Generation of conditional alleles for Foxc1 and Foxc2 in mice
Identifieur interne : 003C96 ( Istex/Corpus ); précédent : 003C95; suivant : 003C97Generation of conditional alleles for Foxc1 and Foxc2 in mice
Auteurs : Amy Sasman ; Carey Nassano-Miller ; Kyoo Seok Shim ; Hyun Young Koo ; Ting Liu ; Kathryn M. Schultz ; Meredith Millay ; Atsushi Nanano ; Myengmo Kang ; Takashi Suzuki ; Tsutomu KumeSource :
- genesis [ 1526-954X ] ; 2012-10.
Abstract
The Forkhead box transcription factors, Foxc1 and Foxc2, are crucial for development of the eye, cardiovascular network, and other physiological systems, but their cell‐type specific and postdevelopmental functions are unknown, in part because conventional (i.e., whole‐organism) homozygous‐null mutations of either factor result in perinatal death. Here, we describe the generation of mice with conditional‐null Foxc1flox and Foxc2flox mutations that are induced via Cre‐mediated recombination. Mice homozygous for the unrecombined alleles are viable and fertile, indicating that the conditional alleles retain their wild‐type function. The embryos of Foxc1flox or Foxc2flox mice crossed with Cre‐deleter mice that are homozygous for the recombined allele (i.e., Foxc1Δ/Δ or Foxc2Δ/Δ embryos) lack expression of the corresponding gene and show the same developmental defects observed in conventional homozygous mutant embryos. We expect these conditional mutations to enable characterization of the cell‐type specific functions of Foxc1 and Foxc2 in development, disease, and adult animals. genesis 50:766–774, 2012. © 2012 Wiley Periodicals, Inc.
Url:
DOI: 10.1002/dvg.22036
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ISTEX:814AB4C97D2BAA7D95908A7B7F70742F780C0185Le document en format XML
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Schultz</name><affiliation><mods:affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</mods:affiliation></affiliation></author><author><name sortKey="Millay, Meredith" sort="Millay, Meredith" uniqKey="Millay M" first="Meredith" last="Millay">Meredith Millay</name><affiliation><mods:affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</mods:affiliation></affiliation></author><author><name sortKey="Nanano, Atsushi" sort="Nanano, Atsushi" uniqKey="Nanano A" first="Atsushi" last="Nanano">Atsushi Nanano</name><affiliation><mods:affiliation>Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee</mods:affiliation></affiliation></author><author><name sortKey="Kang, Myengmo" sort="Kang, Myengmo" uniqKey="Kang M" first="Myengmo" last="Kang">Myengmo Kang</name><affiliation><mods:affiliation>Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee</mods:affiliation></affiliation></author><author><name sortKey="Suzuki, Takashi" sort="Suzuki, Takashi" uniqKey="Suzuki T" first="Takashi" last="Suzuki">Takashi Suzuki</name><affiliation><mods:affiliation>Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee</mods:affiliation></affiliation></author><author><name sortKey="Kume, Tsutomu" sort="Kume, Tsutomu" uniqKey="Kume T" first="Tsutomu" last="Kume">Tsutomu Kume</name><affiliation><mods:affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</mods:affiliation></affiliation><affiliation><mods:affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, 303E Chicago Ave, Chicago, IL 60611</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">genesis</title><title level="j" type="alt">GENESIS</title><idno type="ISSN">1526-954X</idno><idno type="eISSN">1526-968X</idno><imprint><biblScope unit="vol">50</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="766">766</biblScope><biblScope unit="page" to="774">774</biblScope><biblScope unit="page-count">9</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2012-10">2012-10</date></imprint><idno type="ISSN">1526-954X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1526-954X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The Forkhead box transcription factors, Foxc1 and Foxc2, are crucial for development of the eye, cardiovascular network, and other physiological systems, but their cell‐type specific and postdevelopmental functions are unknown, in part because conventional (i.e., whole‐organism) homozygous‐null mutations of either factor result in perinatal death. Here, we describe the generation of mice with conditional‐null Foxc1flox and Foxc2flox mutations that are induced via Cre‐mediated recombination. Mice homozygous for the unrecombined alleles are viable and fertile, indicating that the conditional alleles retain their wild‐type function. The embryos of Foxc1flox or Foxc2flox mice crossed with Cre‐deleter mice that are homozygous for the recombined allele (i.e., Foxc1Δ/Δ or Foxc2Δ/Δ embryos) lack expression of the corresponding gene and show the same developmental defects observed in conventional homozygous mutant embryos. 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Here, we describe the generation of mice with conditional‐null Foxc1flox and Foxc2flox mutations that are induced via Cre‐mediated recombination. Mice homozygous for the unrecombined alleles are viable and fertile, indicating that the conditional alleles retain their wild‐type function. The embryos of Foxc1flox or Foxc2flox mice crossed with Cre‐deleter mice that are homozygous for the recombined allele (i.e., Foxc1Δ/Δ or Foxc2Δ/Δ embryos) lack expression of the corresponding gene and show the same developmental defects observed in conventional homozygous mutant embryos. We expect these conditional mutations to enable characterization of the cell‐type specific functions of Foxc1 and Foxc2 in development, disease, and adult animals. genesis 50:766–774, 2012. © 2012 Wiley Periodicals, Inc.</abstract><qualityIndicators><score>5.916</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1148</abstractCharCount><pdfWordCount>4056</pdfWordCount><pdfCharCount>25582</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>155</abstractWordCount></qualityIndicators><title>Generation of conditional alleles for Foxc1 and Foxc2 in 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type="first">Amy</forename><surname>Sasman</surname></persName><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois<address><country key="US"></country></address></affiliation><note type="foot">A.S., C.N.‐M., K.S.S., and H.Y.K. contributed equally to this work</note></author><author xml:id="author-0001"><persName><forename type="first">Carey</forename><surname>Nassano‐Miller</surname></persName><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois<address><country key="US"></country></address></affiliation><note type="foot">A.S., C.N.‐M., K.S.S., and H.Y.K. contributed equally to this work</note></author><author xml:id="author-0002"><persName><forename type="first">Kyoo Seok</forename><surname>Shim</surname></persName><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois<address><country key="US"></country></address></affiliation><note type="foot">A.S., C.N.‐M., K.S.S., and H.Y.K. contributed equally to this work</note></author><author xml:id="author-0003"><persName><forename type="first">Hyun Young</forename><surname>Koo</surname></persName><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois<address><country key="US"></country></address></affiliation><note type="foot">A.S., C.N.‐M., K.S.S., and H.Y.K. contributed equally to this work</note></author><author xml:id="author-0004"><persName><forename type="first">Ting</forename><surname>Liu</surname></persName><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois<address><country key="US"></country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Kathryn M.</forename><surname>Schultz</surname></persName><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois<address><country key="US"></country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Meredith</forename><surname>Millay</surname></persName><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois<address><country key="US"></country></address></affiliation></author><author xml:id="author-0007"><persName><forename type="first">Atsushi</forename><surname>Nanano</surname></persName><affiliation>Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee<address><country key="US"></country></address></affiliation></author><author xml:id="author-0008"><persName><forename type="first">Myengmo</forename><surname>Kang</surname></persName><affiliation>Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee<address><country key="US"></country></address></affiliation></author><author xml:id="author-0009"><persName><forename type="first">Takashi</forename><surname>Suzuki</surname></persName><affiliation>Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee<address><country key="US"></country></address></affiliation></author><author xml:id="author-0010" role="corresp"><persName><forename type="first">Tsutomu</forename><surname>Kume</surname></persName><email>t‐kume@northwestern.edu</email><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois<address><country key="US"></country></address></affiliation><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, 303E Chicago Ave, Chicago, IL 60611</affiliation></author><idno 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style="main"><head>Abstract</head><p>The Forkhead box transcription factors, Foxc1 and Foxc2, are crucial for development of the eye, cardiovascular network, and other physiological systems, but their cell‐type specific and postdevelopmental functions are unknown, in part because conventional (i.e., whole‐organism) homozygous‐null mutations of either factor result in perinatal death. Here, we describe the generation of mice with conditional‐null <hi rend="italic">Foxc1<hi rend="superscript">flox</hi></hi> and <hi rend="italic">Foxc2<hi rend="superscript">flox</hi></hi> mutations that are induced via Cre‐mediated recombination. Mice homozygous for the unrecombined alleles are viable and fertile, indicating that the conditional alleles retain their wild‐type function. The embryos of <hi rend="italic">Foxc1<hi rend="superscript">flox</hi></hi> or <hi rend="italic">Foxc2<hi rend="superscript">flox</hi></hi> mice crossed with <hi rend="italic">Cre</hi>‐deleter mice that are homozygous for the recombined allele (i.e., <hi rend="italic">Foxc1<hi rend="superscript">Δ/Δ</hi></hi> or <hi rend="italic">Foxc2<hi rend="superscript">Δ/Δ</hi></hi> embryos) lack expression of the corresponding gene and show the same developmental defects observed in conventional homozygous mutant embryos. We expect these conditional mutations to enable characterization of the cell‐type specific functions of Foxc1 and Foxc2 in development, disease, and adult animals. genesis 50:766–774, 2012. © 2012 Wiley Periodicals, Inc.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="kwd1">conditional knockout</term><term xml:id="kwd2">gene targeting</term><term xml:id="kwd3">Cre recombination</term><term xml:id="kwd4">Foxc1</term><term xml:id="kwd5">Foxc2</term></keywords><classCode scheme="articleCategory">Technology Report</classCode><classCode scheme="tocHeading1">Technology Reports</classCode></textClass><langUsage><language ident="EN"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/814AB4C97D2BAA7D95908A7B7F70742F780C0185/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: 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position="100"><doi origin="wiley" registered="yes">10.1002/dvg.v50.10</doi><numberingGroup><numbering type="journalVolume" number="50">50</numbering><numbering type="journalIssue">10</numbering></numberingGroup><coverDate startDate="2012-10">October 2012</coverDate></publicationMeta><publicationMeta level="unit" type="shortCommunication" position="70" status="forIssue"><doi origin="wiley" registered="yes">10.1002/dvg.22036</doi><idGroup><id type="unit" value="DVG22036"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="articleCategory">Technology Report</title><title type="tocHeading1">Technology Reports</title></titleGroup><copyright ownership="publisher">Copyright © 2012 Wiley Periodicals, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2011-11-28"></event><event type="manuscriptRevised" date="2012-04-10"></event><event type="manuscriptAccepted" date="2012-04-14"></event><event type="xmlConverted" 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href="file:DVG.DVG22036.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="5"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="40"></count><count type="wordTotal" number="7523"></count></countGroup><titleGroup><title type="main" xml:lang="en">Generation of conditional alleles for <i>Foxc1</i> and <i>Foxc2</i> in mice</title><title type="short" xml:lang="en">Generation of Conditional Alleles</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" noteRef="#fn1"><personName><givenNames>Amy</givenNames><familyName>Sasman</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1" noteRef="#fn1"><personName><givenNames>Carey</givenNames><familyName>Nassano‐Miller</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1" noteRef="#fn1"><personName><givenNames>Kyoo Seok</givenNames><familyName>Shim</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1" noteRef="#fn1"><personName><givenNames>Hyun Young</givenNames><familyName>Koo</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Ting</givenNames><familyName>Liu</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Kathryn M.</givenNames><familyName>Schultz</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Meredith</givenNames><familyName>Millay</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Atsushi</givenNames><familyName>Nanano</familyName></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Myengmo</givenNames><familyName>Kang</familyName></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Takashi</givenNames><familyName>Suzuki</familyName></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Tsutomu</givenNames><familyName>Kume</familyName></personName><contactDetails><email normalForm="t-kume@northwestern.edu">t‐kume@northwestern.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">conditional knockout</keyword><keyword xml:id="kwd2">gene targeting</keyword><keyword xml:id="kwd3">Cre recombination</keyword><keyword xml:id="kwd4">Foxc1</keyword><keyword xml:id="kwd5">Foxc2</keyword></keywordGroup><fundingInfo><fundingAgency>US National Institutes of Health (NIH)</fundingAgency><fundingNumber>HL074121</fundingNumber><fundingNumber>EY019484</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The Forkhead box transcription factors, Foxc1 and Foxc2, are crucial for development of the eye, cardiovascular network, and other physiological systems, but their cell‐type specific and postdevelopmental functions are unknown, in part because conventional (i.e., whole‐organism) homozygous‐null mutations of either factor result in perinatal death. Here, we describe the generation of mice with conditional‐null <i>Foxc1<sup>flox</sup></i> and <i>Foxc2<sup>flox</sup></i> mutations that are induced via Cre‐mediated recombination. Mice homozygous for the unrecombined alleles are viable and fertile, indicating that the conditional alleles retain their wild‐type function. The embryos of <i>Foxc1<sup>flox</sup></i> or <i>Foxc2<sup>flox</sup></i> mice crossed with <i>Cre</i>‐deleter mice that are homozygous for the recombined allele (i.e., <i>Foxc1<sup>Δ/Δ</sup></i> or <i>Foxc2<sup>Δ/Δ</sup></i> embryos) lack expression of the corresponding gene and show the same developmental defects observed in conventional homozygous mutant embryos. We expect these conditional mutations to enable characterization of the cell‐type specific functions of Foxc1 and Foxc2 in development, disease, and adult animals. genesis 50:766–774, 2012. © 2012 Wiley Periodicals, Inc.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>A.S., C.N.‐M., K.S.S., and H.Y.K. contributed equally to this work</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Generation of conditional alleles for Foxc1 and Foxc2 in mice</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Generation of Conditional Alleles</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Generation of conditional alleles for Foxc1 and Foxc2 in mice</title></titleInfo><name type="personal"><namePart type="given">Amy</namePart><namePart type="family">Sasman</namePart><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</affiliation><description>A.S., C.N.‐M., K.S.S., and H.Y.K. contributed equally to this work</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carey</namePart><namePart type="family">Nassano‐Miller</namePart><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</affiliation><description>A.S., C.N.‐M., K.S.S., and H.Y.K. contributed equally to this work</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kyoo Seok</namePart><namePart type="family">Shim</namePart><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</affiliation><description>A.S., C.N.‐M., K.S.S., and H.Y.K. contributed equally to this work</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hyun Young</namePart><namePart type="family">Koo</namePart><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</affiliation><description>A.S., C.N.‐M., K.S.S., and H.Y.K. contributed equally to this work</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ting</namePart><namePart type="family">Liu</namePart><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kathryn M.</namePart><namePart type="family">Schultz</namePart><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Meredith</namePart><namePart type="family">Millay</namePart><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Atsushi</namePart><namePart type="family">Nanano</namePart><affiliation>Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Myengmo</namePart><namePart type="family">Kang</namePart><affiliation>Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takashi</namePart><namePart type="family">Suzuki</namePart><affiliation>Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tsutomu</namePart><namePart type="family">Kume</namePart><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</affiliation><affiliation>Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, 303E Chicago Ave, Chicago, IL 60611</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief-communication" displayLabel="shortCommunication"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2012-10</dateIssued><dateCaptured encoding="w3cdtf">2011-11-28</dateCaptured><dateValid encoding="w3cdtf">2012-04-14</dateValid><copyrightDate encoding="w3cdtf">2012</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent><extent unit="references">40</extent><extent unit="words">7523</extent></physicalDescription><abstract lang="en">The Forkhead box transcription factors, Foxc1 and Foxc2, are crucial for development of the eye, cardiovascular network, and other physiological systems, but their cell‐type specific and postdevelopmental functions are unknown, in part because conventional (i.e., whole‐organism) homozygous‐null mutations of either factor result in perinatal death. Here, we describe the generation of mice with conditional‐null Foxc1flox and Foxc2flox mutations that are induced via Cre‐mediated recombination. Mice homozygous for the unrecombined alleles are viable and fertile, indicating that the conditional alleles retain their wild‐type function. The embryos of Foxc1flox or Foxc2flox mice crossed with Cre‐deleter mice that are homozygous for the recombined allele (i.e., Foxc1Δ/Δ or Foxc2Δ/Δ embryos) lack expression of the corresponding gene and show the same developmental defects observed in conventional homozygous mutant embryos. We expect these conditional mutations to enable characterization of the cell‐type specific functions of Foxc1 and Foxc2 in development, disease, and adult animals. genesis 50:766–774, 2012. © 2012 Wiley Periodicals, Inc.</abstract><note type="funding">US National Institutes of Health (NIH) - No. HL074121; No. EY019484; </note><subject lang="en"><genre>keywords</genre><topic>conditional knockout</topic><topic>gene targeting</topic><topic>Cre recombination</topic><topic>Foxc1</topic><topic>Foxc2</topic></subject><relatedItem type="host"><titleInfo><title>genesis</title></titleInfo><titleInfo type="abbreviated"><title>Genesis</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Technology Report</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>2012</date><detail type="volume"><caption>vol.</caption><number>50</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>766</start><end>774</end><total>9</total></extent></part></relatedItem><relatedItem type="preceding"><titleInfo><title>Developmental Genetics</title></titleInfo><identifier type="ISSN">0192-253X</identifier><part><date point="end">1999</date><detail type="volume"><caption>last vol.</caption><number>25</number></detail><detail type="issue"><caption>last no.</caption><number>4</number></detail></part></relatedItem><identifier type="istex">814AB4C97D2BAA7D95908A7B7F70742F780C0185</identifier><identifier type="DOI">10.1002/dvg.22036</identifier><identifier type="ArticleID">DVG22036</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2012 Wiley Periodicals, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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