WT1 controls antagonistic FGF and BMP-pSMAD pathways in early renal progenitors.
Identifieur interne : 003644 ( PubMed/Corpus ); précédent : 003643; suivant : 003645WT1 controls antagonistic FGF and BMP-pSMAD pathways in early renal progenitors.
Auteurs : Fariba Jian Motamedi ; Danielle A. Badro ; Michael Clarkson ; M Rita Lecca ; Stephen T. Bradford ; Fabian A. Buske ; Kathrin Saar ; Norbert Hübner ; André W. Br Ndli ; Andreas SchedlSource :
- Nature communications [ 2041-1723 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Bone Morphogenetic Proteins (genetics), Bone Morphogenetic Proteins (metabolism), Cell Differentiation (genetics), Cell Differentiation (physiology), Computational Biology, Fibroblast Growth Factors (genetics), Fibroblast Growth Factors (metabolism), Fluorescent Antibody Technique, Gene Expression Regulation, Developmental (genetics), Gene Expression Regulation, Developmental (physiology), In Situ Hybridization, In Situ Nick-End Labeling, Mice, Mice, Mutant Strains, Organ Culture Techniques, Repressor Proteins (genetics), Repressor Proteins (metabolism), Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction (genetics), Signal Transduction (physiology), Stem Cells (metabolism).
- MESH :
- chemical , genetics : Bone Morphogenetic Proteins, Fibroblast Growth Factors, Repressor Proteins.
- chemical , metabolism : Bone Morphogenetic Proteins, Fibroblast Growth Factors, Repressor Proteins.
- genetics : Cell Differentiation, Gene Expression Regulation, Developmental, Signal Transduction.
- metabolism : Stem Cells.
- physiology : Cell Differentiation, Gene Expression Regulation, Developmental, Signal Transduction.
- Animals, Computational Biology, Fluorescent Antibody Technique, In Situ Hybridization, In Situ Nick-End Labeling, Mice, Mice, Mutant Strains, Organ Culture Techniques, Reverse Transcriptase Polymerase Chain Reaction.
Abstract
Kidney organogenesis requires the tight control of proliferation, differentiation and apoptosis of renal progenitor cells. How the balance between these cellular decisions is achieved remains elusive. The Wilms' tumour suppressor Wt1 is required for progenitor survival, but the molecular cause for renal agenesis in mutants is poorly understood. Here we demonstrate that lack of Wt1 abolishes fibroblast growth factor (FGF) and induces BMP/pSMAD signalling within the metanephric mesenchyme. Addition of recombinant FGFs or inhibition of pSMAD signalling rescues progenitor cell apoptosis induced by the loss of Wt1. We further show that recombinant BMP4, but not BMP7, induces an apoptotic response within the early kidney that can be suppressed by simultaneous addition of FGFs. These data reveal a hitherto unknown sensitivity of early renal progenitors to pSMAD signalling, establishes FGF and pSMAD signalling as antagonistic forces in early kidney development and places WT1 as a key regulator of pro-survival FGF signalling pathway genes.
DOI: 10.1038/ncomms5444
PubMed: 25031030
Links to Exploration step
pubmed:25031030Le document en format XML
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Br Ndli</name><affiliation><nlm:affiliation>1] Institute of Pharmaceutical Sciences, Department of Chemistry and Applied Biosciences, ETH Zurich, Zurich, Switzerland [2] Walter Brendel Center of Experimental Medicine, Ludwig-Maximilians-University, 81377 Munich, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Schedl, Andreas" sort="Schedl, Andreas" uniqKey="Schedl A" first="Andreas" last="Schedl">Andreas Schedl</name><affiliation><nlm:affiliation>1] Institute of Biology Valrose, Université de Nice-Sophia, F-06108 Nice, France [2] Inserm, UMR1091, F-06108 Nice, France [3] CNRS, UMR7277, F-06108 Nice, France.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:25031030</idno><idno type="pmid">25031030</idno><idno type="doi">10.1038/ncomms5444</idno><idno type="wicri:Area/PubMed/Corpus">003644</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">003644</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">WT1 controls antagonistic FGF and BMP-pSMAD pathways in early renal progenitors.</title><author><name sortKey="Motamedi, Fariba Jian" sort="Motamedi, Fariba Jian" uniqKey="Motamedi F" first="Fariba Jian" last="Motamedi">Fariba Jian Motamedi</name><affiliation><nlm:affiliation>1] Institute of Biology Valrose, Université de Nice-Sophia, F-06108 Nice, France [2] Inserm, UMR1091, F-06108 Nice, France [3] CNRS, UMR7277, F-06108 Nice, France [4].</nlm:affiliation></affiliation></author><author><name sortKey="Badro, Danielle A" sort="Badro, Danielle A" uniqKey="Badro D" first="Danielle A" last="Badro">Danielle A. Badro</name><affiliation><nlm:affiliation>1] Institute of Biology Valrose, Université de Nice-Sophia, F-06108 Nice, France [2] Inserm, UMR1091, F-06108 Nice, France [3] CNRS, UMR7277, F-06108 Nice, France [4].</nlm:affiliation></affiliation></author><author><name sortKey="Clarkson, Michael" sort="Clarkson, Michael" uniqKey="Clarkson M" first="Michael" last="Clarkson">Michael Clarkson</name><affiliation><nlm:affiliation>1] Institute of Biology Valrose, Université de Nice-Sophia, F-06108 Nice, France [2] Inserm, UMR1091, F-06108 Nice, France [3] CNRS, UMR7277, F-06108 Nice, France [4].</nlm:affiliation></affiliation></author><author><name sortKey="Lecca, M Rita" sort="Lecca, M Rita" uniqKey="Lecca M" first="M Rita" last="Lecca">M Rita Lecca</name><affiliation><nlm:affiliation>1] Institute of Pharmaceutical Sciences, Department of Chemistry and Applied Biosciences, ETH Zurich, Zurich, Switzerland [2] Functional Genomics Center Zurich, UZH/ETH Zurich, CH-8057 Zurich, Switzerland.</nlm:affiliation></affiliation></author><author><name sortKey="Bradford, Stephen T" sort="Bradford, Stephen T" uniqKey="Bradford S" first="Stephen T" last="Bradford">Stephen T. Bradford</name><affiliation><nlm:affiliation>1] Institute of Biology Valrose, Université de Nice-Sophia, F-06108 Nice, France [2] Inserm, UMR1091, F-06108 Nice, France [3] CNRS, UMR7277, F-06108 Nice, France [4] Garvan Institute of Medical Research, Darlinghurst, New South Wales 2010, Australia [5] CSIRO Animal, Food & Health Sciences, Preventative Health Flagship, North Ryde, New South Wales 2113, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Buske, Fabian A" sort="Buske, Fabian A" uniqKey="Buske F" first="Fabian A" last="Buske">Fabian A. Buske</name><affiliation><nlm:affiliation>1] Garvan Institute of Medical Research, Darlinghurst, New South Wales 2010, Australia [2] St Vincent's Clinical School, University of NSW Australia, Sydney, New South Wales 2010, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Saar, Kathrin" sort="Saar, Kathrin" uniqKey="Saar K" first="Kathrin" last="Saar">Kathrin Saar</name><affiliation><nlm:affiliation>MDC for Molecular Medicine, 13092 Berlin, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Hubner, Norbert" sort="Hubner, Norbert" uniqKey="Hubner N" first="Norbert" last="Hübner">Norbert Hübner</name><affiliation><nlm:affiliation>MDC for Molecular Medicine, 13092 Berlin, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Br Ndli, Andre W" sort="Br Ndli, Andre W" uniqKey="Br Ndli A" first="André W" last="Br Ndli">André W. Br Ndli</name><affiliation><nlm:affiliation>1] Institute of Pharmaceutical Sciences, Department of Chemistry and Applied Biosciences, ETH Zurich, Zurich, Switzerland [2] Walter Brendel Center of Experimental Medicine, Ludwig-Maximilians-University, 81377 Munich, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Schedl, Andreas" sort="Schedl, Andreas" uniqKey="Schedl A" first="Andreas" last="Schedl">Andreas Schedl</name><affiliation><nlm:affiliation>1] Institute of Biology Valrose, Université de Nice-Sophia, F-06108 Nice, France [2] Inserm, UMR1091, F-06108 Nice, France [3] CNRS, UMR7277, F-06108 Nice, France.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Nature communications</title><idno type="eISSN">2041-1723</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Bone Morphogenetic Proteins (genetics)</term><term>Bone Morphogenetic Proteins (metabolism)</term><term>Cell Differentiation (genetics)</term><term>Cell Differentiation (physiology)</term><term>Computational Biology</term><term>Fibroblast Growth Factors (genetics)</term><term>Fibroblast Growth Factors (metabolism)</term><term>Fluorescent Antibody Technique</term><term>Gene Expression Regulation, Developmental (genetics)</term><term>Gene Expression Regulation, Developmental (physiology)</term><term>In Situ Hybridization</term><term>In Situ Nick-End Labeling</term><term>Mice</term><term>Mice, Mutant Strains</term><term>Organ Culture Techniques</term><term>Repressor Proteins (genetics)</term><term>Repressor Proteins (metabolism)</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Signal Transduction (genetics)</term><term>Signal Transduction (physiology)</term><term>Stem Cells (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Bone Morphogenetic Proteins</term><term>Fibroblast Growth Factors</term><term>Repressor Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Bone Morphogenetic Proteins</term><term>Fibroblast Growth Factors</term><term>Repressor Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Differentiation</term><term>Gene Expression Regulation, Developmental</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Stem Cells</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Differentiation</term><term>Gene Expression Regulation, Developmental</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Computational Biology</term><term>Fluorescent Antibody Technique</term><term>In Situ Hybridization</term><term>In Situ Nick-End Labeling</term><term>Mice</term><term>Mice, Mutant Strains</term><term>Organ Culture Techniques</term><term>Reverse Transcriptase Polymerase Chain Reaction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Kidney organogenesis requires the tight control of proliferation, differentiation and apoptosis of renal progenitor cells. How the balance between these cellular decisions is achieved remains elusive. The Wilms' tumour suppressor Wt1 is required for progenitor survival, but the molecular cause for renal agenesis in mutants is poorly understood. Here we demonstrate that lack of Wt1 abolishes fibroblast growth factor (FGF) and induces BMP/pSMAD signalling within the metanephric mesenchyme. Addition of recombinant FGFs or inhibition of pSMAD signalling rescues progenitor cell apoptosis induced by the loss of Wt1. We further show that recombinant BMP4, but not BMP7, induces an apoptotic response within the early kidney that can be suppressed by simultaneous addition of FGFs. These data reveal a hitherto unknown sensitivity of early renal progenitors to pSMAD signalling, establishes FGF and pSMAD signalling as antagonistic forces in early kidney development and places WT1 as a key regulator of pro-survival FGF signalling pathway genes.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25031030</PMID><DateCreated><Year>2014</Year><Month>07</Month><Day>17</Day></DateCreated><DateCompleted><Year>2015</Year><Month>12</Month><Day>14</Day></DateCompleted><DateRevised><Year>2014</Year><Month>07</Month><Day>17</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2041-1723</ISSN><JournalIssue CitedMedium="Internet"><Volume>5</Volume><PubDate><Year>2014</Year><Month>Jul</Month><Day>17</Day></PubDate></JournalIssue><Title>Nature communications</Title><ISOAbbreviation>Nat Commun</ISOAbbreviation></Journal><ArticleTitle>WT1 controls antagonistic FGF and BMP-pSMAD pathways in early renal progenitors.</ArticleTitle><Pagination><MedlinePgn>4444</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/ncomms5444</ELocationID><Abstract><AbstractText>Kidney organogenesis requires the tight control of proliferation, differentiation and apoptosis of renal progenitor cells. How the balance between these cellular decisions is achieved remains elusive. The Wilms' tumour suppressor Wt1 is required for progenitor survival, but the molecular cause for renal agenesis in mutants is poorly understood. Here we demonstrate that lack of Wt1 abolishes fibroblast growth factor (FGF) and induces BMP/pSMAD signalling within the metanephric mesenchyme. Addition of recombinant FGFs or inhibition of pSMAD signalling rescues progenitor cell apoptosis induced by the loss of Wt1. We further show that recombinant BMP4, but not BMP7, induces an apoptotic response within the early kidney that can be suppressed by simultaneous addition of FGFs. These data reveal a hitherto unknown sensitivity of early renal progenitors to pSMAD signalling, establishes FGF and pSMAD signalling as antagonistic forces in early kidney development and places WT1 as a key regulator of pro-survival FGF signalling pathway genes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Motamedi</LastName><ForeName>Fariba Jian</ForeName><Initials>FJ</Initials><AffiliationInfo><Affiliation>1] Institute of Biology Valrose, Université de Nice-Sophia, F-06108 Nice, France [2] Inserm, UMR1091, F-06108 Nice, France [3] CNRS, UMR7277, F-06108 Nice, France [4].</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Badro</LastName><ForeName>Danielle A</ForeName><Initials>DA</Initials><AffiliationInfo><Affiliation>1] Institute of Biology Valrose, Université de Nice-Sophia, F-06108 Nice, France [2] Inserm, UMR1091, F-06108 Nice, France [3] CNRS, UMR7277, F-06108 Nice, France [4].</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Clarkson</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>1] Institute of Biology Valrose, Université de Nice-Sophia, F-06108 Nice, France [2] Inserm, UMR1091, F-06108 Nice, France [3] CNRS, UMR7277, F-06108 Nice, France [4].</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lecca</LastName><ForeName>M Rita</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>1] Institute of Pharmaceutical Sciences, Department of Chemistry and Applied Biosciences, ETH Zurich, Zurich, Switzerland [2] Functional Genomics Center Zurich, UZH/ETH Zurich, CH-8057 Zurich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bradford</LastName><ForeName>Stephen T</ForeName><Initials>ST</Initials><AffiliationInfo><Affiliation>1] Institute of Biology Valrose, Université de Nice-Sophia, F-06108 Nice, France [2] Inserm, UMR1091, F-06108 Nice, France [3] CNRS, UMR7277, F-06108 Nice, France [4] Garvan Institute of Medical Research, Darlinghurst, New South Wales 2010, Australia [5] CSIRO Animal, Food & Health Sciences, Preventative Health Flagship, North Ryde, New South Wales 2113, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Buske</LastName><ForeName>Fabian A</ForeName><Initials>FA</Initials><AffiliationInfo><Affiliation>1] Garvan Institute of Medical Research, Darlinghurst, New South Wales 2010, Australia [2] St Vincent's Clinical School, University of NSW Australia, Sydney, New South Wales 2010, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saar</LastName><ForeName>Kathrin</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>MDC for Molecular Medicine, 13092 Berlin, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hübner</LastName><ForeName>Norbert</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>MDC for Molecular Medicine, 13092 Berlin, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brändli</LastName><ForeName>André W</ForeName><Initials>AW</Initials><AffiliationInfo><Affiliation>1] Institute of Pharmaceutical Sciences, Department of Chemistry and Applied Biosciences, ETH Zurich, Zurich, Switzerland [2] Walter Brendel Center of Experimental Medicine, Ludwig-Maximilians-University, 81377 Munich, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schedl</LastName><ForeName>Andreas</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>1] Institute of Biology Valrose, Université de Nice-Sophia, F-06108 Nice, France [2] Inserm, UMR1091, F-06108 Nice, France [3] CNRS, UMR7277, F-06108 Nice, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList 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