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Genome-wide Expression Analysis of Mouse Liver Reveals CLOCK-regulated Circadian Output Genes
CLOCK is a positive component of a transcription/translation-based negative feedback loop of the central circadian oscillator in the suprachiasmatic nucleus in mammals. To examine CLOCK-regulated circadian transcription in peripheral tissues, we performed microarray analyses using liver RNA isolated...
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Published in: | The Journal of biological chemistry 2003-10, Vol.278 (42), p.41519-41527 |
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creator | Oishi, Katsutaka Miyazaki, Koyomi Kadota, Koji Kikuno, Reiko Nagase, Takahiro Atsumi, Gen-ichi Ohkura, Naoki Azama, Takashi Mesaki, Miho Yukimasa, Shima Kobayashi, Hisato Iitaka, Chisato Umehara, Takashi Horikoshi, Masami Kudo, Takashi Shimizu, Yoshihisa Yano, Masahiko Monden, Morito Machida, Kazuhiko Matsuda, Juzo Horie, Shuichi Todo, Takeshi Ishida, Norio |
description | CLOCK is a positive component of a transcription/translation-based negative feedback loop of the central circadian oscillator in the suprachiasmatic nucleus in mammals. To examine CLOCK-regulated circadian transcription in peripheral tissues, we performed microarray analyses using liver RNA isolated from Clock mutant mice. We also compared expression profiles with those of Cryptochromes (Cry1 and Cry2) double knockout mice. We identified more than 100 genes that fluctuated from day to night and of which expression levels were decreased in Clock mutant mice. In Cry-deficient mice, the expression levels of most CLOCK-regulated genes were elevated to the upper range of normal oscillation. Most of the screened genes had a CLOCK/BMAL1 binding site (E box) in the 5′-flanking region. We found that CLOCK was absolutely concerned with the circadian transcription of one type of liver genes (such as DBP, TEF, and Usp2) and partially with another (such as mPer1, mPer2, mDec1, Nocturnin, P450 oxidoreductase, and FKBP51) because the latter were damped but remained rhythmic in the mutant mice. Our results showed that CLOCK and CRY proteins are involved in the transcriptional regulation of many circadian output genes in the mouse liver. In addition to being a core component of the negative feedback loop that drives the circadian oscillator, CLOCK also appears to be involved in various physiological functions such as cell cycle, lipid metabolism, immune functions, and proteolysis in peripheral tissues. |
doi_str_mv | 10.1074/jbc.M304564200 |
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To examine CLOCK-regulated circadian transcription in peripheral tissues, we performed microarray analyses using liver RNA isolated from Clock mutant mice. We also compared expression profiles with those of Cryptochromes (Cry1 and Cry2) double knockout mice. We identified more than 100 genes that fluctuated from day to night and of which expression levels were decreased in Clock mutant mice. In Cry-deficient mice, the expression levels of most CLOCK-regulated genes were elevated to the upper range of normal oscillation. Most of the screened genes had a CLOCK/BMAL1 binding site (E box) in the 5′-flanking region. We found that CLOCK was absolutely concerned with the circadian transcription of one type of liver genes (such as DBP, TEF, and Usp2) and partially with another (such as mPer1, mPer2, mDec1, Nocturnin, P450 oxidoreductase, and FKBP51) because the latter were damped but remained rhythmic in the mutant mice. Our results showed that CLOCK and CRY proteins are involved in the transcriptional regulation of many circadian output genes in the mouse liver. In addition to being a core component of the negative feedback loop that drives the circadian oscillator, CLOCK also appears to be involved in various physiological functions such as cell cycle, lipid metabolism, immune functions, and proteolysis in peripheral tissues.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M304564200</identifier><identifier>PMID: 12865428</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Amino Acid Motifs ; Animals ; Base Sequence ; Binding Sites ; Blotting, Northern ; Circadian Rhythm ; CLOCK Proteins ; Fatty Acids - metabolism ; Genome ; Humans ; In Situ Hybridization ; Lipid Metabolism ; Liver - metabolism ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; Oligonucleotide Array Sequence Analysis ; Reverse Transcriptase Polymerase Chain Reaction ; RNA - metabolism ; RNA, Messenger - metabolism ; Sequence Homology, Nucleic Acid ; Time Factors ; Trans-Activators - genetics ; Trans-Activators - metabolism ; Transcription, Genetic</subject><ispartof>The Journal of biological chemistry, 2003-10, Vol.278 (42), p.41519-41527</ispartof><rights>2003 © 2003 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c553t-7a7217fabb74af3aeea86d2935df716f9756f76d8dfddb4da08f8ec55932131d3</citedby><cites>FETCH-LOGICAL-c553t-7a7217fabb74af3aeea86d2935df716f9756f76d8dfddb4da08f8ec55932131d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S002192582082955X$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3549,27924,27925,45780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12865428$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Oishi, Katsutaka</creatorcontrib><creatorcontrib>Miyazaki, Koyomi</creatorcontrib><creatorcontrib>Kadota, Koji</creatorcontrib><creatorcontrib>Kikuno, Reiko</creatorcontrib><creatorcontrib>Nagase, Takahiro</creatorcontrib><creatorcontrib>Atsumi, Gen-ichi</creatorcontrib><creatorcontrib>Ohkura, Naoki</creatorcontrib><creatorcontrib>Azama, Takashi</creatorcontrib><creatorcontrib>Mesaki, Miho</creatorcontrib><creatorcontrib>Yukimasa, Shima</creatorcontrib><creatorcontrib>Kobayashi, Hisato</creatorcontrib><creatorcontrib>Iitaka, Chisato</creatorcontrib><creatorcontrib>Umehara, Takashi</creatorcontrib><creatorcontrib>Horikoshi, Masami</creatorcontrib><creatorcontrib>Kudo, Takashi</creatorcontrib><creatorcontrib>Shimizu, Yoshihisa</creatorcontrib><creatorcontrib>Yano, Masahiko</creatorcontrib><creatorcontrib>Monden, Morito</creatorcontrib><creatorcontrib>Machida, Kazuhiko</creatorcontrib><creatorcontrib>Matsuda, Juzo</creatorcontrib><creatorcontrib>Horie, Shuichi</creatorcontrib><creatorcontrib>Todo, Takeshi</creatorcontrib><creatorcontrib>Ishida, Norio</creatorcontrib><title>Genome-wide Expression Analysis of Mouse Liver Reveals CLOCK-regulated Circadian Output Genes</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>CLOCK is a positive component of a transcription/translation-based negative feedback loop of the central circadian oscillator in the suprachiasmatic nucleus in mammals. To examine CLOCK-regulated circadian transcription in peripheral tissues, we performed microarray analyses using liver RNA isolated from Clock mutant mice. We also compared expression profiles with those of Cryptochromes (Cry1 and Cry2) double knockout mice. We identified more than 100 genes that fluctuated from day to night and of which expression levels were decreased in Clock mutant mice. In Cry-deficient mice, the expression levels of most CLOCK-regulated genes were elevated to the upper range of normal oscillation. Most of the screened genes had a CLOCK/BMAL1 binding site (E box) in the 5′-flanking region. We found that CLOCK was absolutely concerned with the circadian transcription of one type of liver genes (such as DBP, TEF, and Usp2) and partially with another (such as mPer1, mPer2, mDec1, Nocturnin, P450 oxidoreductase, and FKBP51) because the latter were damped but remained rhythmic in the mutant mice. Our results showed that CLOCK and CRY proteins are involved in the transcriptional regulation of many circadian output genes in the mouse liver. In addition to being a core component of the negative feedback loop that drives the circadian oscillator, CLOCK also appears to be involved in various physiological functions such as cell cycle, lipid metabolism, immune functions, and proteolysis in peripheral tissues.</description><subject>Amino Acid Motifs</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Binding Sites</subject><subject>Blotting, Northern</subject><subject>Circadian Rhythm</subject><subject>CLOCK Proteins</subject><subject>Fatty Acids - metabolism</subject><subject>Genome</subject><subject>Humans</subject><subject>In Situ Hybridization</subject><subject>Lipid Metabolism</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Molecular Sequence Data</subject><subject>Mutation</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Sequence Homology, Nucleic Acid</subject><subject>Time Factors</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription, Genetic</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNqFkM1rFDEYxoModlu9epQcxNus-ZxkjmVoa3HLgih4kZBJ3nRT5mNNZrb2vzeyCz2J7-W9_J6Hhx9C7yhZU6LEp4fOre84EbIWjJAXaEWJ5hWX9MdLtCKE0aphUp-h85wfSDnR0NfojDJdS8H0Cv28gXEaoHqMHvDV732CnOM04svR9k85ZjwFfDctGfAmHiDhr3AA22fcbrbtlyrB_dLbGTxuY3LWRzvi7TLvlxmXXshv0KtQaHh7-hfo-_XVt_Zztdne3LaXm8pJyedKWcWoCrbrlLCBWwCra88aLn1QtA6NknVQtdc-eN8Jb4kOGkq24Yxy6vkF-njs3afp1wJ5NkPMDvrejlDGG0VZTThX_wWp1kw2NS_g-gi6NOWcIJh9ioNNT4YS89e8KebNs_kSeH9qXroB_DN-Ul2AD0dgF-93jzGB6eLkdjAYprQRzAgqaVMwfcSg-DpESCa7CKMDXyJuNn6K_5rwB8Hjnbs</recordid><startdate>20031017</startdate><enddate>20031017</enddate><creator>Oishi, Katsutaka</creator><creator>Miyazaki, Koyomi</creator><creator>Kadota, Koji</creator><creator>Kikuno, Reiko</creator><creator>Nagase, Takahiro</creator><creator>Atsumi, Gen-ichi</creator><creator>Ohkura, Naoki</creator><creator>Azama, Takashi</creator><creator>Mesaki, Miho</creator><creator>Yukimasa, Shima</creator><creator>Kobayashi, Hisato</creator><creator>Iitaka, Chisato</creator><creator>Umehara, Takashi</creator><creator>Horikoshi, Masami</creator><creator>Kudo, Takashi</creator><creator>Shimizu, Yoshihisa</creator><creator>Yano, Masahiko</creator><creator>Monden, Morito</creator><creator>Machida, Kazuhiko</creator><creator>Matsuda, Juzo</creator><creator>Horie, Shuichi</creator><creator>Todo, Takeshi</creator><creator>Ishida, Norio</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</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>7TM</scope><scope>7X8</scope></search><sort><creationdate>20031017</creationdate><title>Genome-wide Expression Analysis of Mouse Liver Reveals CLOCK-regulated Circadian Output Genes</title><author>Oishi, Katsutaka ; 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To examine CLOCK-regulated circadian transcription in peripheral tissues, we performed microarray analyses using liver RNA isolated from Clock mutant mice. We also compared expression profiles with those of Cryptochromes (Cry1 and Cry2) double knockout mice. We identified more than 100 genes that fluctuated from day to night and of which expression levels were decreased in Clock mutant mice. In Cry-deficient mice, the expression levels of most CLOCK-regulated genes were elevated to the upper range of normal oscillation. Most of the screened genes had a CLOCK/BMAL1 binding site (E box) in the 5′-flanking region. We found that CLOCK was absolutely concerned with the circadian transcription of one type of liver genes (such as DBP, TEF, and Usp2) and partially with another (such as mPer1, mPer2, mDec1, Nocturnin, P450 oxidoreductase, and FKBP51) because the latter were damped but remained rhythmic in the mutant mice. Our results showed that CLOCK and CRY proteins are involved in the transcriptional regulation of many circadian output genes in the mouse liver. In addition to being a core component of the negative feedback loop that drives the circadian oscillator, CLOCK also appears to be involved in various physiological functions such as cell cycle, lipid metabolism, immune functions, and proteolysis in peripheral tissues.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12865428</pmid><doi>10.1074/jbc.M304564200</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Amino Acid Motifs Animals Base Sequence Binding Sites Blotting, Northern Circadian Rhythm CLOCK Proteins Fatty Acids - metabolism Genome Humans In Situ Hybridization Lipid Metabolism Liver - metabolism Male Mice Mice, Knockout Molecular Sequence Data Mutation Oligonucleotide Array Sequence Analysis Reverse Transcriptase Polymerase Chain Reaction RNA - metabolism RNA, Messenger - metabolism Sequence Homology, Nucleic Acid Time Factors Trans-Activators - genetics Trans-Activators - metabolism Transcription, Genetic |
title | Genome-wide Expression Analysis of Mouse Liver Reveals CLOCK-regulated Circadian Output Genes |
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