Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF‐1 signaling pathways in C. elegans
Summary Target of rapamycin (TOR) signaling is an evolutionarily well‐conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of ye...
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| Veröffentlicht in: | Aging cell 2013-12, Vol.12 (6), p.1073-1081 |
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| creator | Seo, Keunhee Choi, Eunseok Lee, Dongyeop Jeong, Dae‐Eun Jang, Sung Key Lee, Seung‐Jae |
| description | Summary
Target of rapamycin (TOR) signaling is an evolutionarily well‐conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF‐1), a crucial longevity transcription factor known to act downstream of the insulin/IGF‐1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks‐1). We found that hsf‐1 is required for the longevity caused by down‐regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat‐shock protein hsp‐16, a transcriptional target of HSF‐1, mediates the long lifespan of rsks‐1 mutants. Moreover, we show that synergistic activation of HSF‐1 is required for the further enhanced longevity caused by simultaneous down‐regulation of TOR and IIS pathways. Our findings suggest that HSF‐1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways. |
| doi_str_mv | 10.1111/acel.12140 |
| format | Article |
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Target of rapamycin (TOR) signaling is an evolutionarily well‐conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF‐1), a crucial longevity transcription factor known to act downstream of the insulin/IGF‐1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks‐1). We found that hsf‐1 is required for the longevity caused by down‐regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat‐shock protein hsp‐16, a transcriptional target of HSF‐1, mediates the long lifespan of rsks‐1 mutants. Moreover, we show that synergistic activation of HSF‐1 is required for the further enhanced longevity caused by simultaneous down‐regulation of TOR and IIS pathways. Our findings suggest that HSF‐1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways.</description><identifier>ISSN: 1474-9718</identifier><identifier>EISSN: 1474-9726</identifier><identifier>DOI: 10.1111/acel.12140</identifier><identifier>PMID: 23879233</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>aging ; Animals ; Caenorhabditis elegans ; Caenorhabditis elegans - physiology ; Caenorhabditis elegans Proteins - antagonists & inhibitors ; Caenorhabditis elegans Proteins - metabolism ; Down-Regulation ; HSF‐1 ; Insulin - metabolism ; Insulin-Like Growth Factor I - metabolism ; insulin/IGF‐1 signaling ; Longevity ; Mice ; mRNA translation ; Mutation - genetics ; Oxidative Stress ; Peptides - metabolism ; Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors ; Phosphotransferases (Alcohol Group Acceptor) - metabolism ; Protein Structure, Quaternary ; Ribosomal Protein S6 Kinases, 70-kDa - antagonists & inhibitors ; Ribosomal Protein S6 Kinases, 70-kDa - metabolism ; S6 kinase ; Signal Transduction ; target of rapamycin ; Transcription Factors - metabolism</subject><ispartof>Aging cell, 2013-12, Vol.12 (6), p.1073-1081</ispartof><rights>2013 the Anatomical Society and John Wiley & Sons Ltd</rights><rights>2013 the Anatomical Society and John Wiley & Sons Ltd.</rights><rights>2013 The Anatomical Society and John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3930-d451ff1c1557ac2d337e4d219125b80df216fb12a9deac6fff4940ee91ea1a113</citedby><cites>FETCH-LOGICAL-c3930-d451ff1c1557ac2d337e4d219125b80df216fb12a9deac6fff4940ee91ea1a113</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Facel.12140$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Facel.12140$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,11553,27915,27916,45565,45566,46043,46467</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Facel.12140$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23879233$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Seo, Keunhee</creatorcontrib><creatorcontrib>Choi, Eunseok</creatorcontrib><creatorcontrib>Lee, Dongyeop</creatorcontrib><creatorcontrib>Jeong, Dae‐Eun</creatorcontrib><creatorcontrib>Jang, Sung Key</creatorcontrib><creatorcontrib>Lee, Seung‐Jae</creatorcontrib><title>Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF‐1 signaling pathways in C. elegans</title><title>Aging cell</title><addtitle>Aging Cell</addtitle><description>Summary
Target of rapamycin (TOR) signaling is an evolutionarily well‐conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF‐1), a crucial longevity transcription factor known to act downstream of the insulin/IGF‐1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks‐1). We found that hsf‐1 is required for the longevity caused by down‐regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat‐shock protein hsp‐16, a transcriptional target of HSF‐1, mediates the long lifespan of rsks‐1 mutants. Moreover, we show that synergistic activation of HSF‐1 is required for the further enhanced longevity caused by simultaneous down‐regulation of TOR and IIS pathways. Our findings suggest that HSF‐1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways.</description><subject>aging</subject><subject>Animals</subject><subject>Caenorhabditis elegans</subject><subject>Caenorhabditis elegans - physiology</subject><subject>Caenorhabditis elegans Proteins - antagonists & inhibitors</subject><subject>Caenorhabditis elegans Proteins - metabolism</subject><subject>Down-Regulation</subject><subject>HSF‐1</subject><subject>Insulin - metabolism</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>insulin/IGF‐1 signaling</subject><subject>Longevity</subject><subject>Mice</subject><subject>mRNA translation</subject><subject>Mutation - genetics</subject><subject>Oxidative Stress</subject><subject>Peptides - metabolism</subject><subject>Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors</subject><subject>Phosphotransferases (Alcohol Group Acceptor) - metabolism</subject><subject>Protein Structure, Quaternary</subject><subject>Ribosomal Protein S6 Kinases, 70-kDa - antagonists & inhibitors</subject><subject>Ribosomal Protein S6 Kinases, 70-kDa - metabolism</subject><subject>S6 kinase</subject><subject>Signal Transduction</subject><subject>target of rapamycin</subject><subject>Transcription Factors - metabolism</subject><issn>1474-9718</issn><issn>1474-9726</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90ctqGzEUBmBRGppLu-kDFEE3JWBHR9LMWMtgcgNDIKTrQaM5spWOJUeaaZhN6SPkGfMkleskiyyijcTh40fST8hXYFPI60Qb7KbAQbIP5ABkJSeq4uXH1zPM9slhSneMQaWY-ET2uZhVigtxQP5cou5pWgXzi1pt-hAp0DW2TveYaL9C2gW_xN-uH6kJ3mKM2NJmpM6vXON6FzwNlt5e31Dt2zxNQ-f8ydXF-dPfR6DJLb3OgyXd6H71oMeUCZ1PKXa41D59JntWdwm_PO9H5Of52e38crK4vriany4mRijBJq0swFowUBSVNrwVokLZclDAi2bGWsuhtA1wrVrUprTWSiUZogLUoAHEEfmxy93EcD9g6uu1S_nbOu0xDKkGWYIQMyhZpt_f0LswxPyKrSqUkvlCW3W8UyaGlCLaehPdWsexBlZvW6m3rdT_W8n423Pk0OS_faUvNWQAO_DgOhzfiapP52eLXeg_bkWXkA</recordid><startdate>201312</startdate><enddate>201312</enddate><creator>Seo, Keunhee</creator><creator>Choi, Eunseok</creator><creator>Lee, Dongyeop</creator><creator>Jeong, Dae‐Eun</creator><creator>Jang, Sung Key</creator><creator>Lee, Seung‐Jae</creator><general>John Wiley & Sons, Inc</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>7QP</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>201312</creationdate><title>Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF‐1 signaling pathways in C. elegans</title><author>Seo, Keunhee ; Choi, Eunseok ; Lee, Dongyeop ; Jeong, Dae‐Eun ; Jang, Sung Key ; Lee, Seung‐Jae</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3930-d451ff1c1557ac2d337e4d219125b80df216fb12a9deac6fff4940ee91ea1a113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>aging</topic><topic>Animals</topic><topic>Caenorhabditis elegans</topic><topic>Caenorhabditis elegans - physiology</topic><topic>Caenorhabditis elegans Proteins - antagonists & inhibitors</topic><topic>Caenorhabditis elegans Proteins - metabolism</topic><topic>Down-Regulation</topic><topic>HSF‐1</topic><topic>Insulin - metabolism</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>insulin/IGF‐1 signaling</topic><topic>Longevity</topic><topic>Mice</topic><topic>mRNA translation</topic><topic>Mutation - genetics</topic><topic>Oxidative Stress</topic><topic>Peptides - metabolism</topic><topic>Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors</topic><topic>Phosphotransferases (Alcohol Group Acceptor) - metabolism</topic><topic>Protein Structure, Quaternary</topic><topic>Ribosomal Protein S6 Kinases, 70-kDa - antagonists & inhibitors</topic><topic>Ribosomal Protein S6 Kinases, 70-kDa - metabolism</topic><topic>S6 kinase</topic><topic>Signal Transduction</topic><topic>target of rapamycin</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Seo, Keunhee</creatorcontrib><creatorcontrib>Choi, Eunseok</creatorcontrib><creatorcontrib>Lee, Dongyeop</creatorcontrib><creatorcontrib>Jeong, Dae‐Eun</creatorcontrib><creatorcontrib>Jang, Sung Key</creatorcontrib><creatorcontrib>Lee, Seung‐Jae</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Aging cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Seo, Keunhee</au><au>Choi, Eunseok</au><au>Lee, Dongyeop</au><au>Jeong, Dae‐Eun</au><au>Jang, Sung Key</au><au>Lee, Seung‐Jae</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF‐1 signaling pathways in C. elegans</atitle><jtitle>Aging cell</jtitle><addtitle>Aging Cell</addtitle><date>2013-12</date><risdate>2013</risdate><volume>12</volume><issue>6</issue><spage>1073</spage><epage>1081</epage><pages>1073-1081</pages><issn>1474-9718</issn><eissn>1474-9726</eissn><abstract>Summary
Target of rapamycin (TOR) signaling is an evolutionarily well‐conserved pathway that regulates various physiologic processes, including aging and metabolism. One of the key downstream components of TOR signaling is ribosomal protein S6 kinase (S6K) whose inhibition extends the lifespan of yeast, Caenorhabditis elegans, Drosophila, and mice. Here, we demonstrate that the activation of heat shock factor 1 (HSF‐1), a crucial longevity transcription factor known to act downstream of the insulin/IGF‐1 signaling (IIS) pathway, mediates the prolonged lifespan conferred by mutations in C. elegans S6K (rsks‐1). We found that hsf‐1 is required for the longevity caused by down‐regulation of components in TOR signaling pathways, including TOR and S6K. The induction of a small heat‐shock protein hsp‐16, a transcriptional target of HSF‐1, mediates the long lifespan of rsks‐1 mutants. Moreover, we show that synergistic activation of HSF‐1 is required for the further enhanced longevity caused by simultaneous down‐regulation of TOR and IIS pathways. Our findings suggest that HSF‐1 acts as an essential longevity factor that intersects both IIS and TOR signaling pathways.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>23879233</pmid><doi>10.1111/acel.12140</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | aging Animals Caenorhabditis elegans Caenorhabditis elegans - physiology Caenorhabditis elegans Proteins - antagonists & inhibitors Caenorhabditis elegans Proteins - metabolism Down-Regulation HSF‐1 Insulin - metabolism Insulin-Like Growth Factor I - metabolism insulin/IGF‐1 signaling Longevity Mice mRNA translation Mutation - genetics Oxidative Stress Peptides - metabolism Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors Phosphotransferases (Alcohol Group Acceptor) - metabolism Protein Structure, Quaternary Ribosomal Protein S6 Kinases, 70-kDa - antagonists & inhibitors Ribosomal Protein S6 Kinases, 70-kDa - metabolism S6 kinase Signal Transduction target of rapamycin Transcription Factors - metabolism |
| title | Heat shock factor 1 mediates the longevity conferred by inhibition of TOR and insulin/IGF‐1 signaling pathways in C. elegans |
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