants led to the forced attachment of these neurons. We propose that both homophilic and heterophilic interactions of SAX‐7 are essential for maintenance of neuronal positions in organized ganglia.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>15775964</pmid><doi>10.1038/sj.emboj.7600621</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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language | eng |
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source | Open Access: PubMed Central |
subjects | Adhesion Animals Baculoviridae Blotting, Western Bombyx C. elegans Caenorhabditis elegans Caenorhabditis elegans - metabolism Caenorhabditis elegans Proteins - genetics Caenorhabditis elegans Proteins - metabolism Cell Adhesion - physiology Cell Aggregation - genetics Cell Aggregation - physiology Cells, Cultured Cloning, Molecular DNA, Complementary - genetics EMBO11 EMBO27 Ganglia, Invertebrate - metabolism Gene Components Genetic Vectors Green Fluorescent Proteins L1 family Membrane Proteins - metabolism Models, Biological Mutants Mutation Mutation - genetics Neural Cell Adhesion Molecule L1 - genetics Neural Cell Adhesion Molecules - genetics Neural Cell Adhesion Molecules - metabolism neuronal adhesion neuronal placement Neurons - metabolism organization of ganglia Phylogeny |
title | Maintenance of neuronal positions in organized ganglia by SAX-7, a Caenorhabditis elegans homologue of L1 |
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