GATA2 is required for lymphatic vessel valve development and maintenance.
Identifieur interne : 000D50 ( PubMed/Curation ); précédent : 000D49; suivant : 000D51GATA2 is required for lymphatic vessel valve development and maintenance.
Auteurs : Jan Kazenwadel ; Kelly L. Betterman ; Chan-Eng Chong ; Philippa H. Stokes ; Young K. Lee ; Genevieve A. Secker ; Yan Agalarov ; Cansaran Saygili Demir ; David M. Lawrence ; Drew L. Sutton ; Sebastien P. Tabruyn ; Naoyuki Miura ; Marjo Salminen ; Tatiana V. Petrova ; Jacqueline M. Matthews ; Christopher N. Hahn ; Hamish S. Scott ; Natasha L. HarveySource :
- The Journal of clinical investigation [ 1558-8238 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux, Cellules K562, Délétion de gène, Facteur de transcription GATA-2 (génétique), Facteur de transcription GATA-2 (métabolisme), Facteurs de transcription Forkhead (génétique), Facteurs de transcription Forkhead (métabolisme), Facteurs de transcription NFATC (génétique), Facteurs de transcription NFATC (métabolisme), Humains, Lymphoedème (anatomopathologie), Lymphoedème (embryologie), Lymphoedème (génétique), Mutation, Protéines suppresseurs de tumeurs (génétique), Protéines suppresseurs de tumeurs (métabolisme), Protéines à homéodomaine (génétique), Protéines à homéodomaine (métabolisme), Souris, Vaisseaux lymphatiques (anatomopathologie), Vaisseaux lymphatiques (embryologie), Éléments activateurs (génétique).
- MESH :
- anatomopathologie : Lymphoedème, Vaisseaux lymphatiques.
- embryologie : Lymphoedème, Vaisseaux lymphatiques.
- génétique : Facteur de transcription GATA-2, Facteurs de transcription Forkhead, Facteurs de transcription NFATC, Lymphoedème, Protéines suppresseurs de tumeurs, Protéines à homéodomaine.
- métabolisme : Facteur de transcription GATA-2, Facteurs de transcription Forkhead, Facteurs de transcription NFATC, Protéines suppresseurs de tumeurs, Protéines à homéodomaine.
- Animaux, Cellules K562, Délétion de gène, Humains, Mutation, Souris, Éléments activateurs (génétique).
English descriptors
- KwdEn :
- Animals, Enhancer Elements, Genetic, Forkhead Transcription Factors (genetics), Forkhead Transcription Factors (metabolism), GATA2 Transcription Factor (genetics), GATA2 Transcription Factor (metabolism), Gene Deletion, Homeodomain Proteins (genetics), Homeodomain Proteins (metabolism), Humans, K562 Cells, Lymphatic Vessels (embryology), Lymphatic Vessels (pathology), Lymphedema (embryology), Lymphedema (genetics), Lymphedema (pathology), Mice, Mutation, NFATC Transcription Factors (genetics), NFATC Transcription Factors (metabolism), Tumor Suppressor Proteins (genetics), Tumor Suppressor Proteins (metabolism).
- MESH :
- chemical , genetics : Forkhead Transcription Factors, GATA2 Transcription Factor, Homeodomain Proteins, NFATC Transcription Factors, Tumor Suppressor Proteins.
- chemical , metabolism : Forkhead Transcription Factors, GATA2 Transcription Factor, Homeodomain Proteins, NFATC Transcription Factors, Tumor Suppressor Proteins.
- embryology : Lymphatic Vessels, Lymphedema.
- genetics : Lymphedema.
- pathology : Lymphatic Vessels, Lymphedema.
- Animals, Enhancer Elements, Genetic, Gene Deletion, Humans, K562 Cells, Mice, Mutation.
Abstract
Heterozygous germline mutations in the zinc finger transcription factor GATA2 have recently been shown to underlie a range of clinical phenotypes, including Emberger syndrome, a disorder characterized by lymphedema and predisposition to myelodysplastic syndrome/acute myeloid leukemia (MDS/AML). Despite well-defined roles in hematopoiesis, the functions of GATA2 in the lymphatic vasculature and the mechanisms by which GATA2 mutations result in lymphedema have not been characterized. Here, we have provided a molecular explanation for lymphedema predisposition in a subset of patients with germline GATA2 mutations. Specifically, we demonstrated that Emberger-associated GATA2 missense mutations result in complete loss of GATA2 function, with respect to the capacity to regulate the transcription of genes that are important for lymphatic vessel valve development. We identified a putative enhancer element upstream of the key lymphatic transcriptional regulator PROX1 that is bound by GATA2, and the transcription factors FOXC2 and NFATC1. Emberger GATA2 missense mutants had a profoundly reduced capacity to bind this element. Conditional Gata2 deletion in mice revealed that GATA2 is required for both development and maintenance of lymphovenous and lymphatic vessel valves. Together, our data unveil essential roles for GATA2 in the lymphatic vasculature and explain why a select catalogue of human GATA2 mutations results in lymphedema.
DOI: 10.1172/JCI78888
PubMed: 26214525
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Betterman</name></author><author><name sortKey="Chong, Chan Eng" sort="Chong, Chan Eng" uniqKey="Chong C" first="Chan-Eng" last="Chong">Chan-Eng Chong</name></author><author><name sortKey="Stokes, Philippa H" sort="Stokes, Philippa H" uniqKey="Stokes P" first="Philippa H" last="Stokes">Philippa H. Stokes</name></author><author><name sortKey="Lee, Young K" sort="Lee, Young K" uniqKey="Lee Y" first="Young K" last="Lee">Young K. Lee</name></author><author><name sortKey="Secker, Genevieve A" sort="Secker, Genevieve A" uniqKey="Secker G" first="Genevieve A" last="Secker">Genevieve A. Secker</name></author><author><name sortKey="Agalarov, Yan" sort="Agalarov, Yan" uniqKey="Agalarov Y" first="Yan" last="Agalarov">Yan Agalarov</name></author><author><name sortKey="Demir, Cansaran Saygili" sort="Demir, Cansaran Saygili" uniqKey="Demir C" first="Cansaran Saygili" last="Demir">Cansaran Saygili Demir</name></author><author><name sortKey="Lawrence, David M" sort="Lawrence, David M" uniqKey="Lawrence D" first="David M" last="Lawrence">David M. Lawrence</name></author><author><name sortKey="Sutton, Drew L" sort="Sutton, Drew L" uniqKey="Sutton D" first="Drew L" last="Sutton">Drew L. Sutton</name></author><author><name sortKey="Tabruyn, Sebastien P" sort="Tabruyn, Sebastien P" uniqKey="Tabruyn S" first="Sebastien P" last="Tabruyn">Sebastien P. Tabruyn</name></author><author><name sortKey="Miura, Naoyuki" sort="Miura, Naoyuki" uniqKey="Miura N" first="Naoyuki" last="Miura">Naoyuki Miura</name></author><author><name sortKey="Salminen, Marjo" sort="Salminen, Marjo" uniqKey="Salminen M" first="Marjo" last="Salminen">Marjo Salminen</name></author><author><name sortKey="Petrova, Tatiana V" sort="Petrova, Tatiana V" uniqKey="Petrova T" first="Tatiana V" last="Petrova">Tatiana V. Petrova</name></author><author><name sortKey="Matthews, Jacqueline M" sort="Matthews, Jacqueline M" uniqKey="Matthews J" first="Jacqueline M" last="Matthews">Jacqueline M. Matthews</name></author><author><name sortKey="Hahn, Christopher N" sort="Hahn, Christopher N" uniqKey="Hahn C" first="Christopher N" last="Hahn">Christopher N. Hahn</name></author><author><name sortKey="Scott, Hamish S" sort="Scott, Hamish S" uniqKey="Scott H" first="Hamish S" last="Scott">Hamish S. Scott</name></author><author><name sortKey="Harvey, Natasha L" sort="Harvey, Natasha L" uniqKey="Harvey N" first="Natasha L" last="Harvey">Natasha L. Harvey</name></author></analytic><series><title level="j">The Journal of clinical investigation</title><idno type="eISSN">1558-8238</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Enhancer Elements, Genetic</term><term>Forkhead Transcription Factors (genetics)</term><term>Forkhead Transcription Factors (metabolism)</term><term>GATA2 Transcription Factor (genetics)</term><term>GATA2 Transcription Factor (metabolism)</term><term>Gene Deletion</term><term>Homeodomain Proteins (genetics)</term><term>Homeodomain Proteins (metabolism)</term><term>Humans</term><term>K562 Cells</term><term>Lymphatic Vessels (embryology)</term><term>Lymphatic Vessels (pathology)</term><term>Lymphedema (embryology)</term><term>Lymphedema (genetics)</term><term>Lymphedema (pathology)</term><term>Mice</term><term>Mutation</term><term>NFATC Transcription Factors (genetics)</term><term>NFATC Transcription Factors (metabolism)</term><term>Tumor Suppressor Proteins (genetics)</term><term>Tumor Suppressor Proteins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Cellules K562</term><term>Délétion de gène</term><term>Facteur de transcription GATA-2 (génétique)</term><term>Facteur de transcription GATA-2 (métabolisme)</term><term>Facteurs de transcription Forkhead (génétique)</term><term>Facteurs de transcription Forkhead (métabolisme)</term><term>Facteurs de transcription NFATC (génétique)</term><term>Facteurs de transcription NFATC (métabolisme)</term><term>Humains</term><term>Lymphoedème (anatomopathologie)</term><term>Lymphoedème (embryologie)</term><term>Lymphoedème (génétique)</term><term>Mutation</term><term>Protéines suppresseurs de tumeurs (génétique)</term><term>Protéines suppresseurs de tumeurs (métabolisme)</term><term>Protéines à homéodomaine (génétique)</term><term>Protéines à homéodomaine (métabolisme)</term><term>Souris</term><term>Vaisseaux lymphatiques (anatomopathologie)</term><term>Vaisseaux lymphatiques (embryologie)</term><term>Éléments activateurs (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Forkhead Transcription Factors</term><term>GATA2 Transcription Factor</term><term>Homeodomain Proteins</term><term>NFATC Transcription Factors</term><term>Tumor Suppressor Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Forkhead Transcription Factors</term><term>GATA2 Transcription Factor</term><term>Homeodomain Proteins</term><term>NFATC Transcription Factors</term><term>Tumor Suppressor Proteins</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Lymphoedème</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="embryologie" xml:lang="fr"><term>Lymphoedème</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="embryology" xml:lang="en"><term>Lymphatic Vessels</term><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur de transcription GATA-2</term><term>Facteurs de transcription Forkhead</term><term>Facteurs de transcription NFATC</term><term>Lymphoedème</term><term>Protéines suppresseurs de tumeurs</term><term>Protéines à homéodomaine</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de transcription GATA-2</term><term>Facteurs de transcription Forkhead</term><term>Facteurs de transcription NFATC</term><term>Protéines suppresseurs de tumeurs</term><term>Protéines à homéodomaine</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lymphatic Vessels</term><term>Lymphedema</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Enhancer Elements, Genetic</term><term>Gene Deletion</term><term>Humans</term><term>K562 Cells</term><term>Mice</term><term>Mutation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules K562</term><term>Délétion de gène</term><term>Humains</term><term>Mutation</term><term>Souris</term><term>Éléments activateurs (génétique)</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Heterozygous germline mutations in the zinc finger transcription factor GATA2 have recently been shown to underlie a range of clinical phenotypes, including Emberger syndrome, a disorder characterized by lymphedema and predisposition to myelodysplastic syndrome/acute myeloid leukemia (MDS/AML). Despite well-defined roles in hematopoiesis, the functions of GATA2 in the lymphatic vasculature and the mechanisms by which GATA2 mutations result in lymphedema have not been characterized. Here, we have provided a molecular explanation for lymphedema predisposition in a subset of patients with germline GATA2 mutations. Specifically, we demonstrated that Emberger-associated GATA2 missense mutations result in complete loss of GATA2 function, with respect to the capacity to regulate the transcription of genes that are important for lymphatic vessel valve development. We identified a putative enhancer element upstream of the key lymphatic transcriptional regulator PROX1 that is bound by GATA2, and the transcription factors FOXC2 and NFATC1. Emberger GATA2 missense mutants had a profoundly reduced capacity to bind this element. Conditional Gata2 deletion in mice revealed that GATA2 is required for both development and maintenance of lymphovenous and lymphatic vessel valves. Together, our data unveil essential roles for GATA2 in the lymphatic vasculature and explain why a select catalogue of human GATA2 mutations results in lymphedema.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26214525</PMID><DateCreated><Year>2015</Year><Month>08</Month><Day>04</Day></DateCreated><DateCompleted><Year>2015</Year><Month>10</Month><Day>23</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1558-8238</ISSN><JournalIssue CitedMedium="Internet"><Volume>125</Volume><Issue>8</Issue><PubDate><Year>2015</Year><Month>Aug</Month><Day>03</Day></PubDate></JournalIssue><Title>The Journal of clinical investigation</Title><ISOAbbreviation>J. Clin. Invest.</ISOAbbreviation></Journal><ArticleTitle>GATA2 is required for lymphatic vessel valve development and maintenance.</ArticleTitle><Pagination><MedlinePgn>2979-94</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1172/JCI78888</ELocationID><ELocationID EIdType="pii" ValidYN="Y">78888</ELocationID><Abstract><AbstractText>Heterozygous germline mutations in the zinc finger transcription factor GATA2 have recently been shown to underlie a range of clinical phenotypes, including Emberger syndrome, a disorder characterized by lymphedema and predisposition to myelodysplastic syndrome/acute myeloid leukemia (MDS/AML). Despite well-defined roles in hematopoiesis, the functions of GATA2 in the lymphatic vasculature and the mechanisms by which GATA2 mutations result in lymphedema have not been characterized. Here, we have provided a molecular explanation for lymphedema predisposition in a subset of patients with germline GATA2 mutations. Specifically, we demonstrated that Emberger-associated GATA2 missense mutations result in complete loss of GATA2 function, with respect to the capacity to regulate the transcription of genes that are important for lymphatic vessel valve development. We identified a putative enhancer element upstream of the key lymphatic transcriptional regulator PROX1 that is bound by GATA2, and the transcription factors FOXC2 and NFATC1. Emberger GATA2 missense mutants had a profoundly reduced capacity to bind this element. Conditional Gata2 deletion in mice revealed that GATA2 is required for both development and maintenance of lymphovenous and lymphatic vessel valves. Together, our data unveil essential roles for GATA2 in the lymphatic vasculature and explain why a select catalogue of human GATA2 mutations results in lymphedema.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kazenwadel</LastName><ForeName>Jan</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Betterman</LastName><ForeName>Kelly L</ForeName><Initials>KL</Initials></Author><Author ValidYN="Y"><LastName>Chong</LastName><ForeName>Chan-Eng</ForeName><Initials>CE</Initials></Author><Author ValidYN="Y"><LastName>Stokes</LastName><ForeName>Philippa H</ForeName><Initials>PH</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Young K</ForeName><Initials>YK</Initials></Author><Author ValidYN="Y"><LastName>Secker</LastName><ForeName>Genevieve A</ForeName><Initials>GA</Initials></Author><Author ValidYN="Y"><LastName>Agalarov</LastName><ForeName>Yan</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Demir</LastName><ForeName>Cansaran Saygili</ForeName><Initials>CS</Initials></Author><Author ValidYN="Y"><LastName>Lawrence</LastName><ForeName>David M</ForeName><Initials>DM</Initials></Author><Author ValidYN="Y"><LastName>Sutton</LastName><ForeName>Drew L</ForeName><Initials>DL</Initials></Author><Author ValidYN="Y"><LastName>Tabruyn</LastName><ForeName>Sebastien P</ForeName><Initials>SP</Initials></Author><Author ValidYN="Y"><LastName>Miura</LastName><ForeName>Naoyuki</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Salminen</LastName><ForeName>Marjo</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Petrova</LastName><ForeName>Tatiana V</ForeName><Initials>TV</Initials></Author><Author ValidYN="Y"><LastName>Matthews</LastName><ForeName>Jacqueline M</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Hahn</LastName><ForeName>Christopher N</ForeName><Initials>CN</Initials></Author><Author ValidYN="Y"><LastName>Scott</LastName><ForeName>Hamish S</ForeName><Initials>HS</Initials></Author><Author ValidYN="Y"><LastName>Harvey</LastName><ForeName>Natasha L</ForeName><Initials>NL</Initials></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>BioProject</DataBankName><AccessionNumberList><AccessionNumber>PRJEB9436</AccessionNumber></AccessionNumberList></DataBank></DataBankList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>07</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Clin Invest</MedlineTA><NlmUniqueID>7802877</NlmUniqueID><ISSNLinking>0021-9738</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051858">Forkhead Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050989">GATA2 Transcription Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494711">GATA2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494712">Gata2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018398">Homeodomain Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050778">NFATC Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494003">NFATC1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494005">Nfatc1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D025521">Tumor Suppressor Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C082078">mesenchyme fork head 1 protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C102225">prospero-related homeobox 1 protein</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Dev Biol. 2014 Feb 1;386(1):25-33</RefSource><PMID Version="1">24361262</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Blood. 2014 Feb 6;123(6):809-21</RefSource><PMID Version="1">24227816</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2014 Jan;124(1):273-84</RefSource><PMID 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Source="NLM">PMC4563742</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>09</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>05</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>7</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>7</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>10</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26214525</ArticleId><ArticleId IdType="pii">78888</ArticleId><ArticleId IdType="doi">10.1172/JCI78888</ArticleId><ArticleId IdType="pmc">PMC4563742</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix 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