lin-28 controls the succession of cell fate choices via two distinct activities
lin-28 is a conserved regulator of cell fate succession in animals. In Caenorhabditis elegans, it is a component of the heterochronic gene pathway that governs larval developmental timing, while its vertebrate homologs promote pluripotency and control differentiation in diverse tissues. The RNA bind...
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description | lin-28 is a conserved regulator of cell fate succession in animals. In Caenorhabditis elegans, it is a component of the heterochronic gene pathway that governs larval developmental timing, while its vertebrate homologs promote pluripotency and control differentiation in diverse tissues. The RNA binding protein encoded by lin-28 can directly inhibit let-7 microRNA processing by a novel mechanism that is conserved from worms to humans. We found that C. elegans LIN-28 protein can interact with four distinct let-7 family pre-microRNAs, but in vivo inhibits the premature accumulation of only let-7. Surprisingly, however, lin-28 does not require let-7 or its relatives for its characteristic promotion of second larval stage cell fates. In other words, we find that the premature accumulation of mature let-7 does not account for lin-28's precocious phenotype. To explain let-7's role in lin-28 activity, we provide evidence that lin-28 acts in two steps: first, the let-7-independent positive regulation of hbl-1 through its 3'UTR to control L2 stage-specific cell fates; and second, a let-7-dependent step that controls subsequent fates via repression of lin-41. Our evidence also indicates that let-7 functions one stage earlier in C. elegans development than previously thought. Importantly, lin-28's two-step mechanism resembles that of the heterochronic gene lin-14, and the overlap of their activities suggests a clockwork mechanism for developmental timing. Furthermore, this model explains the previous observation that mammalian Lin28 has two genetically separable activities. Thus, lin-28's two-step mechanism may be an essential feature of its evolutionarily conserved role in cell fate succession. |
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In Caenorhabditis elegans, it is a component of the heterochronic gene pathway that governs larval developmental timing, while its vertebrate homologs promote pluripotency and control differentiation in diverse tissues. The RNA binding protein encoded by lin-28 can directly inhibit let-7 microRNA processing by a novel mechanism that is conserved from worms to humans. We found that C. elegans LIN-28 protein can interact with four distinct let-7 family pre-microRNAs, but in vivo inhibits the premature accumulation of only let-7. Surprisingly, however, lin-28 does not require let-7 or its relatives for its characteristic promotion of second larval stage cell fates. In other words, we find that the premature accumulation of mature let-7 does not account for lin-28's precocious phenotype. To explain let-7's role in lin-28 activity, we provide evidence that lin-28 acts in two steps: first, the let-7-independent positive regulation of hbl-1 through its 3'UTR to control L2 stage-specific cell fates; and second, a let-7-dependent step that controls subsequent fates via repression of lin-41. Our evidence also indicates that let-7 functions one stage earlier in C. elegans development than previously thought. Importantly, lin-28's two-step mechanism resembles that of the heterochronic gene lin-14, and the overlap of their activities suggests a clockwork mechanism for developmental timing. Furthermore, this model explains the previous observation that mammalian Lin28 has two genetically separable activities. Thus, lin-28's two-step mechanism may be an essential feature of its evolutionarily conserved role in cell fate succession.</description><identifier>ISSN: 1553-7404</identifier><identifier>ISSN: 1553-7390</identifier><identifier>EISSN: 1553-7404</identifier><identifier>DOI: 10.1371/journal.pgen.1002588</identifier><identifier>PMID: 22457637</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>3' Untranslated Regions - genetics ; Animals ; Bacterial genetics ; Binding proteins ; Biology ; Caenorhabditis elegans ; Caenorhabditis elegans - genetics ; Caenorhabditis elegans - growth & development ; Caenorhabditis elegans Proteins - genetics ; Caenorhabditis elegans Proteins - metabolism ; Cell Differentiation - genetics ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Gene Expression Regulation, Developmental ; Genes ; Genetic aspects ; Genetics ; Larva - genetics ; Larva - growth & development ; MicroRNAs ; Nematodes ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Phenotype ; Physiological aspects ; Proteins ; Repressor Proteins - genetics ; RNA ; Transcription Factors - genetics ; Transcription Factors - metabolism</subject><ispartof>PLoS genetics, 2012-03, Vol.8 (3), p.e1002588-e1002588</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Vadla et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Vadla B, Kemper K, Alaimo J, Heine C, Moss EG (2012) lin-28 Controls the Succession of Cell Fate Choices via Two Distinct Activities. PLoS Genet 8(3): e1002588. doi:10.1371/journal.pgen.1002588</rights><rights>Vadla et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c791t-d845eed39db8567b4ab94e6184fdb28643e11f2b24e0a833cbe15b28d1097ce53</citedby><cites>FETCH-LOGICAL-c791t-d845eed39db8567b4ab94e6184fdb28643e11f2b24e0a833cbe15b28d1097ce53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310729/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310729/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22457637$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Mango, Susan E.</contributor><creatorcontrib>Vadla, Bhaskar</creatorcontrib><creatorcontrib>Kemper, Kevin</creatorcontrib><creatorcontrib>Alaimo, Jennifer</creatorcontrib><creatorcontrib>Heine, Christian</creatorcontrib><creatorcontrib>Moss, Eric G</creatorcontrib><title>lin-28 controls the succession of cell fate choices via two distinct activities</title><title>PLoS genetics</title><addtitle>PLoS Genet</addtitle><description>lin-28 is a conserved regulator of cell fate succession in animals. In Caenorhabditis elegans, it is a component of the heterochronic gene pathway that governs larval developmental timing, while its vertebrate homologs promote pluripotency and control differentiation in diverse tissues. The RNA binding protein encoded by lin-28 can directly inhibit let-7 microRNA processing by a novel mechanism that is conserved from worms to humans. We found that C. elegans LIN-28 protein can interact with four distinct let-7 family pre-microRNAs, but in vivo inhibits the premature accumulation of only let-7. Surprisingly, however, lin-28 does not require let-7 or its relatives for its characteristic promotion of second larval stage cell fates. In other words, we find that the premature accumulation of mature let-7 does not account for lin-28's precocious phenotype. To explain let-7's role in lin-28 activity, we provide evidence that lin-28 acts in two steps: first, the let-7-independent positive regulation of hbl-1 through its 3'UTR to control L2 stage-specific cell fates; and second, a let-7-dependent step that controls subsequent fates via repression of lin-41. Our evidence also indicates that let-7 functions one stage earlier in C. elegans development than previously thought. Importantly, lin-28's two-step mechanism resembles that of the heterochronic gene lin-14, and the overlap of their activities suggests a clockwork mechanism for developmental timing. Furthermore, this model explains the previous observation that mammalian Lin28 has two genetically separable activities. 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genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Phenotype</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Repressor Proteins - genetics</subject><subject>RNA</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><issn>1553-7404</issn><issn>1553-7390</issn><issn>1553-7404</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqVk1uL1DAUx4so7kW_gWhAUHyYMbc2zYuwLF4GFge8vYY0OZ3J0Glmm3Rcv72p012msg9KHhJyfuef5H9ysuwZwXPCBHm78X3X6ma-W0E7JxjTvCwfZKckz9lMcMwfHq1PsrMQNhizvJTicXZCKc9FwcRptmxcO6MlMr6NnW8CimtAoTcGQnC-Rb5GBpoG1ToCMmvvUgDtnUbxp0fWhehaE5E20e1ddBCeZI9q3QR4Os7n2fcP779dfppdLT8uLi-uZkZIEme25DmAZdJWZV6IiutKcihIyWtb0bLgDAipaUU5YF0yZiogeQpYgqUwkLPz7MVBd9f4oEYvgiKMsFwSwUkiFgfCer1Ru85tdfdLee3Unw3frZTuojMNqORGYXFl61oAtwWXVUEwVFgYwwsQZdJ6N57WV1uwBpJZupmITiOtW6uV3yvGCBZUJoHXo0Dnr3sIUW1dGIzVLfg-KFkwLjktaCJf_kXe_7iRWul0f9fWPh1rBk11QUvBJBZyMGl-D5WGha1LFYfapf1JwptJwvAr4CaudB-CWnz98h_s539nlz-m7Ksjdg26ievgmz6m7ximID-ApvMhdFDf1YNgNbTIrXNqaBE1tkhKe35cy7uk255gvwEN1gpt</recordid><startdate>20120301</startdate><enddate>20120301</enddate><creator>Vadla, Bhaskar</creator><creator>Kemper, Kevin</creator><creator>Alaimo, Jennifer</creator><creator>Heine, Christian</creator><creator>Moss, Eric G</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISN</scope><scope>ISR</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120301</creationdate><title>lin-28 controls the succession of cell fate choices via two distinct activities</title><author>Vadla, Bhaskar ; Kemper, Kevin ; Alaimo, Jennifer ; Heine, Christian ; Moss, Eric G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c791t-d845eed39db8567b4ab94e6184fdb28643e11f2b24e0a833cbe15b28d1097ce53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>3' Untranslated Regions - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PLoS genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vadla, Bhaskar</au><au>Kemper, Kevin</au><au>Alaimo, Jennifer</au><au>Heine, Christian</au><au>Moss, Eric G</au><au>Mango, Susan E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>lin-28 controls the succession of cell fate choices via two distinct activities</atitle><jtitle>PLoS genetics</jtitle><addtitle>PLoS Genet</addtitle><date>2012-03-01</date><risdate>2012</risdate><volume>8</volume><issue>3</issue><spage>e1002588</spage><epage>e1002588</epage><pages>e1002588-e1002588</pages><issn>1553-7404</issn><issn>1553-7390</issn><eissn>1553-7404</eissn><abstract>lin-28 is a conserved regulator of cell fate succession in animals. In Caenorhabditis elegans, it is a component of the heterochronic gene pathway that governs larval developmental timing, while its vertebrate homologs promote pluripotency and control differentiation in diverse tissues. The RNA binding protein encoded by lin-28 can directly inhibit let-7 microRNA processing by a novel mechanism that is conserved from worms to humans. We found that C. elegans LIN-28 protein can interact with four distinct let-7 family pre-microRNAs, but in vivo inhibits the premature accumulation of only let-7. Surprisingly, however, lin-28 does not require let-7 or its relatives for its characteristic promotion of second larval stage cell fates. In other words, we find that the premature accumulation of mature let-7 does not account for lin-28's precocious phenotype. To explain let-7's role in lin-28 activity, we provide evidence that lin-28 acts in two steps: first, the let-7-independent positive regulation of hbl-1 through its 3'UTR to control L2 stage-specific cell fates; and second, a let-7-dependent step that controls subsequent fates via repression of lin-41. Our evidence also indicates that let-7 functions one stage earlier in C. elegans development than previously thought. Importantly, lin-28's two-step mechanism resembles that of the heterochronic gene lin-14, and the overlap of their activities suggests a clockwork mechanism for developmental timing. Furthermore, this model explains the previous observation that mammalian Lin28 has two genetically separable activities. Thus, lin-28's two-step mechanism may be an essential feature of its evolutionarily conserved role in cell fate succession.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22457637</pmid><doi>10.1371/journal.pgen.1002588</doi><oa>free_for_read</oa></addata></record> |
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subjects | 3' Untranslated Regions - genetics Animals Bacterial genetics Binding proteins Biology Caenorhabditis elegans Caenorhabditis elegans - genetics Caenorhabditis elegans - growth & development Caenorhabditis elegans Proteins - genetics Caenorhabditis elegans Proteins - metabolism Cell Differentiation - genetics DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Gene Expression Regulation, Developmental Genes Genetic aspects Genetics Larva - genetics Larva - growth & development MicroRNAs Nematodes Nuclear Proteins - genetics Nuclear Proteins - metabolism Phenotype Physiological aspects Proteins Repressor Proteins - genetics RNA Transcription Factors - genetics Transcription Factors - metabolism |
title | lin-28 controls the succession of cell fate choices via two distinct activities |
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