Scratch2 modulates neurogenesis and cell migration through antagonism of bHLH proteins in the developing neocortex.
Identifieur interne : 000098 ( Main/Exploration ); précédent : 000097; suivant : 000099Scratch2 modulates neurogenesis and cell migration through antagonism of bHLH proteins in the developing neocortex.
Auteurs : Vanessa Paul [Allemagne] ; Anton B. Tonchev ; Kristine A. Henningfeld ; Evangelos Pavlakis ; Barbara Rust ; Tomas Pieler ; Anastassia StoykovaSource :
- Cerebral cortex (New York, N.Y. : 1991) [ 1460-2199 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Animaux nouveau-nés (MeSH), Cellules cultivées (MeSH), Embryon de mammifère (MeSH), Facteurs de transcription (génétique), Facteurs de transcription (métabolisme), Facteurs de transcription à motif basique hélice-boucle-hélice (métabolisme), Humains (MeSH), Lignée de cellules transformées (MeSH), Mouvement cellulaire (génétique), Neurogenèse (génétique), Neurones (physiologie), Néocortex (cytologie), Néocortex (physiologie), Protéines de tissu nerveux (métabolisme), Protéines à fluorescence verte (génétique), Protéines à fluorescence verte (métabolisme), Protéines à homéodomaine (génétique), Protéines à homéodomaine (métabolisme), Régulation de l'expression des gènes au cours du développement (génétique), Souris (MeSH), Souris transgéniques (MeSH), Xenopus (MeSH), beta-Galactosidase (génétique), beta-Galactosidase (métabolisme).
- MESH :
- cytologie : Néocortex.
- génétique : Facteurs de transcription, Mouvement cellulaire, Neurogenèse, Protéines à fluorescence verte, Protéines à homéodomaine, Régulation de l'expression des gènes au cours du développement, beta-Galactosidase.
- métabolisme : Facteurs de transcription, Facteurs de transcription à motif basique hélice-boucle-hélice, Protéines de tissu nerveux, Protéines à fluorescence verte, Protéines à homéodomaine, beta-Galactosidase.
- physiologie : Neurones, Néocortex.
- Animaux, Animaux nouveau-nés, Cellules cultivées, Embryon de mammifère, Humains, Lignée de cellules transformées, Souris, Souris transgéniques, Xenopus.
English descriptors
- KwdEn :
- Animals (MeSH), Animals, Newborn (MeSH), Basic Helix-Loop-Helix Transcription Factors (metabolism), Cell Line, Transformed (MeSH), Cell Movement (genetics), Cells, Cultured (MeSH), Embryo, Mammalian (MeSH), Gene Expression Regulation, Developmental (genetics), Green Fluorescent Proteins (genetics), Green Fluorescent Proteins (metabolism), Homeodomain Proteins (genetics), Homeodomain Proteins (metabolism), Humans (MeSH), Mice (MeSH), Mice, Transgenic (MeSH), Neocortex (cytology), Neocortex (physiology), Nerve Tissue Proteins (metabolism), Neurogenesis (genetics), Neurons (physiology), Transcription Factors (genetics), Transcription Factors (metabolism), Xenopus (MeSH), beta-Galactosidase (genetics), beta-Galactosidase (metabolism).
- MESH :
- chemical , genetics : Green Fluorescent Proteins, Homeodomain Proteins, Transcription Factors, beta-Galactosidase.
- chemical , metabolism : Basic Helix-Loop-Helix Transcription Factors, Green Fluorescent Proteins, Homeodomain Proteins, Nerve Tissue Proteins, Transcription Factors, beta-Galactosidase.
- cytology : Neocortex.
- genetics : Cell Movement, Gene Expression Regulation, Developmental, Neurogenesis.
- physiology : Neocortex, Neurons.
- Animals, Animals, Newborn, Cell Line, Transformed, Cells, Cultured, Embryo, Mammalian, Humans, Mice, Mice, Transgenic, Xenopus.
Abstract
Scratch genes (Scrt) are neural-specific zinc-finger transcription factors (TFs) with an unknown function in the developing brain. Here, we show that, in addition to the reported expression of mammalian Scrt2 in postmitotic differentiating and mature neurons in the developing and early postnatal brain, Scrt2 is also localized in subsets of mitotic and neurogenic radial glial (RGP) and intermediate (IP) progenitors, as well as in their descendants-postmitotic IPs and differentiating neurons at the border subventricular/intermediate zone. Conditional activation of transgenic Scrt2 in cortical progenitors in mice promotes neuronal differentiation by favoring the direct mode of neurogenesis of RGPs at the onset of neurogenesis, at the expense of IP generation. Neuronal amplification via indirect IP neurogenesis is thereby extenuated, leading to a mild postnatal reduction of cortical thickness. Forced in vivo overexpression of Scrt2 suppressed the generation of IPs from RGPs and caused a delay in the radial migration of upper layer neurons toward the cortical plate. Mechanistically, our results indicate that Scrt2 negatively regulates the transcriptional activation of the basic helix loop helix TFs Ngn2/NeuroD1 on E-box containing common target genes, including Rnd2, a well-known major effector for migrational defects in developing cortex. Altogether, these findings reveal a modulatory role of Scrt2 protein in cortical neurogenesis and neuronal migration.
DOI: 10.1093/cercor/bhs356
PubMed: 23180754
Affiliations:
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Tonchev</name></author><author><name sortKey="Henningfeld, Kristine A" sort="Henningfeld, Kristine A" uniqKey="Henningfeld K" first="Kristine A" last="Henningfeld">Kristine A. Henningfeld</name></author><author><name sortKey="Pavlakis, Evangelos" sort="Pavlakis, Evangelos" uniqKey="Pavlakis E" first="Evangelos" last="Pavlakis">Evangelos Pavlakis</name></author><author><name sortKey="Rust, Barbara" sort="Rust, Barbara" uniqKey="Rust B" first="Barbara" last="Rust">Barbara Rust</name></author><author><name sortKey="Pieler, Tomas" sort="Pieler, Tomas" uniqKey="Pieler T" first="Tomas" last="Pieler">Tomas Pieler</name></author><author><name sortKey="Stoykova, Anastassia" sort="Stoykova, Anastassia" uniqKey="Stoykova A" first="Anastassia" last="Stoykova">Anastassia Stoykova</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:23180754</idno><idno type="pmid">23180754</idno><idno type="doi">10.1093/cercor/bhs356</idno><idno type="wicri:Area/Main/Corpus">000117</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000117</idno><idno type="wicri:Area/Main/Curation">000117</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000117</idno><idno type="wicri:Area/Main/Exploration">000117</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Scratch2 modulates neurogenesis and cell migration through antagonism of bHLH proteins in the developing neocortex.</title><author><name sortKey="Paul, Vanessa" sort="Paul, Vanessa" uniqKey="Paul V" first="Vanessa" last="Paul">Vanessa Paul</name><affiliation wicri:level="3"><nlm:affiliation>Research Group Molecular Developmental Neurobiology, Max-Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Research Group Molecular Developmental Neurobiology, Max-Planck Institute for Biophysical Chemistry, 37077 Göttingen</wicri:regionArea><placeName><region type="land" nuts="2">Basse-Saxe</region><settlement type="city">Göttingen</settlement></placeName></affiliation></author><author><name sortKey="Tonchev, Anton B" sort="Tonchev, Anton B" uniqKey="Tonchev A" first="Anton B" last="Tonchev">Anton B. 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Henningfeld</name></author><author><name sortKey="Pavlakis, Evangelos" sort="Pavlakis, Evangelos" uniqKey="Pavlakis E" first="Evangelos" last="Pavlakis">Evangelos Pavlakis</name></author><author><name sortKey="Rust, Barbara" sort="Rust, Barbara" uniqKey="Rust B" first="Barbara" last="Rust">Barbara Rust</name></author><author><name sortKey="Pieler, Tomas" sort="Pieler, Tomas" uniqKey="Pieler T" first="Tomas" last="Pieler">Tomas Pieler</name></author><author><name sortKey="Stoykova, Anastassia" sort="Stoykova, Anastassia" uniqKey="Stoykova A" first="Anastassia" last="Stoykova">Anastassia Stoykova</name></author></analytic><series><title level="j">Cerebral cortex (New York, N.Y. : 1991)</title><idno type="eISSN">1460-2199</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Animals, Newborn (MeSH)</term><term>Basic Helix-Loop-Helix Transcription Factors (metabolism)</term><term>Cell Line, Transformed (MeSH)</term><term>Cell Movement (genetics)</term><term>Cells, Cultured (MeSH)</term><term>Embryo, Mammalian (MeSH)</term><term>Gene Expression Regulation, Developmental (genetics)</term><term>Green Fluorescent Proteins (genetics)</term><term>Green Fluorescent Proteins (metabolism)</term><term>Homeodomain Proteins (genetics)</term><term>Homeodomain Proteins (metabolism)</term><term>Humans (MeSH)</term><term>Mice (MeSH)</term><term>Mice, Transgenic (MeSH)</term><term>Neocortex (cytology)</term><term>Neocortex (physiology)</term><term>Nerve Tissue Proteins (metabolism)</term><term>Neurogenesis (genetics)</term><term>Neurons (physiology)</term><term>Transcription Factors (genetics)</term><term>Transcription Factors (metabolism)</term><term>Xenopus (MeSH)</term><term>beta-Galactosidase (genetics)</term><term>beta-Galactosidase (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Animaux nouveau-nés (MeSH)</term><term>Cellules cultivées (MeSH)</term><term>Embryon de mammifère (MeSH)</term><term>Facteurs de transcription (génétique)</term><term>Facteurs de transcription (métabolisme)</term><term>Facteurs de transcription à motif basique hélice-boucle-hélice (métabolisme)</term><term>Humains (MeSH)</term><term>Lignée de cellules transformées (MeSH)</term><term>Mouvement cellulaire (génétique)</term><term>Neurogenèse (génétique)</term><term>Neurones (physiologie)</term><term>Néocortex (cytologie)</term><term>Néocortex (physiologie)</term><term>Protéines de tissu nerveux (métabolisme)</term><term>Protéines à fluorescence verte (génétique)</term><term>Protéines à fluorescence verte (métabolisme)</term><term>Protéines à homéodomaine (génétique)</term><term>Protéines à homéodomaine (métabolisme)</term><term>Régulation de l'expression des gènes au cours du développement (génétique)</term><term>Souris (MeSH)</term><term>Souris transgéniques (MeSH)</term><term>Xenopus (MeSH)</term><term>beta-Galactosidase (génétique)</term><term>beta-Galactosidase (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Green Fluorescent Proteins</term><term>Homeodomain Proteins</term><term>Transcription Factors</term><term>beta-Galactosidase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Basic Helix-Loop-Helix Transcription Factors</term><term>Green Fluorescent Proteins</term><term>Homeodomain Proteins</term><term>Nerve Tissue Proteins</term><term>Transcription Factors</term><term>beta-Galactosidase</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Néocortex</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Neocortex</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Movement</term><term>Gene Expression Regulation, Developmental</term><term>Neurogenesis</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteurs de transcription</term><term>Mouvement cellulaire</term><term>Neurogenèse</term><term>Protéines à fluorescence verte</term><term>Protéines à homéodomaine</term><term>Régulation de l'expression des gènes au cours du développement</term><term>beta-Galactosidase</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs de transcription</term><term>Facteurs de transcription à motif basique hélice-boucle-hélice</term><term>Protéines de tissu nerveux</term><term>Protéines à fluorescence verte</term><term>Protéines à homéodomaine</term><term>beta-Galactosidase</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Neurones</term><term>Néocortex</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Neocortex</term><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Animals, Newborn</term><term>Cell Line, Transformed</term><term>Cells, Cultured</term><term>Embryo, Mammalian</term><term>Humans</term><term>Mice</term><term>Mice, Transgenic</term><term>Xenopus</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Animaux nouveau-nés</term><term>Cellules cultivées</term><term>Embryon de mammifère</term><term>Humains</term><term>Lignée de cellules transformées</term><term>Souris</term><term>Souris transgéniques</term><term>Xenopus</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Scratch genes (Scrt) are neural-specific zinc-finger transcription factors (TFs) with an unknown function in the developing brain. Here, we show that, in addition to the reported expression of mammalian Scrt2 in postmitotic differentiating and mature neurons in the developing and early postnatal brain, Scrt2 is also localized in subsets of mitotic and neurogenic radial glial (RGP) and intermediate (IP) progenitors, as well as in their descendants-postmitotic IPs and differentiating neurons at the border subventricular/intermediate zone. Conditional activation of transgenic Scrt2 in cortical progenitors in mice promotes neuronal differentiation by favoring the direct mode of neurogenesis of RGPs at the onset of neurogenesis, at the expense of IP generation. Neuronal amplification via indirect IP neurogenesis is thereby extenuated, leading to a mild postnatal reduction of cortical thickness. Forced in vivo overexpression of Scrt2 suppressed the generation of IPs from RGPs and caused a delay in the radial migration of upper layer neurons toward the cortical plate. Mechanistically, our results indicate that Scrt2 negatively regulates the transcriptional activation of the basic helix loop helix TFs Ngn2/NeuroD1 on E-box containing common target genes, including Rnd2, a well-known major effector for migrational defects in developing cortex. Altogether, these findings reveal a modulatory role of Scrt2 protein in cortical neurogenesis and neuronal migration. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23180754</PMID><DateCompleted><Year>2014</Year><Month>10</Month><Day>03</Day></DateCompleted><DateRevised><Year>2014</Year><Month>02</Month><Day>12</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2199</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>3</Issue><PubDate><Year>2014</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Cerebral cortex (New York, N.Y. : 1991)</Title><ISOAbbreviation>Cereb Cortex</ISOAbbreviation></Journal><ArticleTitle>Scratch2 modulates neurogenesis and cell migration through antagonism of bHLH proteins in the developing neocortex.</ArticleTitle><Pagination><MedlinePgn>754-72</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/cercor/bhs356</ELocationID><Abstract><AbstractText>Scratch genes (Scrt) are neural-specific zinc-finger transcription factors (TFs) with an unknown function in the developing brain. Here, we show that, in addition to the reported expression of mammalian Scrt2 in postmitotic differentiating and mature neurons in the developing and early postnatal brain, Scrt2 is also localized in subsets of mitotic and neurogenic radial glial (RGP) and intermediate (IP) progenitors, as well as in their descendants-postmitotic IPs and differentiating neurons at the border subventricular/intermediate zone. Conditional activation of transgenic Scrt2 in cortical progenitors in mice promotes neuronal differentiation by favoring the direct mode of neurogenesis of RGPs at the onset of neurogenesis, at the expense of IP generation. Neuronal amplification via indirect IP neurogenesis is thereby extenuated, leading to a mild postnatal reduction of cortical thickness. Forced in vivo overexpression of Scrt2 suppressed the generation of IPs from RGPs and caused a delay in the radial migration of upper layer neurons toward the cortical plate. Mechanistically, our results indicate that Scrt2 negatively regulates the transcriptional activation of the basic helix loop helix TFs Ngn2/NeuroD1 on E-box containing common target genes, including Rnd2, a well-known major effector for migrational defects in developing cortex. Altogether, these findings reveal a modulatory role of Scrt2 protein in cortical neurogenesis and neuronal migration. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Paul</LastName><ForeName>Vanessa</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Research Group Molecular Developmental Neurobiology, Max-Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tonchev</LastName><ForeName>Anton B</ForeName><Initials>AB</Initials></Author><Author ValidYN="Y"><LastName>Henningfeld</LastName><ForeName>Kristine A</ForeName><Initials>KA</Initials></Author><Author ValidYN="Y"><LastName>Pavlakis</LastName><ForeName>Evangelos</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Rust</LastName><ForeName>Barbara</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Pieler</LastName><ForeName>Tomas</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Stoykova</LastName><ForeName>Anastassia</ForeName><Initials>A</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>11</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cereb Cortex</MedlineTA><NlmUniqueID>9110718</NlmUniqueID><ISSNLinking>1047-3211</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051792">Basic Helix-Loop-Helix Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018398">Homeodomain Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009419">Nerve Tissue Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000591999">SCRATCH2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C098425">empty spiracles homeobox proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>147336-22-9</RegistryNumber><NameOfSubstance UI="D049452">Green Fluorescent Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.2.1.23</RegistryNumber><NameOfSubstance UI="D001616">beta-Galactosidase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" 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UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049452" MajorTopicYN="N">Green Fluorescent Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018398" MajorTopicYN="N">Homeodomain Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019579" MajorTopicYN="N">Neocortex</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009419" MajorTopicYN="N">Nerve Tissue Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055495" MajorTopicYN="N">Neurogenesis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014981" MajorTopicYN="N">Xenopus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001616" MajorTopicYN="N">beta-Galactosidase</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Scratch2</Keyword><Keyword MajorTopicYN="N">cortex</Keyword><Keyword MajorTopicYN="N">migration</Keyword><Keyword MajorTopicYN="N">neurogenesis</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>11</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>11</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>10</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23180754</ArticleId><ArticleId IdType="pii">bhs356</ArticleId><ArticleId IdType="doi">10.1093/cercor/bhs356</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country><region><li>Basse-Saxe</li></region><settlement><li>Göttingen</li></settlement></list><tree><noCountry><name sortKey="Henningfeld, Kristine A" sort="Henningfeld, Kristine A" uniqKey="Henningfeld K" first="Kristine A" last="Henningfeld">Kristine A. Henningfeld</name><name sortKey="Pavlakis, Evangelos" sort="Pavlakis, Evangelos" uniqKey="Pavlakis E" first="Evangelos" last="Pavlakis">Evangelos Pavlakis</name><name sortKey="Pieler, Tomas" sort="Pieler, Tomas" uniqKey="Pieler T" first="Tomas" last="Pieler">Tomas Pieler</name><name sortKey="Rust, Barbara" sort="Rust, Barbara" uniqKey="Rust B" first="Barbara" last="Rust">Barbara Rust</name><name sortKey="Stoykova, Anastassia" sort="Stoykova, Anastassia" uniqKey="Stoykova A" first="Anastassia" last="Stoykova">Anastassia Stoykova</name><name sortKey="Tonchev, Anton B" sort="Tonchev, Anton B" uniqKey="Tonchev A" first="Anton B" last="Tonchev">Anton B. Tonchev</name></noCountry><country name="Allemagne"><region name="Basse-Saxe"><name sortKey="Paul, Vanessa" sort="Paul, Vanessa" uniqKey="Paul V" first="Vanessa" last="Paul">Vanessa Paul</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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