Embryonic forebrain transcriptome of mice with polyalanine expansion mutations in the ARX homeobox gene.
Identifieur interne : 001493 ( PubMed/Curation ); précédent : 001492; suivant : 001494Embryonic forebrain transcriptome of mice with polyalanine expansion mutations in the ARX homeobox gene.
Auteurs : Tessa Mattiske ; Kristie Lee ; Jozef Gecz ; Gaelle Friocourt [France] ; Cheryl ShoubridgeSource :
- Human molecular genetics [ 1460-2083 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux, Biosynthèse des protéines (génétique), Déficience intellectuelle (anatomopathologie), Déficience intellectuelle (génétique), Facteurs de transcription (génétique), Histone deacetylases (génétique), Humains, Modèles animaux de maladie humaine, Mutation, Peptides (génétique), Phénotype, Prosencéphale (embryologie), Prosencéphale (métabolisme), Protéines à homéodomaine (génétique), Régulation de l'expression des gènes au cours du développement, Souris, Transcriptome (génétique), Transduction du signal, Télencéphale (embryologie), Télencéphale (métabolisme), Épilepsie (anatomopathologie), Épilepsie (génétique).
- MESH :
- anatomopathologie : Déficience intellectuelle, Épilepsie.
- embryologie : Prosencéphale, Télencéphale.
- génétique : Biosynthèse des protéines, Déficience intellectuelle, Facteurs de transcription, Histone deacetylases, Peptides, Protéines à homéodomaine, Transcriptome, Épilepsie.
- métabolisme : Prosencéphale, Télencéphale.
- Animaux, Humains, Modèles animaux de maladie humaine, Mutation, Phénotype, Régulation de l'expression des gènes au cours du développement, Souris, Transduction du signal.
English descriptors
- KwdEn :
- Animals, Disease Models, Animal, Epilepsy (genetics), Epilepsy (pathology), Gene Expression Regulation, Developmental, Histone Deacetylases (genetics), Homeodomain Proteins (genetics), Humans, Intellectual Disability (genetics), Intellectual Disability (pathology), Mice, Mutation, Peptides (genetics), Phenotype, Prosencephalon (embryology), Prosencephalon (metabolism), Protein Biosynthesis (genetics), Signal Transduction, Telencephalon (embryology), Telencephalon (metabolism), Transcription Factors (genetics), Transcriptome (genetics).
- MESH :
- chemical , genetics : Histone Deacetylases, Homeodomain Proteins, Peptides, Transcription Factors.
- embryology : Prosencephalon, Telencephalon.
- genetics : Epilepsy, Intellectual Disability, Protein Biosynthesis, Transcriptome.
- metabolism : Prosencephalon, Telencephalon.
- pathology : Epilepsy, Intellectual Disability.
- Animals, Disease Models, Animal, Gene Expression Regulation, Developmental, Humans, Mice, Mutation, Phenotype, Signal Transduction.
Abstract
The Aristaless-related homeobox (ARX) gene encodes a paired-type homeodomain transcription factor with critical roles in embryonic development. Mutations in ARX give rise to intellectual disability (ID), epilepsy and brain malformation syndromes. To capture the genetics and molecular disruptions that underpin the ARX-associated clinical phenotypes, we undertook a transcriptome wide RNASeq approach to analyse developing (12.5 dpc) telencephalon of mice modelling two recurrent polyalanine expansion mutations with different phenotypic severities in the ARX gene. Here we report 238 genes significantly deregulated (Log2FC > +/-1.1, P-value <0.05) when both mutations are compared to wild-type (WT) animals. When each mutation is considered separately, a greater number of genes were deregulated in the severe PA1 mice (825) than in the PA2 animals (78). Analysing genes deregulated in either or both mutant strains, we identified 12% as implicated in ID, epilepsy and autism (99/858), with ∼5% of them as putative or known direct targets of ARX transcriptional regulation. We propose a core pathway of transcription regulators, including Hdac4, involved in chromatin condensation and transcriptional repression, and one of its targets, the transcription factor Twist1, as potential drivers of the ID and infantile spasms in patients with ARX polyalanine expansion mutations. We predict that the subsequent disturbance to this pathway is a consequence of ARX protein reduction with a broader and more significant level of disruption in the PA1 in comparison to the PA2 mice. Identifying early triggers of ARX-associated phenotypes contributes to our understanding of particular clusters/pathways underpinning comorbid phenotypes that are shared by many neurodevelopmental disorders.
DOI: 10.1093/hmg/ddw360
PubMed: 27798109
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Tessa Mattiske<affiliation><nlm:affiliation>Department of Paediatrics, Adelaide Medical School.</nlm:affiliation><wicri:noCountry code="subField">Adelaide Medical School</wicri:noCountry></affiliation><affiliation><nlm:affiliation>Department of Paediatrics, Adelaide Medical School.</nlm:affiliation><wicri:noCountry code="subField">Adelaide Medical School</wicri:noCountry></affiliation><affiliation><nlm:affiliation>Department of Paediatrics, Adelaide Medical School.</nlm:affiliation><wicri:noCountry code="subField">Adelaide Medical School</wicri:noCountry></affiliation><affiliation><nlm:affiliation>Department of Paediatrics, Adelaide Medical School.</nlm:affiliation><wicri:noCountry code="subField">Adelaide Medical School</wicri:noCountry></affiliation>Le document en format XML
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Lee</name><affiliation><nlm:affiliation>Department of Paediatrics, Adelaide Medical School.</nlm:affiliation><wicri:noCountry code="subField">Adelaide Medical School</wicri:noCountry></affiliation></author><author><name sortKey="Gecz, Jozef" sort="Gecz, Jozef" uniqKey="Gecz J" first="Jozef" last="Gecz">Jozef Gecz</name><affiliation><nlm:affiliation>Department of Paediatrics, Adelaide Medical School.</nlm:affiliation><wicri:noCountry code="subField">Adelaide Medical School</wicri:noCountry></affiliation></author><author><name sortKey="Friocourt, Gaelle" sort="Friocourt, Gaelle" uniqKey="Friocourt G" first="Gaelle" last="Friocourt">Gaelle Friocourt</name><affiliation wicri:level="1"><nlm:affiliation>Inserm, UMR1078, Brest, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Inserm, UMR1078, Brest</wicri:regionArea></affiliation></author><author><name sortKey="Shoubridge, Cheryl" sort="Shoubridge, Cheryl" uniqKey="Shoubridge C" first="Cheryl" last="Shoubridge">Cheryl Shoubridge</name><affiliation><nlm:affiliation>Department of Paediatrics, Adelaide Medical School.</nlm:affiliation><wicri:noCountry code="subField">Adelaide Medical School</wicri:noCountry></affiliation></author></analytic><series><title level="j">Human molecular genetics</title><idno type="eISSN">1460-2083</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Epilepsy (genetics)</term><term>Epilepsy (pathology)</term><term>Gene Expression Regulation, Developmental</term><term>Histone Deacetylases (genetics)</term><term>Homeodomain Proteins (genetics)</term><term>Humans</term><term>Intellectual Disability (genetics)</term><term>Intellectual Disability (pathology)</term><term>Mice</term><term>Mutation</term><term>Peptides (genetics)</term><term>Phenotype</term><term>Prosencephalon (embryology)</term><term>Prosencephalon (metabolism)</term><term>Protein Biosynthesis (genetics)</term><term>Signal Transduction</term><term>Telencephalon (embryology)</term><term>Telencephalon (metabolism)</term><term>Transcription Factors (genetics)</term><term>Transcriptome (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Biosynthèse des protéines (génétique)</term><term>Déficience intellectuelle (anatomopathologie)</term><term>Déficience intellectuelle (génétique)</term><term>Facteurs de transcription (génétique)</term><term>Histone deacetylases (génétique)</term><term>Humains</term><term>Modèles animaux de maladie humaine</term><term>Mutation</term><term>Peptides (génétique)</term><term>Phénotype</term><term>Prosencéphale (embryologie)</term><term>Prosencéphale (métabolisme)</term><term>Protéines à homéodomaine (génétique)</term><term>Régulation de l'expression des gènes au cours du développement</term><term>Souris</term><term>Transcriptome (génétique)</term><term>Transduction du signal</term><term>Télencéphale (embryologie)</term><term>Télencéphale (métabolisme)</term><term>Épilepsie (anatomopathologie)</term><term>Épilepsie (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Histone Deacetylases</term><term>Homeodomain Proteins</term><term>Peptides</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Déficience intellectuelle</term><term>Épilepsie</term></keywords><keywords scheme="MESH" qualifier="embryologie" xml:lang="fr"><term>Prosencéphale</term><term>Télencéphale</term></keywords><keywords scheme="MESH" qualifier="embryology" xml:lang="en"><term>Prosencephalon</term><term>Telencephalon</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Epilepsy</term><term>Intellectual Disability</term><term>Protein Biosynthesis</term><term>Transcriptome</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Biosynthèse des protéines</term><term>Déficience intellectuelle</term><term>Facteurs de transcription</term><term>Histone deacetylases</term><term>Peptides</term><term>Protéines à homéodomaine</term><term>Transcriptome</term><term>Épilepsie</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Prosencephalon</term><term>Telencephalon</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Prosencéphale</term><term>Télencéphale</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Epilepsy</term><term>Intellectual Disability</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Gene Expression Regulation, Developmental</term><term>Humans</term><term>Mice</term><term>Mutation</term><term>Phenotype</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Modèles animaux de maladie humaine</term><term>Mutation</term><term>Phénotype</term><term>Régulation de l'expression des gènes au cours du développement</term><term>Souris</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The Aristaless-related homeobox (ARX) gene encodes a paired-type homeodomain transcription factor with critical roles in embryonic development. Mutations in ARX give rise to intellectual disability (ID), epilepsy and brain malformation syndromes. To capture the genetics and molecular disruptions that underpin the ARX-associated clinical phenotypes, we undertook a transcriptome wide RNASeq approach to analyse developing (12.5 dpc) telencephalon of mice modelling two recurrent polyalanine expansion mutations with different phenotypic severities in the ARX gene. Here we report 238 genes significantly deregulated (Log2FC > +/-1.1, P-value <0.05) when both mutations are compared to wild-type (WT) animals. When each mutation is considered separately, a greater number of genes were deregulated in the severe PA1 mice (825) than in the PA2 animals (78). Analysing genes deregulated in either or both mutant strains, we identified 12% as implicated in ID, epilepsy and autism (99/858), with ∼5% of them as putative or known direct targets of ARX transcriptional regulation. We propose a core pathway of transcription regulators, including Hdac4, involved in chromatin condensation and transcriptional repression, and one of its targets, the transcription factor Twist1, as potential drivers of the ID and infantile spasms in patients with ARX polyalanine expansion mutations. We predict that the subsequent disturbance to this pathway is a consequence of ARX protein reduction with a broader and more significant level of disruption in the PA1 in comparison to the PA2 mice. Identifying early triggers of ARX-associated phenotypes contributes to our understanding of particular clusters/pathways underpinning comorbid phenotypes that are shared by many neurodevelopmental disorders.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27798109</PMID><DateCreated><Year>2016</Year><Month>10</Month><Day>31</Day></DateCreated><DateCompleted><Year>2017</Year><Month>06</Month><Day>09</Day></DateCompleted><DateRevised><Year>2017</Year><Month>06</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1460-2083</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>24</Issue><PubDate><Year>2016</Year><Month>Dec</Month><Day>15</Day></PubDate></JournalIssue><Title>Human molecular genetics</Title><ISOAbbreviation>Hum. Mol. Genet.</ISOAbbreviation></Journal><ArticleTitle>Embryonic forebrain transcriptome of mice with polyalanine expansion mutations in the ARX homeobox gene.</ArticleTitle><Pagination><MedlinePgn>5433-5443</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/hmg/ddw360</ELocationID><Abstract><AbstractText>The Aristaless-related homeobox (ARX) gene encodes a paired-type homeodomain transcription factor with critical roles in embryonic development. Mutations in ARX give rise to intellectual disability (ID), epilepsy and brain malformation syndromes. To capture the genetics and molecular disruptions that underpin the ARX-associated clinical phenotypes, we undertook a transcriptome wide RNASeq approach to analyse developing (12.5 dpc) telencephalon of mice modelling two recurrent polyalanine expansion mutations with different phenotypic severities in the ARX gene. Here we report 238 genes significantly deregulated (Log2FC > +/-1.1, P-value <0.05) when both mutations are compared to wild-type (WT) animals. When each mutation is considered separately, a greater number of genes were deregulated in the severe PA1 mice (825) than in the PA2 animals (78). Analysing genes deregulated in either or both mutant strains, we identified 12% as implicated in ID, epilepsy and autism (99/858), with ∼5% of them as putative or known direct targets of ARX transcriptional regulation. We propose a core pathway of transcription regulators, including Hdac4, involved in chromatin condensation and transcriptional repression, and one of its targets, the transcription factor Twist1, as potential drivers of the ID and infantile spasms in patients with ARX polyalanine expansion mutations. We predict that the subsequent disturbance to this pathway is a consequence of ARX protein reduction with a broader and more significant level of disruption in the PA1 in comparison to the PA2 mice. Identifying early triggers of ARX-associated phenotypes contributes to our understanding of particular clusters/pathways underpinning comorbid phenotypes that are shared by many neurodevelopmental disorders.</AbstractText><CopyrightInformation>© The Author 2016. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mattiske</LastName><ForeName>Tessa</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, Adelaide Medical School.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Robinson Research Institute, University of Adelaide, SA, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Kristie</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, Adelaide Medical School.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Robinson Research Institute, University of Adelaide, SA, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gecz</LastName><ForeName>Jozef</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, Adelaide Medical School.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Robinson Research Institute, University of Adelaide, SA, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Friocourt</LastName><ForeName>Gaelle</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Inserm, UMR1078, Brest, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Brest University, Faculté de Médecine et des Sciences de la Santé, Sfr ScInBioS, Brest, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shoubridge</LastName><ForeName>Cheryl</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Paediatrics, Adelaide Medical School.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Robinson Research Institute, University of Adelaide, SA, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Hum Mol Genet</MedlineTA><NlmUniqueID>9208958</NlmUniqueID><ISSNLinking>0964-6906</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C469265">ARX protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018398">Homeodomain Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010455">Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>25191-17-7</RegistryNumber><NameOfSubstance UI="C019529">polyalanine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.5.1.98</RegistryNumber><NameOfSubstance UI="C498618">Hdac5 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.5.1.98</RegistryNumber><NameOfSubstance UI="D006655">Histone Deacetylases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004827" MajorTopicYN="N">Epilepsy</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018507" MajorTopicYN="N">Gene Expression Regulation, Developmental</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006655" MajorTopicYN="N">Histone Deacetylases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018398" MajorTopicYN="N">Homeodomain Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008607" MajorTopicYN="N">Intellectual Disability</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010455" MajorTopicYN="N">Peptides</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016548" MajorTopicYN="N">Prosencephalon</DescriptorName><QualifierName UI="Q000196" MajorTopicYN="N">embryology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014176" MajorTopicYN="N">Protein Biosynthesis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013687" MajorTopicYN="N">Telencephalon</DescriptorName><QualifierName UI="Q000196" MajorTopicYN="N">embryology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059467" MajorTopicYN="N">Transcriptome</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>08</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>10</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>11</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>6</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>11</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27798109</ArticleId><ArticleId 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