Loss of Bardet-Biedl syndrome proteins causes defects in peripheral sensory innervation and function
Reception and interpretation of environmental stimuli is critical for the survival of all organisms. Here, we show that the ablation of BBS1 and BBS4, two genes mutated in Bardet-Biedl syndrome and that encode proteins that localize near the centrioles of sensory neurons, leads to alterations of s.c...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2007-10, Vol.104 (44), p.17524-17529 |
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| creator | Tan, Perciliz L Barr, Travis Inglis, Peter N Mitsuma, Norimasa Huang, Susan M Garcia-Gonzalez, Miguel A Bradley, Brian A Coforio, Stephanie Albrecht, Phillip J Watnick, Terry Germino, Gregory G Beales, Philip L Caterina, Michael J Leroux, Michel R Rice, Frank L Katsanis, Nicholas |
| description | Reception and interpretation of environmental stimuli is critical for the survival of all organisms. Here, we show that the ablation of BBS1 and BBS4, two genes mutated in Bardet-Biedl syndrome and that encode proteins that localize near the centrioles of sensory neurons, leads to alterations of s.c. sensory innervation and trafficking of the thermosensory channel TRPV1 and the mechanosensory channel STOML3, with concomitant defects in peripheral thermosensation and mechanosensation. The thermosensory phenotype is recapitulated in Caenorhabditis elegans, because BBS mutants manifest deficient thermosensory responses at both physiological and nociceptive temperatures and defective trafficking of OSM-9, a polymodal sensory channel protein and a functional homolog of TRPV1 or TRPV4. Our findings suggest a hitherto unrecognized, but essential, role for mammalian basal body proteins in the acquisition of mechano- and thermosensory stimuli and highlight potentially clinical features of ciliopathies in humans. |
| doi_str_mv | 10.1073/pnas.0706618104 |
| format | Article |
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Here, we show that the ablation of BBS1 and BBS4, two genes mutated in Bardet-Biedl syndrome and that encode proteins that localize near the centrioles of sensory neurons, leads to alterations of s.c. sensory innervation and trafficking of the thermosensory channel TRPV1 and the mechanosensory channel STOML3, with concomitant defects in peripheral thermosensation and mechanosensation. The thermosensory phenotype is recapitulated in Caenorhabditis elegans, because BBS mutants manifest deficient thermosensory responses at both physiological and nociceptive temperatures and defective trafficking of OSM-9, a polymodal sensory channel protein and a functional homolog of TRPV1 or TRPV4. Our findings suggest a hitherto unrecognized, but essential, role for mammalian basal body proteins in the acquisition of mechano- and thermosensory stimuli and highlight potentially clinical features of ciliopathies in humans.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0706618104</identifier><identifier>PMID: 17959775</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Adolescent ; Adult ; Animals ; Animals, Genetically Modified ; Antibodies ; Bardet-Biedl Syndrome - metabolism ; Bardet-Biedl Syndrome - pathology ; Biological Sciences ; Caenorhabditis elegans ; Caenorhabditis elegans - genetics ; Caenorhabditis elegans - metabolism ; Central Nervous System - metabolism ; Cilia ; Female ; Gene Expression Regulation ; Genes ; Genotype & phenotype ; Genotypes ; Humans ; Innervation ; Male ; Mammals ; Mice ; Microscopy, Electron ; Mutation ; Mutation - genetics ; Nematodes ; Nerve Tissue Proteins - deficiency ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Neurons ; Papillae ; Phenotype ; Phenotypes ; Proteins ; Sensory disorders ; Sensory neurons ; Temperature</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2007-10, Vol.104 (44), p.17524-17529</ispartof><rights>Copyright 2007 The National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Oct 30, 2007</rights><rights>2007 by The National Academy of Sciences of the USA 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c620t-322a95ee433480650836ece01fcb3d6371b8e771ac9743f3c433c67d48fe3eac3</citedby><cites>FETCH-LOGICAL-c620t-322a95ee433480650836ece01fcb3d6371b8e771ac9743f3c433c67d48fe3eac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/104/44.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/25450268$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/25450268$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,315,729,782,786,805,887,27931,27932,53798,53800,58024,58257</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17959775$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tan, Perciliz L</creatorcontrib><creatorcontrib>Barr, Travis</creatorcontrib><creatorcontrib>Inglis, Peter N</creatorcontrib><creatorcontrib>Mitsuma, Norimasa</creatorcontrib><creatorcontrib>Huang, Susan M</creatorcontrib><creatorcontrib>Garcia-Gonzalez, Miguel A</creatorcontrib><creatorcontrib>Bradley, Brian A</creatorcontrib><creatorcontrib>Coforio, Stephanie</creatorcontrib><creatorcontrib>Albrecht, Phillip J</creatorcontrib><creatorcontrib>Watnick, Terry</creatorcontrib><creatorcontrib>Germino, Gregory G</creatorcontrib><creatorcontrib>Beales, Philip L</creatorcontrib><creatorcontrib>Caterina, Michael J</creatorcontrib><creatorcontrib>Leroux, Michel R</creatorcontrib><creatorcontrib>Rice, Frank L</creatorcontrib><creatorcontrib>Katsanis, Nicholas</creatorcontrib><title>Loss of Bardet-Biedl syndrome proteins causes defects in peripheral sensory innervation and function</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Reception and interpretation of environmental stimuli is critical for the survival of all organisms. Here, we show that the ablation of BBS1 and BBS4, two genes mutated in Bardet-Biedl syndrome and that encode proteins that localize near the centrioles of sensory neurons, leads to alterations of s.c. sensory innervation and trafficking of the thermosensory channel TRPV1 and the mechanosensory channel STOML3, with concomitant defects in peripheral thermosensation and mechanosensation. The thermosensory phenotype is recapitulated in Caenorhabditis elegans, because BBS mutants manifest deficient thermosensory responses at both physiological and nociceptive temperatures and defective trafficking of OSM-9, a polymodal sensory channel protein and a functional homolog of TRPV1 or TRPV4. Our findings suggest a hitherto unrecognized, but essential, role for mammalian basal body proteins in the acquisition of mechano- and thermosensory stimuli and highlight potentially clinical features of ciliopathies in humans.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Antibodies</subject><subject>Bardet-Biedl Syndrome - metabolism</subject><subject>Bardet-Biedl Syndrome - pathology</subject><subject>Biological Sciences</subject><subject>Caenorhabditis elegans</subject><subject>Caenorhabditis elegans - genetics</subject><subject>Caenorhabditis elegans - metabolism</subject><subject>Central Nervous System - metabolism</subject><subject>Cilia</subject><subject>Female</subject><subject>Gene Expression Regulation</subject><subject>Genes</subject><subject>Genotype & phenotype</subject><subject>Genotypes</subject><subject>Humans</subject><subject>Innervation</subject><subject>Male</subject><subject>Mammals</subject><subject>Mice</subject><subject>Microscopy, Electron</subject><subject>Mutation</subject><subject>Mutation - genetics</subject><subject>Nematodes</subject><subject>Nerve Tissue Proteins - deficiency</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Neurons</subject><subject>Papillae</subject><subject>Phenotype</subject><subject>Phenotypes</subject><subject>Proteins</subject><subject>Sensory disorders</subject><subject>Sensory neurons</subject><subject>Temperature</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0Utv1DAUBeAIgWgprFkBFgskFmmv384GiVa8pJFYQNeWx7lpM8rYwU4q5t_jaEYdYNNV5NzPR7ZPVb2kcE5B84sxuHwOGpSihoJ4VJ1SaGitRAOPq1MApmsjmDipnuW8AYBGGnhanVDdyEZreVq1q5gziR25dKnFqb7ssR1I3oU2xS2SMcUJ-5CJd3PGTFrs0E-Z9IGMmPrxFpMrHEOOaVf-Bkx3bupjIC60pJuDXxbPqyedGzK-OHzPquvPn35efa1X3798u_q4qr1iMNWcMddIRMG5MKAkGK7QI9DOr3mruKZrg1pT5xsteMd9gV7pVpgOOTrPz6oP-9xxXm-x9Rimcjw7pn7r0s5G19t_J6G_tTfxzjLQmpmmBLw7BKT4a8Y82W2fPQ6DCxjnbJURWnHDHoQMhJRAVYFv_4ObOKdQXqEYypYSaEEXe-RTaSNhd39kCnbp2S4922PPZcfrv2969IdiCyAHsOw8xgkrRFGSLRnvHyC2m4dhwt9Tsa_2dpOnmO4xk0ICU6bM3-znnYvW3aQ-2-sf5YIcoLwWyIb_ASIY0NI</recordid><startdate>20071030</startdate><enddate>20071030</enddate><creator>Tan, Perciliz L</creator><creator>Barr, Travis</creator><creator>Inglis, Peter N</creator><creator>Mitsuma, Norimasa</creator><creator>Huang, Susan M</creator><creator>Garcia-Gonzalez, Miguel A</creator><creator>Bradley, Brian A</creator><creator>Coforio, Stephanie</creator><creator>Albrecht, Phillip J</creator><creator>Watnick, Terry</creator><creator>Germino, Gregory G</creator><creator>Beales, Philip L</creator><creator>Caterina, Michael J</creator><creator>Leroux, Michel R</creator><creator>Rice, Frank L</creator><creator>Katsanis, Nicholas</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>FBQ</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>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></search><sort><creationdate>20071030</creationdate><title>Loss of Bardet-Biedl syndrome proteins causes defects in peripheral sensory innervation and function</title><author>Tan, Perciliz L ; Barr, Travis ; Inglis, Peter N ; Mitsuma, Norimasa ; Huang, Susan M ; Garcia-Gonzalez, Miguel A ; Bradley, Brian A ; Coforio, Stephanie ; Albrecht, Phillip J ; Watnick, Terry ; Germino, Gregory G ; Beales, Philip L ; Caterina, Michael J ; Leroux, Michel R ; Rice, Frank L ; Katsanis, Nicholas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c620t-322a95ee433480650836ece01fcb3d6371b8e771ac9743f3c433c67d48fe3eac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>Antibodies</topic><topic>Bardet-Biedl Syndrome - 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Here, we show that the ablation of BBS1 and BBS4, two genes mutated in Bardet-Biedl syndrome and that encode proteins that localize near the centrioles of sensory neurons, leads to alterations of s.c. sensory innervation and trafficking of the thermosensory channel TRPV1 and the mechanosensory channel STOML3, with concomitant defects in peripheral thermosensation and mechanosensation. The thermosensory phenotype is recapitulated in Caenorhabditis elegans, because BBS mutants manifest deficient thermosensory responses at both physiological and nociceptive temperatures and defective trafficking of OSM-9, a polymodal sensory channel protein and a functional homolog of TRPV1 or TRPV4. Our findings suggest a hitherto unrecognized, but essential, role for mammalian basal body proteins in the acquisition of mechano- and thermosensory stimuli and highlight potentially clinical features of ciliopathies in humans.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>17959775</pmid><doi>10.1073/pnas.0706618104</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Adult Animals Animals, Genetically Modified Antibodies Bardet-Biedl Syndrome - metabolism Bardet-Biedl Syndrome - pathology Biological Sciences Caenorhabditis elegans Caenorhabditis elegans - genetics Caenorhabditis elegans - metabolism Central Nervous System - metabolism Cilia Female Gene Expression Regulation Genes Genotype & phenotype Genotypes Humans Innervation Male Mammals Mice Microscopy, Electron Mutation Mutation - genetics Nematodes Nerve Tissue Proteins - deficiency Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Neurons Papillae Phenotype Phenotypes Proteins Sensory disorders Sensory neurons Temperature |
| title | Loss of Bardet-Biedl syndrome proteins causes defects in peripheral sensory innervation and function |
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