Engineering subtle targeted mutations into the mouse genome
Identifieur interne : 002399 ( Istex/Corpus ); précédent : 002398; suivant : 002400Engineering subtle targeted mutations into the mouse genome
Auteurs : Douglas B. MenkeSource :
- genesis [ 1526-954X ] ; 2013-09.
English descriptors
- Teeft :
- Acad, Allele, Allelic series, Base pairs, Biallelic mutations, Biol, Biotechnol, Cas9, Cassette, Cell clones, Clone, Coding exons, Conditional alleles, Consortium, Deletion, Dsbs, Eppig, Exon, Extraneous sequences, Gene, Gene expression, Gene function, Genetics, Genome, Genome editing, Genome engineering, Grnas, High frequency, Homology, Human cells, Insertion, Knockout, Locus, Mammalian cells, Menke, Mouse, Mouse alleles, Mouse genome, Mouse models, Mouse mutations, Mouse zygotes, Mrna, Multiple genes, Mutation, Natl, Negative selection, Nhej, Nhej pathway, Nuclease, Nucleic, Nucleic acids, Null alleles, Pathway, Pbase, Piggybac, Point mutation, Point mutations, Positive selection, Proc, Proc natl acad, Recombinase systems, Recombinases, Recombination, Selectable, Selection cassette, Selection cassettes, Small deletions, Small insertions, Stm, Talens, Target sites, Transient expression, Transposon, Ttaa, Wang, Zfns, Zhang.
Abstract
Homologous recombination in embryonic stem (ES) cells offers an exquisitely precise mechanism to introduce targeted modifications to the mouse genome. This ability to produce specific alterations to the mouse genome has become an essential tool for the analysis of gene function and the development of mouse models of human disease. Of the many thousands of mouse alleles that have been generated by gene targeting, the majority are designed to completely ablate gene function, to create conditional alleles that are inactivated in the presence of Cre recombinase, or to produce reporter alleles that label‐specific tissues or cell populations (Eppig et al., 2012, Nucleic Acids Res 40:D881–D886). However, there is a variety of powerful motivations for the introduction of subtle targeted mutations (STMs) such as point mutations, small deletions, or small insertions into the mouse genome. The introduction of STMs allows the ablation of specific transcript isoforms, permits the functional investigation of particular domains or amino acids within a protein, provides the ability to study the role of specific sites with in cis‐regulatory elements, and can result in better mouse models of human genetic disorders. In this review, I examine the current strategies that are commonly used to introduce STMs into the mouse genome and highlight new gene targeting technologies, including TALENs and CRISPR/Cas, which are likely to influence the future of gene targeting in mice. genesis 51:605–618. © 2013 Wiley Periodicals, Inc.
Url:
DOI: 10.1002/dvg.22422
Links to Exploration step
ISTEX:759D7404B5167901ABD206D57087B733DC19B17FLe document en format XML
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The introduction of STMs allows the ablation of specific transcript isoforms, permits the functional investigation of particular domains or amino acids within a protein, provides the ability to study the role of specific sites with in cis‐regulatory elements, and can result in better mouse models of human genetic disorders. In this review, I examine the current strategies that are commonly used to introduce STMs into the mouse genome and highlight new gene targeting technologies, including TALENs and CRISPR/Cas, which are likely to influence the future of gene targeting in mice. genesis 51:605–618. © 2013 Wiley Periodicals, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>mutation</json:string><json:string>genome</json:string><json:string>allele</json:string><json:string>nuclease</json:string><json:string>wang</json:string><json:string>cassette</json:string><json:string>talens</json:string><json:string>mouse genome</json:string><json:string>point mutations</json:string><json:string>stm</json:string><json:string>deletion</json:string><json:string>cas9</json:string><json:string>recombination</json:string><json:string>homology</json:string><json:string>zfns</json:string><json:string>proc</json:string><json:string>proc natl acad</json:string><json:string>acad</json:string><json:string>natl</json:string><json:string>knockout</json:string><json:string>zhang</json:string><json:string>nhej</json:string><json:string>selection cassettes</json:string><json:string>dsbs</json:string><json:string>transposon</json:string><json:string>nucleic acids</json:string><json:string>selection cassette</json:string><json:string>clone</json:string><json:string>mrna</json:string><json:string>biotechnol</json:string><json:string>piggybac</json:string><json:string>exon</json:string><json:string>ttaa</json:string><json:string>pbase</json:string><json:string>menke</json:string><json:string>genetics</json:string><json:string>biol</json:string><json:string>genome editing</json:string><json:string>recombinases</json:string><json:string>consortium</json:string><json:string>grnas</json:string><json:string>selectable</json:string><json:string>pathway</json:string><json:string>small deletions</json:string><json:string>eppig</json:string><json:string>insertion</json:string><json:string>gene function</json:string><json:string>transient expression</json:string><json:string>mouse</json:string><json:string>null alleles</json:string><json:string>extraneous sequences</json:string><json:string>conditional alleles</json:string><json:string>nucleic</json:string><json:string>gene</json:string><json:string>locus</json:string><json:string>biallelic mutations</json:string><json:string>positive selection</json:string><json:string>human cells</json:string><json:string>base pairs</json:string><json:string>gene expression</json:string><json:string>cell clones</json:string><json:string>point mutation</json:string><json:string>mouse zygotes</json:string><json:string>genome engineering</json:string><json:string>target sites</json:string><json:string>coding exons</json:string><json:string>mouse alleles</json:string><json:string>multiple genes</json:string><json:string>nhej pathway</json:string><json:string>high frequency</json:string><json:string>mouse models</json:string><json:string>mammalian cells</json:string><json:string>mouse mutations</json:string><json:string>negative selection</json:string><json:string>allelic series</json:string><json:string>small insertions</json:string><json:string>recombinase systems</json:string></teeft></keywords><author><json:item><name>Douglas B. 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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract style="main"><p>Homologous recombination in embryonic stem (ES) cells offers an exquisitely precise mechanism to introduce targeted modifications to the mouse genome. This ability to produce specific alterations to the mouse genome has become an essential tool for the analysis of gene function and the development of mouse models of human disease. Of the many thousands of mouse alleles that have been generated by gene targeting, the majority are designed to completely ablate gene function, to create conditional alleles that are inactivated in the presence of Cre recombinase, or to produce reporter alleles that label‐specific tissues or cell populations (Eppig <hi rend="italic">et al</hi>., 2012, Nucleic Acids Res 40:D881–D886). However, there is a variety of powerful motivations for the introduction of subtle targeted mutations (STMs) such as point mutations, small deletions, or small insertions into the mouse genome. The introduction of STMs allows the ablation of specific transcript isoforms, permits the functional investigation of particular domains or amino acids within a protein, provides the ability to study the role of specific sites with in cis‐regulatory elements, and can result in better mouse models of human genetic disorders. In this review, I examine the current strategies that are commonly used to introduce STMs into the mouse genome and highlight new gene targeting technologies, including TALENs and CRISPR/Cas, which are likely to influence the future of gene targeting in mice. genesis 51:605–618. © 2013 Wiley Periodicals, Inc.</p></abstract><textClass><keywords><term xml:id="dvg22422-kwd-0001">point mutation</term><term xml:id="dvg22422-kwd-0002">ZFN</term><term xml:id="dvg22422-kwd-0003">TALEN</term><term xml:id="dvg22422-kwd-0004">CRISPR/Cas</term></keywords><keywords rend="articleCategory"><term>Review</term></keywords><keywords rend="tocHeading1"><term>Review</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-9LQH8JN4-C/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en" xml:id="dvg22422"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1002/(ISSN)1526-968X</doi><issn type="print">1526-954X</issn><issn type="electronic">1526-968X</issn><idGroup><id type="product" value="DVG"></id></idGroup><titleGroup><title type="main" sort="GENESIS">genesis</title><title type="short">genesis</title></titleGroup></publicationMeta><publicationMeta level="part" position="90"><doi>10.1002/dvg.v51.9</doi><copyright ownership="publisher">Copyright © 2013 Wiley Periodicals, Inc.</copyright><numberingGroup><numbering type="journalVolume" number="51">51</numbering><numbering type="journalIssue">9</numbering></numberingGroup><coverDate startDate="2013-09">September 2013</coverDate></publicationMeta><publicationMeta level="unit" position="20" type="reviewArticle" status="forIssue"><doi>10.1002/dvg.22422</doi><idGroup><id type="unit" value="DVG22422"></id></idGroup><countGroup><count type="pageTotal" number="14"></count></countGroup><titleGroup><title type="articleCategory">Review</title><title type="tocHeading1">Review</title></titleGroup><copyright ownership="publisher">Copyright © 2013 Wiley Periodicals, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2013-06-28"></event><event type="manuscriptRevised" date="2013-07-25"></event><event type="manuscriptAccepted" date="2013-07-26"></event><event type="xmlCreated" agent="Cenveo Publisher Services" date="2013-08-13"></event><event type="publishedOnlineAccepted" date="2013-08-02"></event><event type="publishedOnlineEarlyUnpaginated" date="2013-08-30"></event><event type="firstOnline" date="2013-08-30"></event><event type="publishedOnlineFinalForm" date="2013-09-19"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-17"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.6.4 mode:FullText" date="2015-10-05"></event></eventGroup><numberingGroup><numbering type="pageFirst">605</numbering><numbering type="pageLast">618</numbering></numberingGroup><correspondenceTo>Correspondence to: Department of Genetics, University of Georgia, Coverdell Building, Room 250A, 500 DW Brooks Drive, Athens, GA 30602, USA. E‐mail: <email>dmenke@uga.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:DVG.DVG22422.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Engineering subtle targeted mutations into the mouse genome</title><title type="short">ENGINEERING MOUSE MUTATIONS</title><title type="shortAuthors">Menke</title></titleGroup><creators><creator affiliationRef="#dvg22422-aff-0001" corresponding="yes" creatorRole="author" xml:id="dvg22422-cr-0001"><personName><givenNames>Douglas B.</givenNames><familyName>Menke</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="US" type="organization" xml:id="dvg22422-aff-0001"><orgDiv>Department of Genetics</orgDiv><orgName>University of Georgia</orgName><address><city>Athens</city><countryPart>Georgia</countryPart></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="dvg22422-kwd-0001">point mutation</keyword><keyword xml:id="dvg22422-kwd-0002">ZFN</keyword><keyword xml:id="dvg22422-kwd-0003">TALEN</keyword><keyword xml:id="dvg22422-kwd-0004">CRISPR/Cas</keyword></keywordGroup><abstractGroup><abstract type="main"><p>Homologous recombination in embryonic stem (ES) cells offers an exquisitely precise mechanism to introduce targeted modifications to the mouse genome. This ability to produce specific alterations to the mouse genome has become an essential tool for the analysis of gene function and the development of mouse models of human disease. Of the many thousands of mouse alleles that have been generated by gene targeting, the majority are designed to completely ablate gene function, to create conditional alleles that are inactivated in the presence of Cre recombinase, or to produce reporter alleles that label‐specific tissues or cell populations (Eppig <i>et al</i>., 2012, Nucleic Acids Res 40:D881–D886). However, there is a variety of powerful motivations for the introduction of subtle targeted mutations (STMs) such as point mutations, small deletions, or small insertions into the mouse genome. The introduction of STMs allows the ablation of specific transcript isoforms, permits the functional investigation of particular domains or amino acids within a protein, provides the ability to study the role of specific sites with in cis‐regulatory elements, and can result in better mouse models of human genetic disorders. In this review, I examine the current strategies that are commonly used to introduce STMs into the mouse genome and highlight new gene targeting technologies, including TALENs and CRISPR/Cas, which are likely to influence the future of gene targeting in mice. genesis 51:605–618. © 2013 Wiley Periodicals, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Engineering subtle targeted mutations into the mouse genome</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>ENGINEERING MOUSE MUTATIONS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Engineering subtle targeted mutations into the mouse genome</title></titleInfo><name type="personal"><namePart type="given">Douglas B.</namePart><namePart type="family">Menke</namePart><affiliation>Department of Genetics, University of Georgia, Georgia, Athens</affiliation><affiliation>E-mail: dmenke@uga.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2013-09</dateIssued><dateCreated encoding="w3cdtf">2013-08-13</dateCreated><dateCaptured encoding="w3cdtf">2013-06-28</dateCaptured><dateValid encoding="w3cdtf">2013-07-26</dateValid><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>Homologous recombination in embryonic stem (ES) cells offers an exquisitely precise mechanism to introduce targeted modifications to the mouse genome. This ability to produce specific alterations to the mouse genome has become an essential tool for the analysis of gene function and the development of mouse models of human disease. Of the many thousands of mouse alleles that have been generated by gene targeting, the majority are designed to completely ablate gene function, to create conditional alleles that are inactivated in the presence of Cre recombinase, or to produce reporter alleles that label‐specific tissues or cell populations (Eppig et al., 2012, Nucleic Acids Res 40:D881–D886). However, there is a variety of powerful motivations for the introduction of subtle targeted mutations (STMs) such as point mutations, small deletions, or small insertions into the mouse genome. The introduction of STMs allows the ablation of specific transcript isoforms, permits the functional investigation of particular domains or amino acids within a protein, provides the ability to study the role of specific sites with in cis‐regulatory elements, and can result in better mouse models of human genetic disorders. In this review, I examine the current strategies that are commonly used to introduce STMs into the mouse genome and highlight new gene targeting technologies, including TALENs and CRISPR/Cas, which are likely to influence the future of gene targeting in mice. genesis 51:605–618. © 2013 Wiley Periodicals, Inc.</abstract><subject><genre>keywords</genre><topic>point mutation</topic><topic>ZFN</topic><topic>TALEN</topic><topic>CRISPR/Cas</topic></subject><relatedItem type="host"><titleInfo><title>genesis</title></titleInfo><titleInfo type="abbreviated"><title>genesis</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>article-category</genre><topic>Review</topic><topic>Review</topic></subject><identifier type="ISSN">1526-954X</identifier><identifier type="eISSN">1526-968X</identifier><identifier type="DOI">10.1002/(ISSN)1526-968X</identifier><identifier type="PublisherID">DVG</identifier><part><date>2013</date><detail type="volume"><caption>vol.</caption><number>51</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>605</start><end>618</end><total>14</total></extent></part></relatedItem><relatedItem type="references" displayLabel="dvg22422-cit-0001"><titleInfo><title>Selective inactivation of Otx2 mRNA isoforms reveals isoform‐specific requirement for visceral endoderm anteriorization and head morphogenesis and highlights cell diversity in the visceral endoderm</title></titleInfo><name type="personal"><namePart type="given">D</namePart><namePart type="family">Acampora</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LG</namePart><namePart type="family">Di Giovannantonio</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Di Salvio</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Mancuso</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Simeone</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Acampora D, Di Giovannantonio LG, Di Salvio M, Mancuso P, Simeone A. 2009. 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