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Mouse development with a single E2F activator
The E2F family is conserved from Caenorhabditis elegans to mammals, with some family members having transcription activation functions and others having repressor functions. Whereas C. elegans and Drosophila melanogaster have a single E2F activator protein and repressor protein, mammals have at leas...
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| Published in: | Nature 2008-08, Vol.454 (7208), p.1137-1141 |
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| Main Authors: | , , , , , , , , , , , , , , , |
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| container_title | Nature |
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| creator | Chong, Jean-Leon Naidu, Shan Timmers, Cynthia Nolan, Eric Leone, Gustavo Feria-Arias, Enrique Sharma, Nidhi Opavska, Jana Opavsky, Rene Rosol, Thomas J Wu, Lizhao Tsai, Shih-Yin de Bruin, Alain Trikha, Prashant Stromberg, Paul Fernandez, Soledad A |
| description | The E2F family is conserved from Caenorhabditis elegans to mammals, with some family members having transcription activation functions and others having repressor functions. Whereas C. elegans and Drosophila melanogaster have a single E2F activator protein and repressor protein, mammals have at least three activator and five repressor proteins. Why such genetic complexity evolved in mammals is not known. To begin to evaluate this genetic complexity, we targeted the inactivation of the entire subset of activators, E2f1, E2f2, E2f3a and E2f3b, singly or in combination in mice. We demonstrate that E2f3a is sufficient to support mouse embryonic and postnatal development. Remarkably, expression of E2f3b or E2f1 from the E2f3a locus (E2f3a3bki or E2f3a1ki, respectively) suppressed all the postnatal phenotypes associated with the inactivation of E2f3a. We conclude that there is significant functional redundancy among activators and that the specific requirement for E2f3a during postnatal development is dictated by regulatory sequences governing its selective spatiotemporal expression and not by its intrinsic protein functions. These findings provide a molecular basis for the observed specificity among E2F activators during development. |
| doi_str_mv | 10.1038/nature07066 |
| format | article |
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Whereas C. elegans and Drosophila melanogaster have a single E2F activator protein and repressor protein, mammals have at least three activator and five repressor proteins. Why such genetic complexity evolved in mammals is not known. To begin to evaluate this genetic complexity, we targeted the inactivation of the entire subset of activators, E2f1, E2f2, E2f3a and E2f3b, singly or in combination in mice. We demonstrate that E2f3a is sufficient to support mouse embryonic and postnatal development. Remarkably, expression of E2f3b or E2f1 from the E2f3a locus (E2f3a3bki or E2f3a1ki, respectively) suppressed all the postnatal phenotypes associated with the inactivation of E2f3a. We conclude that there is significant functional redundancy among activators and that the specific requirement for E2f3a during postnatal development is dictated by regulatory sequences governing its selective spatiotemporal expression and not by its intrinsic protein functions. These findings provide a molecular basis for the observed specificity among E2F activators during development.</description><identifier>ISSN: 0028-0836</identifier><identifier>EISSN: 1476-4687</identifier><identifier>EISSN: 1476-4679</identifier><identifier>DOI: 10.1038/nature07066</identifier><identifier>PMID: 18594513</identifier><identifier>CODEN: NATUAS</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adipose tissue ; Animals ; Biological and medical sciences ; Caenorhabditis elegans ; Cells, Cultured ; DNA binding proteins ; Drosophila ; E2F Transcription Factors - deficiency ; E2F Transcription Factors - genetics ; E2F Transcription Factors - metabolism ; E2F1 Transcription Factor - deficiency ; E2F1 Transcription Factor - genetics ; E2F1 Transcription Factor - metabolism ; E2F2 Transcription Factor - deficiency ; E2F2 Transcription Factor - genetics ; E2F2 Transcription Factor - metabolism ; E2F3 Transcription Factor - deficiency ; E2F3 Transcription Factor - genetics ; E2F3 Transcription Factor - metabolism ; Embryo Loss - genetics ; Embryo, Mammalian - embryology ; Embryo, Mammalian - metabolism ; Embryology: invertebrates and vertebrates. Teratology ; Embryonic Development - genetics ; Fundamental and applied biological sciences. Psychology ; Gene Deletion ; Genetic aspects ; Genomics ; Genotype ; Growth ; Growth - genetics ; Humanities and Social Sciences ; letter ; Mammals ; Mice ; Mice, Knockout ; Molecular embryology ; multidisciplinary ; Phenotype ; Physiological aspects ; Properties ; Proteins ; Rodents ; Science ; Science (multidisciplinary)</subject><ispartof>Nature, 2008-08, Vol.454 (7208), p.1137-1141</ispartof><rights>Macmillan Publishers Limited. All rights reserved 2008</rights><rights>2008 INIST-CNRS</rights><rights>COPYRIGHT 2008 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Aug 28, 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c736t-6ab4c03e11376735176e61a081492e9bb4afd62b5f63b88e0f51037aded9f8583</citedby><cites>FETCH-LOGICAL-c736t-6ab4c03e11376735176e61a081492e9bb4afd62b5f63b88e0f51037aded9f8583</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,2727,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20584171$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18594513$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chong, Jean-Leon</creatorcontrib><creatorcontrib>Naidu, Shan</creatorcontrib><creatorcontrib>Timmers, Cynthia</creatorcontrib><creatorcontrib>Nolan, Eric</creatorcontrib><creatorcontrib>Leone, Gustavo</creatorcontrib><creatorcontrib>Feria-Arias, Enrique</creatorcontrib><creatorcontrib>Sharma, Nidhi</creatorcontrib><creatorcontrib>Opavska, Jana</creatorcontrib><creatorcontrib>Opavsky, Rene</creatorcontrib><creatorcontrib>Rosol, Thomas J</creatorcontrib><creatorcontrib>Wu, Lizhao</creatorcontrib><creatorcontrib>Tsai, Shih-Yin</creatorcontrib><creatorcontrib>de Bruin, Alain</creatorcontrib><creatorcontrib>Trikha, Prashant</creatorcontrib><creatorcontrib>Stromberg, Paul</creatorcontrib><creatorcontrib>Fernandez, Soledad A</creatorcontrib><title>Mouse development with a single E2F activator</title><title>Nature</title><addtitle>Nature</addtitle><addtitle>Nature</addtitle><description>The E2F family is conserved from Caenorhabditis elegans to mammals, with some family members having transcription activation functions and others having repressor functions. Whereas C. elegans and Drosophila melanogaster have a single E2F activator protein and repressor protein, mammals have at least three activator and five repressor proteins. Why such genetic complexity evolved in mammals is not known. To begin to evaluate this genetic complexity, we targeted the inactivation of the entire subset of activators, E2f1, E2f2, E2f3a and E2f3b, singly or in combination in mice. We demonstrate that E2f3a is sufficient to support mouse embryonic and postnatal development. Remarkably, expression of E2f3b or E2f1 from the E2f3a locus (E2f3a3bki or E2f3a1ki, respectively) suppressed all the postnatal phenotypes associated with the inactivation of E2f3a. We conclude that there is significant functional redundancy among activators and that the specific requirement for E2f3a during postnatal development is dictated by regulatory sequences governing its selective spatiotemporal expression and not by its intrinsic protein functions. These findings provide a molecular basis for the observed specificity among E2F activators during development.</description><subject>Adipose tissue</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Caenorhabditis elegans</subject><subject>Cells, Cultured</subject><subject>DNA binding proteins</subject><subject>Drosophila</subject><subject>E2F Transcription Factors - deficiency</subject><subject>E2F Transcription Factors - genetics</subject><subject>E2F Transcription Factors - metabolism</subject><subject>E2F1 Transcription Factor - deficiency</subject><subject>E2F1 Transcription Factor - genetics</subject><subject>E2F1 Transcription Factor - metabolism</subject><subject>E2F2 Transcription Factor - deficiency</subject><subject>E2F2 Transcription Factor - genetics</subject><subject>E2F2 Transcription Factor - metabolism</subject><subject>E2F3 Transcription Factor - deficiency</subject><subject>E2F3 Transcription Factor - genetics</subject><subject>E2F3 Transcription Factor - metabolism</subject><subject>Embryo Loss - genetics</subject><subject>Embryo, Mammalian - embryology</subject><subject>Embryo, Mammalian - metabolism</subject><subject>Embryology: invertebrates and vertebrates. Teratology</subject><subject>Embryonic Development - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Deletion</subject><subject>Genetic aspects</subject><subject>Genomics</subject><subject>Genotype</subject><subject>Growth</subject><subject>Growth - genetics</subject><subject>Humanities and Social Sciences</subject><subject>letter</subject><subject>Mammals</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Molecular embryology</subject><subject>multidisciplinary</subject><subject>Phenotype</subject><subject>Physiological aspects</subject><subject>Properties</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><issn>0028-0836</issn><issn>1476-4687</issn><issn>1476-4679</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNp90t2L1DAQAPAgireePvku9UBFtGfSpEn6IizLnR6cCnriY0jTaS9Hm-4l7ar_vTm67Ies0odA8uvMJDMIPSX4lGAq3zk9jB6wwJzfQzPCBE8Zl-I-mmGcyRRLyo_QoxBuMMY5EewhOiIyL1hO6Ayln_oxQFLBCtp-2YEbkp92uE50EqxrWkjOsvNEm8Gu9ND7x-hBrdsAT9brMfp-fna1-JhefvlwsZhfpkZQPqRcl8xgCoRQwQWNSTlworEkrMigKEum64pnZV5zWkoJuM7jTYSuoCpqmUt6jN5PcZdj2UFlYllet2rpbaf9b9Vrq_ZPnL1WTb9SLJNSZiwGeLUO4PvbEcKgOhsMtK12EC-sBKOUYCbuUr38r8xwwUWOaYQnf8GbfvQuPkM0LKe8ICKidEKNbkFZV_exPNOAg1hl76C2cXtOYpEstiXbBt3zZmlv1S46PYDiV0FnzcGor_d-iGaAX0OjxxDUxbev-_bNv-386sfi80FtfB-Ch3rTE4LV3TSqnWmM-tluG7d2PX4RvFgDHYxua6-dsWHjMpxLRgSJ7u3kQjxyDfjt2x_O-3zi0-Ym3q75A85Y_fM</recordid><startdate>20080828</startdate><enddate>20080828</enddate><creator>Chong, Jean-Leon</creator><creator>Naidu, Shan</creator><creator>Timmers, Cynthia</creator><creator>Nolan, Eric</creator><creator>Leone, Gustavo</creator><creator>Feria-Arias, Enrique</creator><creator>Sharma, Nidhi</creator><creator>Opavska, Jana</creator><creator>Opavsky, Rene</creator><creator>Rosol, Thomas J</creator><creator>Wu, Lizhao</creator><creator>Tsai, Shih-Yin</creator><creator>de Bruin, Alain</creator><creator>Trikha, Prashant</creator><creator>Stromberg, Paul</creator><creator>Fernandez, Soledad A</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>IQODW</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>ATWCN</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7ST</scope><scope>7T5</scope><scope>7TG</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PCBAR</scope><scope>PDBOC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>R05</scope><scope>RC3</scope><scope>S0X</scope><scope>SOI</scope><scope>7SC</scope><scope>7SP</scope><scope>7SR</scope><scope>7TB</scope><scope>7U5</scope><scope>8BQ</scope><scope>F28</scope><scope>JG9</scope><scope>JQ2</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><scope>5PM</scope></search><sort><creationdate>20080828</creationdate><title>Mouse development with a single E2F activator</title><author>Chong, Jean-Leon ; 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Communications Abstracts</collection><collection>Engineered Materials Abstracts</collection><collection>Mechanical & Transportation Engineering Abstracts</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>METADEX</collection><collection>ANTE: Abstracts in New Technology & Engineering</collection><collection>Materials Research Database</collection><collection>ProQuest Computer Science Collection</collection><collection>Civil Engineering Abstracts</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>Computer and Information Systems Abstracts Academic</collection><collection>Computer and Information Systems Abstracts Professional</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chong, Jean-Leon</au><au>Naidu, Shan</au><au>Timmers, Cynthia</au><au>Nolan, Eric</au><au>Leone, Gustavo</au><au>Feria-Arias, Enrique</au><au>Sharma, Nidhi</au><au>Opavska, Jana</au><au>Opavsky, Rene</au><au>Rosol, Thomas J</au><au>Wu, Lizhao</au><au>Tsai, Shih-Yin</au><au>de Bruin, Alain</au><au>Trikha, Prashant</au><au>Stromberg, Paul</au><au>Fernandez, Soledad A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mouse development with a single E2F activator</atitle><jtitle>Nature</jtitle><stitle>Nature</stitle><addtitle>Nature</addtitle><date>2008-08-28</date><risdate>2008</risdate><volume>454</volume><issue>7208</issue><spage>1137</spage><epage>1141</epage><pages>1137-1141</pages><issn>0028-0836</issn><eissn>1476-4687</eissn><eissn>1476-4679</eissn><coden>NATUAS</coden><abstract>The E2F family is conserved from Caenorhabditis elegans to mammals, with some family members having transcription activation functions and others having repressor functions. Whereas C. elegans and Drosophila melanogaster have a single E2F activator protein and repressor protein, mammals have at least three activator and five repressor proteins. Why such genetic complexity evolved in mammals is not known. To begin to evaluate this genetic complexity, we targeted the inactivation of the entire subset of activators, E2f1, E2f2, E2f3a and E2f3b, singly or in combination in mice. We demonstrate that E2f3a is sufficient to support mouse embryonic and postnatal development. Remarkably, expression of E2f3b or E2f1 from the E2f3a locus (E2f3a3bki or E2f3a1ki, respectively) suppressed all the postnatal phenotypes associated with the inactivation of E2f3a. We conclude that there is significant functional redundancy among activators and that the specific requirement for E2f3a during postnatal development is dictated by regulatory sequences governing its selective spatiotemporal expression and not by its intrinsic protein functions. These findings provide a molecular basis for the observed specificity among E2F activators during development.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>18594513</pmid><doi>10.1038/nature07066</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0028-0836 |
| ispartof | Nature, 2008-08, Vol.454 (7208), p.1137-1141 |
| issn | 0028-0836 1476-4687 1476-4679 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4288824 |
| source | Nature |
| subjects | Adipose tissue Animals Biological and medical sciences Caenorhabditis elegans Cells, Cultured DNA binding proteins Drosophila E2F Transcription Factors - deficiency E2F Transcription Factors - genetics E2F Transcription Factors - metabolism E2F1 Transcription Factor - deficiency E2F1 Transcription Factor - genetics E2F1 Transcription Factor - metabolism E2F2 Transcription Factor - deficiency E2F2 Transcription Factor - genetics E2F2 Transcription Factor - metabolism E2F3 Transcription Factor - deficiency E2F3 Transcription Factor - genetics E2F3 Transcription Factor - metabolism Embryo Loss - genetics Embryo, Mammalian - embryology Embryo, Mammalian - metabolism Embryology: invertebrates and vertebrates. Teratology Embryonic Development - genetics Fundamental and applied biological sciences. Psychology Gene Deletion Genetic aspects Genomics Genotype Growth Growth - genetics Humanities and Social Sciences letter Mammals Mice Mice, Knockout Molecular embryology multidisciplinary Phenotype Physiological aspects Properties Proteins Rodents Science Science (multidisciplinary) |
| title | Mouse development with a single E2F activator |
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