The Experts below are selected from a list of 285 Experts worldwide ranked by ideXlab platform
Wieland B Huttner - One of the best experts on this subject based on the ideXlab platform.
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human specific arhgap11b induces hallmarks of neocortical expansion in developing ferret Neocortex
eLife, 2018Co-Authors: Nereo Kalebic, Carlotta Gilardi, Mareike Albert, Takashi Namba, Katherine R Long, Milos Kostic, Barbara Langen, Wieland B HuttnerAbstract:The human brain owes its characteristic wrinkled appearance to its outer layer, the cerebral cortex. All mammals have a cerebral cortex, but its size varies greatly between species. As the brain evolved, the Neocortex, the evolutionarily youngest part of the cerebral cortex, expanded dramatically and so had to fold into wrinkles to fit inside the skull. The human Neocortex is roughly three times bigger than that of our closest relatives, the chimpanzees, and helps support advanced cognitive skills such as reasoning and language. But how did the human Neocortex become so big? The answer may lie in genes that are unique to humans, such as ARHGAP11B. Introducing ARHGAP11B into the Neocortex of mouse embryos increases its size and can induce folding. It does this by increasing the number of neural progenitors, the cells that give rise to neurons. But there are two types of neural progenitors in mammalian Neocortex: apical and basal. A subtype of the latter – basal radial glia – is thought to drive Neocortex growth in human development. Unfortunately, mice have very few basal radial glia. This makes them unsuitable for testing whether ARHGAP11B acts via basal radial glia to enlarge the human Neocortex. Kalebic et al. therefore introduced ARHGAP11B into ferret embryos in the womb. Ferrets have a larger Neocortex than mice and possess more basal radial glia. Unlike in mice, introducing this gene into the ferret Neocortex markedly increased the number of basal radial glia. It also extended the time window during which the basal radial glia produced neurons. These changes increased the number of neurons, particularly of a specific subtype found mainly in animals with large Neocortex and thought to be involved in human cognition. Introducing human-specific ARHGAP11B into embryonic ferrets thus helped expand the ferret Neocortex. This suggests that this gene may have a similar role in human brain development. Further experiments are needed to determine whether ferrets with the ARHGAP11B gene, and thus a larger Neocortex, have enhanced cognitive abilities. If they do, testing these animals could provide insights into human cognition. The animals could also be used to model human brain diseases and to test potential treatments.
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human specific arhgap11b induces hallmarks of neocortical expansion in developing ferret Neocortex
bioRxiv, 2018Co-Authors: Nereo Kalebic, Carlotta Gilardi, Mareike Albert, Takashi Namba, Katherine R Long, Milos Kostic, Barbara Langen, Wieland B HuttnerAbstract:The evolutionary increase in size and complexity of the primate Neocortex is thought to underlie the higher cognitive abilities of humans. ARHGAP11B is a human-specific gene that, based on its expression pattern in fetal human Neocortex and progenitor effects in embryonic mouse Neocortex, has been proposed to have a key function in the evolutionary expansion of the Neocortex. Here, we study the effects of ARHGAP11B expression in the developing Neocortex of the gyrencephalic ferret. In contrast to its effects in mouse, ARHGAP11B markedly increases proliferative basal radial glia, a progenitor cell type thought to be instrumental for neocortical expansion, and results in extension of the neurogenic period and an increase in upper-layer neurons. As a consequence, the postnatal ferret Neocortex exhibits an increased neuron density in the upper cortical layers and expands in the radial dimension. Thus, human-specific ARHGAP11B can elicit hallmarks of neocortical expansion in developing ferret Neocortex.
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neural progenitors neurogenesis and the evolution of the Neocortex
Development, 2014Co-Authors: Marta Florio, Wieland B HuttnerAbstract:The Neocortex is the seat of higher cognitive functions and, in evolutionary terms, is the youngest part of the mammalian brain. Since its origin, the Neocortex has expanded in several mammalian lineages, and this is particularly notable in humans. This expansion reflects an increase in the number of neocortical neurons, which is determined during development and primarily reflects the number of neurogenic divisions of distinct classes of neural progenitor cells. Consequently, the evolutionary expansion of the Neocortex and the concomitant increase in the numbers of neurons produced during development entail interspecies differences in neural progenitor biology. Here, we review the diversity of neocortical neural progenitors, their interspecies variations and their roles in determining the evolutionary increase in neuron numbers and Neocortex size.
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Progenitor Networking in the Fetal Primate Neocortex
Neuron, 2013Co-Authors: Wieland B Huttner, Iva Kelava, Eric LewitusAbstract:Basal radial glia (bRG) is a recently identified major type of neural stem cell in fetal primate, notably human, Neocortex. In this issue of Neuron, Betizeau et al. (2013) now demonstrate that four morphologically distinct bRG subtypes exist in the outer subventricular zone of fetal macaque Neocortex, and reveal an unexpected complexity of lineages generating neurons.
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eLS - Neurogenesis in the Developing Mammalian Neocortex
eLS, 2012Co-Authors: Iva Kelava, Wieland B HuttnerAbstract:The Neocortex is the evolutionarily newest and most complex part of the mammalian brain. The neurons of the Neocortex are born from different neural stem and progenitor cells (for simplicity collectively referred to as progenitors) that reside in proliferative zones during embryonic development. During the neurogenic period, distinct populations of neural progenitors appear, each having specific molecular and cell biological characteristics. These characteristics and the environment of the neural progenitor are responsible for the self-renewing or neurogenic potential of each neural progenitor type. The fate of daughter cells after neural progenitor division is determined by the mode of division, intrinsic factors such as transcription factors or regulatory ribonucleic acids (RNAs), and by extrinsic signals coming from the surrounding cells. This tight regulation controls the rate of production of neural progenitor types and neurons. The ratios of different progenitor types have a huge impact on the final number of neurons in the adult Neocortex, and are partly responsible for vast differences in the brains of different mammals. Key Concepts: Neocortex is a part of the brain characteristic of mammals. Neocortex is a six-layered structure comprised of post-mitotic neurons and glial cells. Neocortical neurons are born from neural progenitor cells, mostly during embryonic development. Neural progenitor cells can be classified into different populations based on molecular and cell-biological features. The molecular and cell-biological features of neural progenitor cells influence their propensity to self-renew or produce neurons. Neural progenitor cells are under tight intrinsic and extrinsic control, in order to maintain the equilibrium between proliferative and neurogenic divisions. The relative abundance of different progenitor populations influences the final number of neurons in the adult Neocortex. Keywords: mammals; neurogenesis; Neocortex; neural progenitor; (a)symmetric division; evolution
Nereo Kalebic - One of the best experts on this subject based on the ideXlab platform.
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human specific arhgap11b induces hallmarks of neocortical expansion in developing ferret Neocortex
eLife, 2018Co-Authors: Nereo Kalebic, Carlotta Gilardi, Mareike Albert, Takashi Namba, Katherine R Long, Milos Kostic, Barbara Langen, Wieland B HuttnerAbstract:The human brain owes its characteristic wrinkled appearance to its outer layer, the cerebral cortex. All mammals have a cerebral cortex, but its size varies greatly between species. As the brain evolved, the Neocortex, the evolutionarily youngest part of the cerebral cortex, expanded dramatically and so had to fold into wrinkles to fit inside the skull. The human Neocortex is roughly three times bigger than that of our closest relatives, the chimpanzees, and helps support advanced cognitive skills such as reasoning and language. But how did the human Neocortex become so big? The answer may lie in genes that are unique to humans, such as ARHGAP11B. Introducing ARHGAP11B into the Neocortex of mouse embryos increases its size and can induce folding. It does this by increasing the number of neural progenitors, the cells that give rise to neurons. But there are two types of neural progenitors in mammalian Neocortex: apical and basal. A subtype of the latter – basal radial glia – is thought to drive Neocortex growth in human development. Unfortunately, mice have very few basal radial glia. This makes them unsuitable for testing whether ARHGAP11B acts via basal radial glia to enlarge the human Neocortex. Kalebic et al. therefore introduced ARHGAP11B into ferret embryos in the womb. Ferrets have a larger Neocortex than mice and possess more basal radial glia. Unlike in mice, introducing this gene into the ferret Neocortex markedly increased the number of basal radial glia. It also extended the time window during which the basal radial glia produced neurons. These changes increased the number of neurons, particularly of a specific subtype found mainly in animals with large Neocortex and thought to be involved in human cognition. Introducing human-specific ARHGAP11B into embryonic ferrets thus helped expand the ferret Neocortex. This suggests that this gene may have a similar role in human brain development. Further experiments are needed to determine whether ferrets with the ARHGAP11B gene, and thus a larger Neocortex, have enhanced cognitive abilities. If they do, testing these animals could provide insights into human cognition. The animals could also be used to model human brain diseases and to test potential treatments.
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human specific arhgap11b induces hallmarks of neocortical expansion in developing ferret Neocortex
bioRxiv, 2018Co-Authors: Nereo Kalebic, Carlotta Gilardi, Mareike Albert, Takashi Namba, Katherine R Long, Milos Kostic, Barbara Langen, Wieland B HuttnerAbstract:The evolutionary increase in size and complexity of the primate Neocortex is thought to underlie the higher cognitive abilities of humans. ARHGAP11B is a human-specific gene that, based on its expression pattern in fetal human Neocortex and progenitor effects in embryonic mouse Neocortex, has been proposed to have a key function in the evolutionary expansion of the Neocortex. Here, we study the effects of ARHGAP11B expression in the developing Neocortex of the gyrencephalic ferret. In contrast to its effects in mouse, ARHGAP11B markedly increases proliferative basal radial glia, a progenitor cell type thought to be instrumental for neocortical expansion, and results in extension of the neurogenic period and an increase in upper-layer neurons. As a consequence, the postnatal ferret Neocortex exhibits an increased neuron density in the upper cortical layers and expands in the radial dimension. Thus, human-specific ARHGAP11B can elicit hallmarks of neocortical expansion in developing ferret Neocortex.
Kazunori Nakajima - One of the best experts on this subject based on the ideXlab platform.
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GABAergic interneuron migration and the evolution of the Neocortex
Development Growth & Differentiation, 2020Co-Authors: Daisuke H. Tanaka, Kazunori NakajimaAbstract:A Neocortex is present in all mammals but is not present in other classes of vertebrates, and the Neocortex is extremely elaborate in humans. Changes in excitatory projection neurons and their progenitors within the developing dorsal pallium in the most recent common ancestor of mammals are thought to have been involved in the evolution of the Neocortex. Our recent findings suggest that changes in the migratory ability of inhibitory interneurons derived from outside the Neocortex may also have been involved in the evolution of the Neocortex. In this article we review the literature on the migratory profile of inhibitory interneurons in several different species and the literature on comparisons between the intrinsic migratory ability of interneurons derived from different species. Finally, we propose a hypothesis about the mammalian-specific evolution of the migratory ability of interneurons and its potential contribution to the establishment of a functional Neocortex.
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Migratory pathways of GABAergic interneurons when they enter the Neocortex
European Journal of Neuroscience, 2012Co-Authors: Daisuke H. Tanaka, Kazunori NakajimaAbstract:Inhibitory gamma-aminobutyric-acid-containing interneurons play important roles in the functions of the Neocortex. During rodent development, most neocortical interneurons are generated in the subpallium and migrate tangentially toward the Neocortex. They migrate through multiple pathways to enter the Neocortex. Failure of interneuron migration through these pathways during development leads to an abnormal distribution and abnormal functions of interneurons in the postnatal brain. Because of recent discoveries regarding the novel origins and migratory pathways of neocortical interneurons, in this article we review the literature on the migratory pathways of interneurons when they enter the Neocortex.
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Cytoarchitecture of mouse and human subventricular zone in developing cerebral Neocortex
Experimental Brain Research, 2012Co-Authors: Hidenori Tabata, Satoshi Yoshinaga, Kazunori NakajimaAbstract:During cerebral neocortical development, excitatory neurons are generated from radial glial cells in the ventricular zone (VZ) or from secondary progenitor cells in the subventricular zone (SVZ); these neurons then migrate toward the pial surface. We have observed that post-mitotic neurons generated directly in the VZ accumulated just above the VZ with a multipolar morphology, while secondary progenitor cells having a long ascending process left the VZ faster than the post-mitotic neurons. Recent observations of human developing Neocortex have revealed the existence of radial glia-like progenitors (oRG cells) in the SVZ. This type of progenitor was first thought to be human specific; however, similar cells have also been found in mouse Neocortex, and the morphology of these cells resembled that of some of the secondary progenitor cells that we had previously observed, suggesting the existence of a common architecture for the developing Neocortex among mammals. In this review, we discuss the nature of the SVZ and its similarities and differences between humans and mice.
Takashi Namba - One of the best experts on this subject based on the ideXlab platform.
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human specific arhgap11b induces hallmarks of neocortical expansion in developing ferret Neocortex
eLife, 2018Co-Authors: Nereo Kalebic, Carlotta Gilardi, Mareike Albert, Takashi Namba, Katherine R Long, Milos Kostic, Barbara Langen, Wieland B HuttnerAbstract:The human brain owes its characteristic wrinkled appearance to its outer layer, the cerebral cortex. All mammals have a cerebral cortex, but its size varies greatly between species. As the brain evolved, the Neocortex, the evolutionarily youngest part of the cerebral cortex, expanded dramatically and so had to fold into wrinkles to fit inside the skull. The human Neocortex is roughly three times bigger than that of our closest relatives, the chimpanzees, and helps support advanced cognitive skills such as reasoning and language. But how did the human Neocortex become so big? The answer may lie in genes that are unique to humans, such as ARHGAP11B. Introducing ARHGAP11B into the Neocortex of mouse embryos increases its size and can induce folding. It does this by increasing the number of neural progenitors, the cells that give rise to neurons. But there are two types of neural progenitors in mammalian Neocortex: apical and basal. A subtype of the latter – basal radial glia – is thought to drive Neocortex growth in human development. Unfortunately, mice have very few basal radial glia. This makes them unsuitable for testing whether ARHGAP11B acts via basal radial glia to enlarge the human Neocortex. Kalebic et al. therefore introduced ARHGAP11B into ferret embryos in the womb. Ferrets have a larger Neocortex than mice and possess more basal radial glia. Unlike in mice, introducing this gene into the ferret Neocortex markedly increased the number of basal radial glia. It also extended the time window during which the basal radial glia produced neurons. These changes increased the number of neurons, particularly of a specific subtype found mainly in animals with large Neocortex and thought to be involved in human cognition. Introducing human-specific ARHGAP11B into embryonic ferrets thus helped expand the ferret Neocortex. This suggests that this gene may have a similar role in human brain development. Further experiments are needed to determine whether ferrets with the ARHGAP11B gene, and thus a larger Neocortex, have enhanced cognitive abilities. If they do, testing these animals could provide insights into human cognition. The animals could also be used to model human brain diseases and to test potential treatments.
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human specific arhgap11b induces hallmarks of neocortical expansion in developing ferret Neocortex
bioRxiv, 2018Co-Authors: Nereo Kalebic, Carlotta Gilardi, Mareike Albert, Takashi Namba, Katherine R Long, Milos Kostic, Barbara Langen, Wieland B HuttnerAbstract:The evolutionary increase in size and complexity of the primate Neocortex is thought to underlie the higher cognitive abilities of humans. ARHGAP11B is a human-specific gene that, based on its expression pattern in fetal human Neocortex and progenitor effects in embryonic mouse Neocortex, has been proposed to have a key function in the evolutionary expansion of the Neocortex. Here, we study the effects of ARHGAP11B expression in the developing Neocortex of the gyrencephalic ferret. In contrast to its effects in mouse, ARHGAP11B markedly increases proliferative basal radial glia, a progenitor cell type thought to be instrumental for neocortical expansion, and results in extension of the neurogenic period and an increase in upper-layer neurons. As a consequence, the postnatal ferret Neocortex exhibits an increased neuron density in the upper cortical layers and expands in the radial dimension. Thus, human-specific ARHGAP11B can elicit hallmarks of neocortical expansion in developing ferret Neocortex.
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human specific gene arhgap11b promotes basal progenitor amplification and Neocortex expansion
Science, 2015Co-Authors: Marta Florio, Mareike Albert, Takashi Namba, Elena Taverna, Holger Brandl, Eric Lewitus, Christiane Haffner, Alex M Sykes, Fong Kuan Wong, Jula PetersAbstract:Evolutionary expansion of the human Neocortex reflects increased amplification of basal progenitors in the subventricular zone, producing more neurons during fetal corticogenesis. In this work, we analyze the transcriptomes of distinct progenitor subpopulations isolated by a cell polarity–based approach from developing mouse and human Neocortex. We identify 56 genes preferentially expressed in human apical and basal radial glia that lack mouse orthologs. Among these, ARHGAP11B has the highest degree of radial glia–specific expression. ARHGAP11B arose from partial duplication of ARHGAP11A (which encodes a Rho guanosine triphosphatase–activating protein) on the human lineage after separation from the chimpanzee lineage. Expression of ARHGAP11B in embryonic mouse Neocortex promotes basal progenitor generation and self-renewal and can increase cortical plate area and induce gyrification. Hence, ARHGAP11B may have contributed to evolutionary expansion of human Neocortex.
Mareike Albert - One of the best experts on this subject based on the ideXlab platform.
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human specific arhgap11b induces hallmarks of neocortical expansion in developing ferret Neocortex
eLife, 2018Co-Authors: Nereo Kalebic, Carlotta Gilardi, Mareike Albert, Takashi Namba, Katherine R Long, Milos Kostic, Barbara Langen, Wieland B HuttnerAbstract:The human brain owes its characteristic wrinkled appearance to its outer layer, the cerebral cortex. All mammals have a cerebral cortex, but its size varies greatly between species. As the brain evolved, the Neocortex, the evolutionarily youngest part of the cerebral cortex, expanded dramatically and so had to fold into wrinkles to fit inside the skull. The human Neocortex is roughly three times bigger than that of our closest relatives, the chimpanzees, and helps support advanced cognitive skills such as reasoning and language. But how did the human Neocortex become so big? The answer may lie in genes that are unique to humans, such as ARHGAP11B. Introducing ARHGAP11B into the Neocortex of mouse embryos increases its size and can induce folding. It does this by increasing the number of neural progenitors, the cells that give rise to neurons. But there are two types of neural progenitors in mammalian Neocortex: apical and basal. A subtype of the latter – basal radial glia – is thought to drive Neocortex growth in human development. Unfortunately, mice have very few basal radial glia. This makes them unsuitable for testing whether ARHGAP11B acts via basal radial glia to enlarge the human Neocortex. Kalebic et al. therefore introduced ARHGAP11B into ferret embryos in the womb. Ferrets have a larger Neocortex than mice and possess more basal radial glia. Unlike in mice, introducing this gene into the ferret Neocortex markedly increased the number of basal radial glia. It also extended the time window during which the basal radial glia produced neurons. These changes increased the number of neurons, particularly of a specific subtype found mainly in animals with large Neocortex and thought to be involved in human cognition. Introducing human-specific ARHGAP11B into embryonic ferrets thus helped expand the ferret Neocortex. This suggests that this gene may have a similar role in human brain development. Further experiments are needed to determine whether ferrets with the ARHGAP11B gene, and thus a larger Neocortex, have enhanced cognitive abilities. If they do, testing these animals could provide insights into human cognition. The animals could also be used to model human brain diseases and to test potential treatments.
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human specific arhgap11b induces hallmarks of neocortical expansion in developing ferret Neocortex
bioRxiv, 2018Co-Authors: Nereo Kalebic, Carlotta Gilardi, Mareike Albert, Takashi Namba, Katherine R Long, Milos Kostic, Barbara Langen, Wieland B HuttnerAbstract:The evolutionary increase in size and complexity of the primate Neocortex is thought to underlie the higher cognitive abilities of humans. ARHGAP11B is a human-specific gene that, based on its expression pattern in fetal human Neocortex and progenitor effects in embryonic mouse Neocortex, has been proposed to have a key function in the evolutionary expansion of the Neocortex. Here, we study the effects of ARHGAP11B expression in the developing Neocortex of the gyrencephalic ferret. In contrast to its effects in mouse, ARHGAP11B markedly increases proliferative basal radial glia, a progenitor cell type thought to be instrumental for neocortical expansion, and results in extension of the neurogenic period and an increase in upper-layer neurons. As a consequence, the postnatal ferret Neocortex exhibits an increased neuron density in the upper cortical layers and expands in the radial dimension. Thus, human-specific ARHGAP11B can elicit hallmarks of neocortical expansion in developing ferret Neocortex.
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human specific gene arhgap11b promotes basal progenitor amplification and Neocortex expansion
Science, 2015Co-Authors: Marta Florio, Mareike Albert, Takashi Namba, Elena Taverna, Holger Brandl, Eric Lewitus, Christiane Haffner, Alex M Sykes, Fong Kuan Wong, Jula PetersAbstract:Evolutionary expansion of the human Neocortex reflects increased amplification of basal progenitors in the subventricular zone, producing more neurons during fetal corticogenesis. In this work, we analyze the transcriptomes of distinct progenitor subpopulations isolated by a cell polarity–based approach from developing mouse and human Neocortex. We identify 56 genes preferentially expressed in human apical and basal radial glia that lack mouse orthologs. Among these, ARHGAP11B has the highest degree of radial glia–specific expression. ARHGAP11B arose from partial duplication of ARHGAP11A (which encodes a Rho guanosine triphosphatase–activating protein) on the human lineage after separation from the chimpanzee lineage. Expression of ARHGAP11B in embryonic mouse Neocortex promotes basal progenitor generation and self-renewal and can increase cortical plate area and induce gyrification. Hence, ARHGAP11B may have contributed to evolutionary expansion of human Neocortex.
