WT1 controls antagonistic FGF and BMP-pSMAD pathways in early renal progenitors.
Identifieur interne : 003366 ( Main/Curation ); précédent : 003365; suivant : 003367WT1 controls antagonistic FGF and BMP-pSMAD pathways in early renal progenitors.
Auteurs : Fariba Jian Motamedi ; Danielle A. Badro ; Michael Clarkson ; M Rita Lecca [Suisse] ; Stephen T. Bradford [Australie] ; Fabian A. Buske [Australie] ; Kathrin Saar [Allemagne] ; Norbert Hübner [Allemagne] ; André W. Br Ndli [Allemagne] ; Andreas Schedl [France]Source :
- Nature communications [ 2041-1723 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Biologie informatique, Cellules souches (métabolisme), Différenciation cellulaire (génétique), Différenciation cellulaire (physiologie), Facteurs de croissance fibroblastique (génétique), Facteurs de croissance fibroblastique (métabolisme), Hybridation in situ, Méthode TUNEL, Protéines de répression (génétique), Protéines de répression (métabolisme), Protéines morphogénétiques osseuses (génétique), Protéines morphogénétiques osseuses (métabolisme), RT-PCR, Régulation de l'expression des gènes au cours du développement (génétique), Régulation de l'expression des gènes au cours du développement (physiologie), Souches mutantes de souris, Souris, Technique d'immunofluorescence, Techniques de culture d'organes, Transduction du signal (génétique), Transduction du signal (physiologie).
- MESH :
- génétique : Différenciation cellulaire, Facteurs de croissance fibroblastique, Protéines de répression, Protéines morphogénétiques osseuses, Régulation de l'expression des gènes au cours du développement, Transduction du signal.
- métabolisme : Cellules souches, Facteurs de croissance fibroblastique, Protéines de répression, Protéines morphogénétiques osseuses.
- physiologie : Différenciation cellulaire, Régulation de l'expression des gènes au cours du développement, Transduction du signal.
- Animaux, Biologie informatique, Hybridation in situ, Méthode TUNEL, RT-PCR, Souches mutantes de souris, Souris, Technique d'immunofluorescence, Techniques de culture d'organes.
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
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Fariba Jian Motamedi<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>
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<term>Différenciation cellulaire (physiologie)</term>
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<term>Facteurs de croissance fibroblastique (métabolisme)</term>
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<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Différenciation cellulaire</term>
<term>Régulation de l'expression des gènes au cours du développement</term>
<term>Transduction du signal</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>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Biologie informatique</term>
<term>Hybridation in situ</term>
<term>Méthode TUNEL</term>
<term>RT-PCR</term>
<term>Souches mutantes de souris</term>
<term>Souris</term>
<term>Technique d'immunofluorescence</term>
<term>Techniques de culture d'organes</term>
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<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>
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