IronSulferCluV1, Main, Curation, bibRecord, 000195

Nubp2 is required for cranial neural crest survival in the mouse.

Identifieur interne : 000195 ( Main/Curation ); précédent : 000194; suivant : 000196

Nubp2 is required for cranial neural crest survival in the mouse.

Auteurs : Andrew Distasio [États-Unis] ; David Paulding [États-Unis] ; Praneet Chaturvedi [États-Unis] ; Rolf W. Stottmann [États-Unis]

Source :

Developmental biology [ 1095-564X ] ; 2020.

RBID : pubmed:31733190

Descripteurs français

KwdFr :
- 1-Éthyl-1-nitroso-urée (MeSH), Animaux (MeSH), Crâne (métabolisme), Crête neurale (embryologie), Crête neurale (métabolisme), Développement embryonnaire (génétique), Femelle (MeSH), Mutagenèse (génétique), Mutation (génétique), Mâle (MeSH), Mésoderme (métabolisme), Phénotype (MeSH), Protéine Wnt1 (métabolisme), Protéines G (génétique), Protéines G (métabolisme), Souris (MeSH), Souris de lignée C57BL (MeSH), Tests de criblage à haut débit (méthodes), Transduction du signal (physiologie).
MESH :
- embryologie : Crête neurale.
- génétique : Développement embryonnaire, Mutagenèse, Mutation, Protéines G.
- métabolisme : Crâne, Crête neurale, Mésoderme, Protéine Wnt1, Protéines G.
- méthodes : Tests de criblage à haut débit.
- physiologie : Transduction du signal.
- 1-Éthyl-1-nitroso-urée, Animaux, Femelle, Mâle, Phénotype, Souris, Souris de lignée C57BL.

English descriptors

KwdEn :
- Animals (MeSH), Embryonic Development (genetics), Ethylnitrosourea (MeSH), Female (MeSH), GTP-Binding Proteins (genetics), GTP-Binding Proteins (metabolism), High-Throughput Screening Assays (methods), Male (MeSH), Mesoderm (metabolism), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mutagenesis (genetics), Mutation (genetics), Neural Crest (embryology), Neural Crest (metabolism), Phenotype (MeSH), Signal Transduction (physiology), Skull (metabolism), Wnt1 Protein (metabolism).
MESH :
- chemical , genetics : GTP-Binding Proteins.
- chemical , metabolism : GTP-Binding Proteins, Wnt1 Protein.
- chemical : Ethylnitrosourea.
- embryology : Neural Crest.
- genetics : Embryonic Development, Mutagenesis, Mutation.
- metabolism : Mesoderm, Neural Crest, Skull.
- methods : High-Throughput Screening Assays.
- physiology : Signal Transduction.
- Animals, Female, Male, Mice, Mice, Inbred C57BL, Phenotype.

Abstract

The N-ethyl-N-nitrosourea (ENU) ←forward genetic screen is a useful tool for the unbiased discovery of novel mechanisms regulating developmental processes. We recovered the dorothy mutation in such a screen designed to recover recessive mutations affecting craniofacial development in the mouse. Dorothy embryos die prenatally and exhibit many striking phenotypes commonly associated with ciliopathies, including a severe midfacial clefting phenotype. We used exome sequencing to discover a missense mutation in nucleotide binding protein 2 (Nubp2) to be causative. This finding was confirmed by a complementation assay with the dorothy allele and an independent Nubp2 null allele (Nubp2^null). We demonstrated that Nubp2 is indispensable for embryogenesis. NUBP2 is implicated in both the cytosolic iron/sulfur cluster assembly pathway and negative regulation of ciliogenesis. Conditional ablation of Nubp2 in the neural crest lineage with Wnt1-cre recapitulates the dorothy craniofacial phenotype. Using this model, we found that the proportion of ciliated cells in the craniofacial mesenchyme was unchanged, and that markers of the SHH, FGF, and BMP signaling pathways are unaltered. Finally, we show evidence that the phenotype results from a marked increase in apoptosis within the craniofacial mesenchyme.

DOI: 10.1016/j.ydbio.2019.10.039
PubMed: 31733190
PubMed Central: PMC6995770

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pubmed:31733190

Le document en format XML

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<term>Embryonic Development (genetics)</term>
<term>Ethylnitrosourea (MeSH)</term>
<term>Female (MeSH)</term>
<term>GTP-Binding Proteins (genetics)</term>
<term>GTP-Binding Proteins (metabolism)</term>
<term>High-Throughput Screening Assays (methods)</term>
<term>Male (MeSH)</term>
<term>Mesoderm (metabolism)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Mutagenesis (genetics)</term>
<term>Mutation (genetics)</term>
<term>Neural Crest (embryology)</term>
<term>Neural Crest (metabolism)</term>
<term>Phenotype (MeSH)</term>
<term>Signal Transduction (physiology)</term>
<term>Skull (metabolism)</term>
<term>Wnt1 Protein (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>1-Éthyl-1-nitroso-urée (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Crâne (métabolisme)</term>
<term>Crête neurale (embryologie)</term>
<term>Crête neurale (métabolisme)</term>
<term>Développement embryonnaire (génétique)</term>
<term>Femelle (MeSH)</term>
<term>Mutagenèse (génétique)</term>
<term>Mutation (génétique)</term>
<term>Mâle (MeSH)</term>
<term>Mésoderme (métabolisme)</term>
<term>Phénotype (MeSH)</term>
<term>Protéine Wnt1 (métabolisme)</term>
<term>Protéines G (génétique)</term>
<term>Protéines G (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Tests de criblage à haut débit (méthodes)</term>
<term>Transduction du signal (physiologie)</term>
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</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>GTP-Binding Proteins</term>
<term>Wnt1 Protein</term>
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<term>Mutagenesis</term>
<term>Mutation</term>
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<term>Mutagenèse</term>
<term>Mutation</term>
<term>Protéines G</term>
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<term>Neural Crest</term>
<term>Skull</term>
</keywords>
<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>High-Throughput Screening Assays</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Crâne</term>
<term>Crête neurale</term>
<term>Mésoderme</term>
<term>Protéine Wnt1</term>
<term>Protéines G</term>
</keywords>
<keywords scheme="MESH" qualifier="méthodes" xml:lang="fr"><term>Tests de criblage à haut débit</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Female</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Phenotype</term>
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<keywords scheme="MESH" xml:lang="fr"><term>1-Éthyl-1-nitroso-urée</term>
<term>Animaux</term>
<term>Femelle</term>
<term>Mâle</term>
<term>Phénotype</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">The N-ethyl-N-nitrosourea (ENU) ←forward genetic screen is a useful tool for the unbiased discovery of novel mechanisms regulating developmental processes. We recovered the dorothy mutation in such a screen designed to recover recessive mutations affecting craniofacial development in the mouse. Dorothy embryos die prenatally and exhibit many striking phenotypes commonly associated with ciliopathies, including a severe midfacial clefting phenotype. We used exome sequencing to discover a missense mutation in nucleotide binding protein 2 (Nubp2) to be causative. This finding was confirmed by a complementation assay with the dorothy allele and an independent Nubp2 null allele (Nubp2<sup>null</sup>
). We demonstrated that Nubp2 is indispensable for embryogenesis. NUBP2 is implicated in both the cytosolic iron/sulfur cluster assembly pathway and negative regulation of ciliogenesis. Conditional ablation of Nubp2 in the neural crest lineage with Wnt1-cre recapitulates the dorothy craniofacial phenotype. Using this model, we found that the proportion of ciliated cells in the craniofacial mesenchyme was unchanged, and that markers of the SHH, FGF, and BMP signaling pathways are unaltered. Finally, we show evidence that the phenotype results from a marked increase in apoptosis within the craniofacial mesenchyme.</div>
</front>
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<Month>09</Month>
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<Month>02</Month>
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<ArticleTitle>Nubp2 is required for cranial neural crest survival in the mouse.</ArticleTitle>
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<Abstract><AbstractText>The N-ethyl-N-nitrosourea (ENU) ←forward genetic screen is a useful tool for the unbiased discovery of novel mechanisms regulating developmental processes. We recovered the dorothy mutation in such a screen designed to recover recessive mutations affecting craniofacial development in the mouse. Dorothy embryos die prenatally and exhibit many striking phenotypes commonly associated with ciliopathies, including a severe midfacial clefting phenotype. We used exome sequencing to discover a missense mutation in nucleotide binding protein 2 (Nubp2) to be causative. This finding was confirmed by a complementation assay with the dorothy allele and an independent Nubp2 null allele (Nubp2<sup>null</sup>
). We demonstrated that Nubp2 is indispensable for embryogenesis. NUBP2 is implicated in both the cytosolic iron/sulfur cluster assembly pathway and negative regulation of ciliogenesis. Conditional ablation of Nubp2 in the neural crest lineage with Wnt1-cre recapitulates the dorothy craniofacial phenotype. Using this model, we found that the proportion of ciliated cells in the craniofacial mesenchyme was unchanged, and that markers of the SHH, FGF, and BMP signaling pathways are unaltered. Finally, we show evidence that the phenotype results from a marked increase in apoptosis within the craniofacial mesenchyme.</AbstractText>
<CopyrightInformation>Copyright © 2019 Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>DiStasio</LastName>
<ForeName>Andrew</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Division of Human Genetics, OH, 45229, USA.</Affiliation>
</AffiliationInfo>
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<Initials>D</Initials>
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</AffiliationInfo>
</Author>
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<ForeName>Praneet</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, OH, 45229, USA.</Affiliation>
</AffiliationInfo>
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</AffiliationInfo>
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<Language>eng</Language>
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<Acronym>DE</Acronym>
<Agency>NIDCR NIH HHS</Agency>
<Country>United States</Country>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C400289">NUBP2 protein, mouse</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D016296" MajorTopicYN="N">Mutagenesis</DescriptorName>
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<MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D009432" MajorTopicYN="N">Neural Crest</DescriptorName>
<QualifierName UI="Q000196" MajorTopicYN="Y">embryology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName>
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<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012886" MajorTopicYN="N">Skull</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051155" MajorTopicYN="N">Wnt1 Protein</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Cilia</Keyword>
<Keyword MajorTopicYN="Y">ENU mutagenesis</Keyword>
<Keyword MajorTopicYN="Y">Neural crest</Keyword>
<Keyword MajorTopicYN="Y">Nubp2</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year>
<Month>06</Month>
<Day>20</Day>
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<PubMedPubDate PubStatus="revised"><Year>2019</Year>
<Month>10</Month>
<Day>16</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2019</Year>
<Month>10</Month>
<Day>26</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pmc-release"><Year>2021</Year>
<Month>02</Month>
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<PubMedPubDate PubStatus="pubmed"><Year>2019</Year>
<Month>11</Month>
<Day>17</Day>
<Hour>6</Hour>
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<Month>9</Month>
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Nubp2 is required for cranial neural crest survival in the mouse.

Nubp2 is required for cranial neural crest survival in the mouse.

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