Peroxisomes Are Signaling Platforms for Antiviral Innate Immunity
Peroxisomes have long been established to play a central role in regulating various metabolic activities in mammalian cells. These organelles act in concert with mitochondria to control the metabolism of lipids and reactive oxygen species. However, while mitochondria have emerged as an important sit...
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| Veröffentlicht in: | Cell 2010-05, Vol.141 (4), p.668-681 |
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| creator | Dixit, Evelyn Boulant, Steeve Zhang, Yijing Lee, Amy S.Y. Odendall, Charlotte Shum, Bennett Hacohen, Nir Chen, Zhijian J. Whelan, Sean P. Fransen, Marc Nibert, Max L. Superti-Furga, Giulio Kagan, Jonathan C. |
| description | Peroxisomes have long been established to play a central role in regulating various metabolic activities in mammalian cells. These organelles act in concert with mitochondria to control the metabolism of lipids and reactive oxygen species. However, while mitochondria have emerged as an important site of antiviral signal transduction, a role for peroxisomes in immune defense is unknown. Here, we report that the RIG-I-like receptor (RLR) adaptor protein MAVS is located on peroxisomes and mitochondria. We find that peroxisomal and mitochondrial MAVS act sequentially to create an antiviral cellular state. Upon viral infection, peroxisomal MAVS induces the rapid interferon-independent expression of defense factors that provide short-term protection, whereas mitochondrial MAVS activates an interferon-dependent signaling pathway with delayed kinetics, which amplifies and stabilizes the antiviral response. The interferon regulatory factor IRF1 plays a crucial role in regulating MAVS-dependent signaling from peroxisomes. These results establish that peroxisomes are an important site of antiviral signal transduction.
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► The antiviral signaling protein MAVS is located on both peroxisomes and mitochondria ► RNA viruses activate MAVS-dependent signaling from peroxisomes ► Peroxisomal signaling induces antiviral gene expression but not interferon production ► MAVS signaling from peroxisomes is sufficient to restrict viral replication |
| doi_str_mv | 10.1016/j.cell.2010.04.018 |
| format | Article |
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► The antiviral signaling protein MAVS is located on both peroxisomes and mitochondria ► RNA viruses activate MAVS-dependent signaling from peroxisomes ► Peroxisomal signaling induces antiviral gene expression but not interferon production ► MAVS signaling from peroxisomes is sufficient to restrict viral replication</description><identifier>ISSN: 0092-8674</identifier><identifier>EISSN: 1097-4172</identifier><identifier>DOI: 10.1016/j.cell.2010.04.018</identifier><identifier>PMID: 20451243</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adaptor Proteins, Signal Transducing - immunology ; Adaptor Proteins, Signal Transducing - metabolism ; Animals ; Cell Line ; CELLIMMUNO ; Cercopithecus aethiops ; Fibroblasts - metabolism ; Hepatocytes - metabolism ; Humans ; Immunity, Innate ; Interferons - metabolism ; Mice ; Mitochondria - metabolism ; Peroxisomes - metabolism ; Signal Transduction ; SIGNALING ; Vero Cells</subject><ispartof>Cell, 2010-05, Vol.141 (4), p.668-681</ispartof><rights>2010 Elsevier Inc.</rights><rights>Copyright (c) 2010 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c535t-3f35a5b46f78bfebfe259b15d556c06da42c550517a9ac00d4d2fb3fc250f1ce3</citedby><cites>FETCH-LOGICAL-c535t-3f35a5b46f78bfebfe259b15d556c06da42c550517a9ac00d4d2fb3fc250f1ce3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.cell.2010.04.018$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,315,782,786,887,3554,27933,27934,46004</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20451243$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dixit, Evelyn</creatorcontrib><creatorcontrib>Boulant, Steeve</creatorcontrib><creatorcontrib>Zhang, Yijing</creatorcontrib><creatorcontrib>Lee, Amy S.Y.</creatorcontrib><creatorcontrib>Odendall, Charlotte</creatorcontrib><creatorcontrib>Shum, Bennett</creatorcontrib><creatorcontrib>Hacohen, Nir</creatorcontrib><creatorcontrib>Chen, Zhijian J.</creatorcontrib><creatorcontrib>Whelan, Sean P.</creatorcontrib><creatorcontrib>Fransen, Marc</creatorcontrib><creatorcontrib>Nibert, Max L.</creatorcontrib><creatorcontrib>Superti-Furga, Giulio</creatorcontrib><creatorcontrib>Kagan, Jonathan C.</creatorcontrib><title>Peroxisomes Are Signaling Platforms for Antiviral Innate Immunity</title><title>Cell</title><addtitle>Cell</addtitle><description>Peroxisomes have long been established to play a central role in regulating various metabolic activities in mammalian cells. These organelles act in concert with mitochondria to control the metabolism of lipids and reactive oxygen species. However, while mitochondria have emerged as an important site of antiviral signal transduction, a role for peroxisomes in immune defense is unknown. Here, we report that the RIG-I-like receptor (RLR) adaptor protein MAVS is located on peroxisomes and mitochondria. We find that peroxisomal and mitochondrial MAVS act sequentially to create an antiviral cellular state. Upon viral infection, peroxisomal MAVS induces the rapid interferon-independent expression of defense factors that provide short-term protection, whereas mitochondrial MAVS activates an interferon-dependent signaling pathway with delayed kinetics, which amplifies and stabilizes the antiviral response. The interferon regulatory factor IRF1 plays a crucial role in regulating MAVS-dependent signaling from peroxisomes. These results establish that peroxisomes are an important site of antiviral signal transduction.
[Display omitted]
► The antiviral signaling protein MAVS is located on both peroxisomes and mitochondria ► RNA viruses activate MAVS-dependent signaling from peroxisomes ► Peroxisomal signaling induces antiviral gene expression but not interferon production ► MAVS signaling from peroxisomes is sufficient to restrict viral replication</description><subject>Adaptor Proteins, Signal Transducing - immunology</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Animals</subject><subject>Cell Line</subject><subject>CELLIMMUNO</subject><subject>Cercopithecus aethiops</subject><subject>Fibroblasts - metabolism</subject><subject>Hepatocytes - metabolism</subject><subject>Humans</subject><subject>Immunity, Innate</subject><subject>Interferons - metabolism</subject><subject>Mice</subject><subject>Mitochondria - metabolism</subject><subject>Peroxisomes - metabolism</subject><subject>Signal Transduction</subject><subject>SIGNALING</subject><subject>Vero Cells</subject><issn>0092-8674</issn><issn>1097-4172</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUU2LFDEUDKK44-of8CB989Tjy8dLd4MIw-LHwIIL6jmk06_HDN3JmvQM7r83w6yLXhTCC-RVFZUqxl5yWHPg-s1-7Wia1gLKA6g18PYRW3HomlrxRjxmK4BO1K1u1AV7lvMeAFpEfMouBCjkQskV29xQij99jjPlapOo-uJ3wU4-7KqbyS5jTHOuyqw2YfFHn-xUbUOwC1XbeT4Ev9w9Z09GO2V6cX9fsm8f3n-9-lRff_64vdpc1w4lLrUcJVrslR6bth-pHIFdz3FA1A70YJVwiIC8sZ11AIMaxNjL0QmEkTuSl-zdWff20M80OApLcWNuk59tujPRevP3JvjvZhePRuqmRINF4PW9QIo_DpQXM_t8StAGiodsWt1hyzul_4tspJRcS9UWpDgjXYo5Jxof_HAwp5LM3pyI5lSSAWWKk0J69edPHii_WymAt2cAlTyPnpLJzlNwNPhEbjFD9P_S_wV-DaRh</recordid><startdate>20100514</startdate><enddate>20100514</enddate><creator>Dixit, Evelyn</creator><creator>Boulant, Steeve</creator><creator>Zhang, Yijing</creator><creator>Lee, Amy S.Y.</creator><creator>Odendall, Charlotte</creator><creator>Shum, Bennett</creator><creator>Hacohen, Nir</creator><creator>Chen, Zhijian J.</creator><creator>Whelan, Sean P.</creator><creator>Fransen, Marc</creator><creator>Nibert, Max L.</creator><creator>Superti-Furga, Giulio</creator><creator>Kagan, Jonathan C.</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>7X8</scope><scope>7T5</scope><scope>7T7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>5PM</scope></search><sort><creationdate>20100514</creationdate><title>Peroxisomes Are Signaling Platforms for Antiviral Innate Immunity</title><author>Dixit, Evelyn ; Boulant, Steeve ; Zhang, Yijing ; Lee, Amy S.Y. ; Odendall, Charlotte ; Shum, Bennett ; Hacohen, Nir ; Chen, Zhijian J. ; Whelan, Sean P. ; Fransen, Marc ; Nibert, Max L. ; Superti-Furga, Giulio ; Kagan, Jonathan C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c535t-3f35a5b46f78bfebfe259b15d556c06da42c550517a9ac00d4d2fb3fc250f1ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adaptor Proteins, Signal Transducing - immunology</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Animals</topic><topic>Cell Line</topic><topic>CELLIMMUNO</topic><topic>Cercopithecus aethiops</topic><topic>Fibroblasts - metabolism</topic><topic>Hepatocytes - metabolism</topic><topic>Humans</topic><topic>Immunity, Innate</topic><topic>Interferons - metabolism</topic><topic>Mice</topic><topic>Mitochondria - metabolism</topic><topic>Peroxisomes - metabolism</topic><topic>Signal Transduction</topic><topic>SIGNALING</topic><topic>Vero Cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dixit, Evelyn</creatorcontrib><creatorcontrib>Boulant, Steeve</creatorcontrib><creatorcontrib>Zhang, Yijing</creatorcontrib><creatorcontrib>Lee, Amy S.Y.</creatorcontrib><creatorcontrib>Odendall, Charlotte</creatorcontrib><creatorcontrib>Shum, Bennett</creatorcontrib><creatorcontrib>Hacohen, Nir</creatorcontrib><creatorcontrib>Chen, Zhijian J.</creatorcontrib><creatorcontrib>Whelan, Sean P.</creatorcontrib><creatorcontrib>Fransen, Marc</creatorcontrib><creatorcontrib>Nibert, Max L.</creatorcontrib><creatorcontrib>Superti-Furga, Giulio</creatorcontrib><creatorcontrib>Kagan, Jonathan C.</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>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</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>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dixit, Evelyn</au><au>Boulant, Steeve</au><au>Zhang, Yijing</au><au>Lee, Amy S.Y.</au><au>Odendall, Charlotte</au><au>Shum, Bennett</au><au>Hacohen, Nir</au><au>Chen, Zhijian J.</au><au>Whelan, Sean P.</au><au>Fransen, Marc</au><au>Nibert, Max L.</au><au>Superti-Furga, Giulio</au><au>Kagan, Jonathan C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peroxisomes Are Signaling Platforms for Antiviral Innate Immunity</atitle><jtitle>Cell</jtitle><addtitle>Cell</addtitle><date>2010-05-14</date><risdate>2010</risdate><volume>141</volume><issue>4</issue><spage>668</spage><epage>681</epage><pages>668-681</pages><issn>0092-8674</issn><eissn>1097-4172</eissn><abstract>Peroxisomes have long been established to play a central role in regulating various metabolic activities in mammalian cells. These organelles act in concert with mitochondria to control the metabolism of lipids and reactive oxygen species. However, while mitochondria have emerged as an important site of antiviral signal transduction, a role for peroxisomes in immune defense is unknown. Here, we report that the RIG-I-like receptor (RLR) adaptor protein MAVS is located on peroxisomes and mitochondria. We find that peroxisomal and mitochondrial MAVS act sequentially to create an antiviral cellular state. Upon viral infection, peroxisomal MAVS induces the rapid interferon-independent expression of defense factors that provide short-term protection, whereas mitochondrial MAVS activates an interferon-dependent signaling pathway with delayed kinetics, which amplifies and stabilizes the antiviral response. The interferon regulatory factor IRF1 plays a crucial role in regulating MAVS-dependent signaling from peroxisomes. These results establish that peroxisomes are an important site of antiviral signal transduction.
[Display omitted]
► The antiviral signaling protein MAVS is located on both peroxisomes and mitochondria ► RNA viruses activate MAVS-dependent signaling from peroxisomes ► Peroxisomal signaling induces antiviral gene expression but not interferon production ► MAVS signaling from peroxisomes is sufficient to restrict viral replication</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>20451243</pmid><doi>10.1016/j.cell.2010.04.018</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - immunology Adaptor Proteins, Signal Transducing - metabolism Animals Cell Line CELLIMMUNO Cercopithecus aethiops Fibroblasts - metabolism Hepatocytes - metabolism Humans Immunity, Innate Interferons - metabolism Mice Mitochondria - metabolism Peroxisomes - metabolism Signal Transduction SIGNALING Vero Cells |
| title | Peroxisomes Are Signaling Platforms for Antiviral Innate Immunity |
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