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:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<term>Cell Line, Transformed (MeSH)</term>
<term>Cell Movement (genetics)</term>
<term>Cells, Cultured (MeSH)</term>
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<term>Green Fluorescent Proteins (genetics)</term>
<term>Green Fluorescent Proteins (metabolism)</term>
<term>Homeodomain Proteins (genetics)</term>
<term>Homeodomain Proteins (metabolism)</term>
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<term>Mice (MeSH)</term>
<term>Mice, Transgenic (MeSH)</term>
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<term>Neocortex (physiology)</term>
<term>Nerve Tissue Proteins (metabolism)</term>
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<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>
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<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>
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<term>Lignée de cellules transformées (MeSH)</term>
<term>Mouvement cellulaire (génétique)</term>
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<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>
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<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>
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<term>Neurogenesis</term>
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<term>Régulation de l'expression des gènes au cours du développement</term>
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<term>Protéines à fluorescence verte</term>
<term>Protéines à homéodomaine</term>
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<term>Néocortex</term>
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<term>Cell Line, Transformed</term>
<term>Cells, Cultured</term>
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<term>Humains</term>
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<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>
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<Title>Cerebral cortex (New York, N.Y. : 1991)</Title>
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<ArticleTitle>Scratch2 modulates neurogenesis and cell migration through antagonism of bHLH proteins in the developing neocortex.</ArticleTitle>
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<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>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Paul</LastName>
<ForeName>Vanessa</ForeName>
<Initials>V</Initials>
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<Author ValidYN="Y"><LastName>Tonchev</LastName>
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<Initials>T</Initials>
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<ArticleId IdType="doi">10.1093/cercor/bhs356</ArticleId>
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<affiliations><list><country><li>Allemagne</li>
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<region><li>Basse-Saxe</li>
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<settlement><li>Göttingen</li>
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<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>
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<country name="Allemagne"><region name="Basse-Saxe"><name sortKey="Paul, Vanessa" sort="Paul, Vanessa" uniqKey="Paul V" first="Vanessa" last="Paul">Vanessa Paul</name>
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