Head formation: OTX2 regulates Dkk1 and Lhx1 activity in the anterior mesendoderm.
Identifieur interne : 003318 ( PubMed/Curation ); précédent : 003317; suivant : 003319Head formation: OTX2 regulates Dkk1 and Lhx1 activity in the anterior mesendoderm.
Auteurs : Chi Kin Ip [Australie] ; Nicolas Fossat [Australie] ; Vanessa Jones [Australie] ; Thomas Lamonerie [France] ; Patrick P L. Tam [Australie]Source :
- Development (Cambridge, England) [ 1477-9129 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Cellules 3T3, Croisements génétiques, Facteurs de transcription (métabolisme), Facteurs de transcription Otx (physiologie), Luciferases (métabolisme), Mutation, Mésoderme (physiologie), Phénotype, Protéines et peptides de signalisation intercellulaire (métabolisme), Protéines à homéodomaine LIM (métabolisme), Régulation de l'expression des gènes au cours du développement, Souris, Tête (embryologie).
- MESH :
- embryologie : Tête.
- métabolisme : Facteurs de transcription, Luciferases, Protéines et peptides de signalisation intercellulaire, Protéines à homéodomaine LIM.
- physiologie : Facteurs de transcription Otx, Mésoderme.
- Animaux, Cellules 3T3, Croisements génétiques, Mutation, Phénotype, Régulation de l'expression des gènes au cours du développement, Souris.
English descriptors
- KwdEn :
- 3T3 Cells, Animals, Crosses, Genetic, Gene Expression Regulation, Developmental, Head (embryology), Intercellular Signaling Peptides and Proteins (metabolism), LIM-Homeodomain Proteins (metabolism), Luciferases (metabolism), Mesoderm (physiology), Mice, Mutation, Otx Transcription Factors (physiology), Phenotype, Transcription Factors (metabolism).
- MESH :
- chemical , metabolism : Intercellular Signaling Peptides and Proteins, LIM-Homeodomain Proteins, Luciferases, Transcription Factors.
- embryology : Head.
- physiology : Mesoderm, Otx Transcription Factors.
- 3T3 Cells, Animals, Crosses, Genetic, Gene Expression Regulation, Developmental, Mice, Mutation, Phenotype.
Abstract
The Otx2 gene encodes a paired-type homeobox transcription factor that is essential for the induction and the patterning of the anterior structures in the mouse embryo. Otx2 knockout embryos fail to form a head. Whereas previous studies have shown that Otx2 is required in the anterior visceral endoderm and the anterior neuroectoderm for head formation, its role in the anterior mesendoderm (AME) has not been assessed specifically. Here, we show that tissue-specific ablation of Otx2 in the AME phenocopies the truncation of the embryonic head of the Otx2 null mutant. Expression of Dkk1 and Lhx1, two genes that are also essential for head formation, is disrupted in the AME of the conditional Otx2-deficient embryos. Consistent with the fact that Dkk1 is a direct target of OTX2, we showed that OTX2 can interact with the H1 regulatory region of Dkk1 to activate its expression. Cross-species comparative analysis, RT-qPCR, ChIP-qPCR and luciferase assays have revealed two conserved regions in the Lhx1 locus to which OTX2 can bind to activate Lhx1 expression. Abnormal development of the embryonic head in Otx2;Lhx1 and Otx2;Dkk1 compound mutant embryos highlights the functional intersection of Otx2, Dkk1 and Lhx1 in the AME for head formation.
DOI: 10.1242/dev.114900
PubMed: 25231759
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Otx2 knockout embryos fail to form a head. Whereas previous studies have shown that Otx2 is required in the anterior visceral endoderm and the anterior neuroectoderm for head formation, its role in the anterior mesendoderm (AME) has not been assessed specifically. Here, we show that tissue-specific ablation of Otx2 in the AME phenocopies the truncation of the embryonic head of the Otx2 null mutant. Expression of Dkk1 and Lhx1, two genes that are also essential for head formation, is disrupted in the AME of the conditional Otx2-deficient embryos. Consistent with the fact that Dkk1 is a direct target of OTX2, we showed that OTX2 can interact with the H1 regulatory region of Dkk1 to activate its expression. Cross-species comparative analysis, RT-qPCR, ChIP-qPCR and luciferase assays have revealed two conserved regions in the Lhx1 locus to which OTX2 can bind to activate Lhx1 expression. Abnormal development of the embryonic head in Otx2;Lhx1 and Otx2;Dkk1 compound mutant embryos highlights the functional intersection of Otx2, Dkk1 and Lhx1 in the AME for head formation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25231759</PMID><DateCreated><Year>2014</Year><Month>10</Month><Day>08</Day></DateCreated><DateCompleted><Year>2014</Year><Month>12</Month><Day>09</Day></DateCompleted><DateRevised><Year>2014</Year><Month>10</Month><Day>08</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1477-9129</ISSN><JournalIssue CitedMedium="Internet"><Volume>141</Volume><Issue>20</Issue><PubDate><Year>2014</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Development (Cambridge, England)</Title><ISOAbbreviation>Development</ISOAbbreviation></Journal><ArticleTitle>Head formation: OTX2 regulates Dkk1 and Lhx1 activity in the anterior mesendoderm.</ArticleTitle><Pagination><MedlinePgn>3859-67</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1242/dev.114900</ELocationID><Abstract><AbstractText>The Otx2 gene encodes a paired-type homeobox transcription factor that is essential for the induction and the patterning of the anterior structures in the mouse embryo. Otx2 knockout embryos fail to form a head. Whereas previous studies have shown that Otx2 is required in the anterior visceral endoderm and the anterior neuroectoderm for head formation, its role in the anterior mesendoderm (AME) has not been assessed specifically. Here, we show that tissue-specific ablation of Otx2 in the AME phenocopies the truncation of the embryonic head of the Otx2 null mutant. Expression of Dkk1 and Lhx1, two genes that are also essential for head formation, is disrupted in the AME of the conditional Otx2-deficient embryos. Consistent with the fact that Dkk1 is a direct target of OTX2, we showed that OTX2 can interact with the H1 regulatory region of Dkk1 to activate its expression. Cross-species comparative analysis, RT-qPCR, ChIP-qPCR and luciferase assays have revealed two conserved regions in the Lhx1 locus to which OTX2 can bind to activate Lhx1 expression. Abnormal development of the embryonic head in Otx2;Lhx1 and Otx2;Dkk1 compound mutant embryos highlights the functional intersection of Otx2, Dkk1 and Lhx1 in the AME for head formation.</AbstractText><CopyrightInformation>© 2014. Published by The Company of Biologists Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ip</LastName><ForeName>Chi Kin</ForeName><Initials>CK</Initials><AffiliationInfo><Affiliation>Embryology Unit, Children's Medical Research Institute, Locked Bag 23, Wentworthville, New South Wales 2145, Australia Discipline of Medicine, Sydney Medical School, University of Sydney, New South Wales 2006, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fossat</LastName><ForeName>Nicolas</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Embryology Unit, Children's Medical Research Institute, Locked Bag 23, Wentworthville, New South Wales 2145, Australia Discipline of Medicine, Sydney Medical School, University of Sydney, New South Wales 2006, Australia nfossat@cmri.org.au.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jones</LastName><ForeName>Vanessa</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Embryology Unit, Children's Medical Research Institute, Locked Bag 23, Wentworthville, New South Wales 2145, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lamonerie</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Equipe Neurodéveloppement, Institut de Biologie Valrose, UMR UNS/CNRS 7277/INSERM 1091, Université Nice Sophia Antipolis, Parc Valrose, 06108 Nice cedex 2, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tam</LastName><ForeName>Patrick P L</ForeName><Initials>PP</Initials><AffiliationInfo><Affiliation>Embryology Unit, Children's Medical Research Institute, Locked Bag 23, Wentworthville, New South Wales 2145, Australia Discipline of Medicine, Sydney Medical School, University of Sydney, New South Wales 2006, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>09</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Development</MedlineTA><NlmUniqueID>8701744</NlmUniqueID><ISSNLinking>0950-1991</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C501127">Dkk1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D036341">Intercellular Signaling Peptides and Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D060850">LIM-Homeodomain Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C499523">Lhx1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051857">Otx Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C497660">Otx2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.13.12.-</RegistryNumber><NameOfSubstance UI="D008156">Luciferases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D016475" MajorTopicYN="N">3T3 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003433" MajorTopicYN="N">Crosses, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018507" MajorTopicYN="Y">Gene Expression Regulation, Developmental</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006257" MajorTopicYN="N">Head</DescriptorName><QualifierName UI="Q000196" MajorTopicYN="Y">embryology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D036341" MajorTopicYN="N">Intercellular Signaling Peptides and Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D060850" MajorTopicYN="N">LIM-Homeodomain Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008156" MajorTopicYN="N">Luciferases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008648" MajorTopicYN="N">Mesoderm</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051857" MajorTopicYN="N">Otx Transcription Factors</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Anterior mesendoderm</Keyword><Keyword MajorTopicYN="N">Dkk1</Keyword><Keyword MajorTopicYN="N">Head formation</Keyword><Keyword MajorTopicYN="N">Lhx1</Keyword><Keyword MajorTopicYN="N">Mouse</Keyword><Keyword MajorTopicYN="N">Otx2</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>9</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>9</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25231759</ArticleId><ArticleId IdType="pii">dev.114900</ArticleId><ArticleId IdType="doi">10.1242/dev.114900</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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