Neural Crest Development - Revision history

Z8600021 at 01:29, 24 August 2023

2023-08-24T01:29:24Z

← Older revision		Revision as of 11:29, 24 August 2023
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	<br>		<br>
	Use the links listed below to study development of specific neural crest populations.		Use the links listed below to study development of specific neural crest populations.
	~~<br>~~
	{{Neural Crest Links}}		{{Neural Crest Links}}

Z8600021 at 18:11, 4 July 2022

2022-07-04T18:11:56Z

← Older revision		Revision as of 04:11, 5 July 2022
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	===Reviews===		===Reviews===
			{{#pmid:35260294}}

	{{#pmid:33723764}}		{{#pmid:33723764}}

Z8600021 at 17:53, 4 July 2022

2022-07-04T17:53:37Z

← Older revision		Revision as of 03:53, 5 July 2022
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	===Reviews===		===Reviews===

	{{#pmid:33723764}}		{{#pmid:33723764}}

			{{#pmid:33548210}}

	{{#pmid:31727473}}		{{#pmid:31727473}}

Z8600021 at 17:51, 4 July 2022

2022-07-04T17:51:34Z

← Older revision		Revision as of 03:51, 5 July 2022
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	===Reviews===		===Reviews===
			{{#pmid:33723764}}

	{{#pmid:31727473}}		{{#pmid:31727473}}

Z8600021 at 07:13, 1 December 2021

2021-12-01T07:13:34Z

← Older revision		Revision as of 17:13, 1 December 2021
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			* '''The mechanosensitive channel Piezo1 cooperates with Semaphorin to control neural crest migration'''{{#pmid:34822717\|PMID34822717}} "We identify that Piezo1 is required for the migration of Xenopus cephalic NC. We show that loss of Piezo1 promotes focal adhesion turnover and cytoskeletal dynamics by controlling Rac1 activity, leading to increased speed of migration. Moreover, overactivation of Rac1, due to Piezo1 inhibition, counteracts cell migration inhibitory signals by Semaphorins 3A and 3F, generating aberrant neural crest invasion in vivo. Thus, we find that, for directional migration in vivo, neural crest cells require a tight regulation of Rac1, by Semaphorins and Piezo1. We reveal here that a balance between a myriad of signals through Rac1 dictates cell migration in vivo, a mechanism that is likely to be conserved in other cell migration processes."

	* '''Nubp2 is required for cranial neural crest survival in the mouse'''{{#pmid:31733190\|PMID31733190}} "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 ([https://omim.org/entry/610779 Nubp2]) to be causative. This finding was confirmed by a complementation assay with the dorothy allele and an independent Nubp2 null allele (Nubp2null). 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 {{Wnt}}1-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."		* '''Nubp2 is required for cranial neural crest survival in the mouse'''{{#pmid:31733190\|PMID31733190}} "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 ([https://omim.org/entry/610779 Nubp2]) to be causative. This finding was confirmed by a complementation assay with the dorothy allele and an independent Nubp2 null allele (Nubp2null). 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 {{Wnt}}1-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."
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	* '''Evolution of the new {{head}} by gradual acquisition of {{neural crest}} regulatory circuits'''{{#pmid:31645763\|PMID31645763}} "The neural crest, an embryonic stem-cell population, is a vertebrate innovation that has been proposed to be a key component of the 'new head', which imbued vertebrates with predatory behaviour1,2. Here, to investigate how the evolution of neural crest cells affected the vertebrate body plan, we examined the molecular circuits that control neural crest development along the anteroposterior axis of a jawless vertebrate, the sea lamprey. Gene expression analysis showed that the cranial subpopulation of the neural crest of the lamprey lacks most components of a transcriptional circuit that is specific to the cranial neural crest in amniotes and confers the ability to form craniofacial cartilage onto non-cranial neural crest subpopulations3. Consistent with this, hierarchical clustering analysis revealed that the transcriptional profile of the lamprey cranial neural crest is more similar to the trunk neural crest of amniotes. Notably, analysis of the cranial neural crest in little skate and zebrafish embryos demonstrated that the transcriptional circuit that is specific to the cranial neural crest emerged via the gradual addition of network components to the neural crest of gnathostomes, which subsequently became restricted to the cephalic region. Our results indicate that the ancestral neural crest at the base of the vertebrate lineage possessed a trunk-like identity. We propose that the emergence of the cranial neural crest, by progressive assembly of an axial-specific regulatory circuit, allowed the elaboration of the new head during vertebrate evolution."		* '''Evolution of the new {{head}} by gradual acquisition of {{neural crest}} regulatory circuits'''{{#pmid:31645763\|PMID31645763}} "The neural crest, an embryonic stem-cell population, is a vertebrate innovation that has been proposed to be a key component of the 'new head', which imbued vertebrates with predatory behaviour1,2. Here, to investigate how the evolution of neural crest cells affected the vertebrate body plan, we examined the molecular circuits that control neural crest development along the anteroposterior axis of a jawless vertebrate, the sea lamprey. Gene expression analysis showed that the cranial subpopulation of the neural crest of the lamprey lacks most components of a transcriptional circuit that is specific to the cranial neural crest in amniotes and confers the ability to form craniofacial cartilage onto non-cranial neural crest subpopulations3. Consistent with this, hierarchical clustering analysis revealed that the transcriptional profile of the lamprey cranial neural crest is more similar to the trunk neural crest of amniotes. Notably, analysis of the cranial neural crest in little skate and zebrafish embryos demonstrated that the transcriptional circuit that is specific to the cranial neural crest emerged via the gradual addition of network components to the neural crest of gnathostomes, which subsequently became restricted to the cephalic region. Our results indicate that the ancestral neural crest at the base of the vertebrate lineage possessed a trunk-like identity. We propose that the emergence of the cranial neural crest, by progressive assembly of an axial-specific regulatory circuit, allowed the elaboration of the new head during vertebrate evolution."

	* '''A genome-wide assessment of the ancestral {{neural crest}} gene regulatory network'''{{#pmid:31619682\|PMID31619682}} "The {{neural crest}} (NC) is an embryonic cell population that contributes to key vertebrate-specific features including the craniofacial skeleton and peripheral nervous system. Here we examine the transcriptional and epigenomic profiles of NC cells in the sea lamprey, in order to gain insight into the ancestral state of the NC gene regulatory network (GRN). Transcriptome analyses identify clusters of co-regulated genes during NC specification and migration that show high conservation across vertebrates but also identify transcription factors (TFs) and cell-adhesion molecules not previously implicated in NC migration. ATAC-seq analysis uncovers an ensemble of cis-regulatory elements, including enhancers of Tfap2B, {{}}SoxE1 and {{Hox}}-α2 validated in the embryo. Cross-species deployment of lamprey elements identifies the deep conservation of lamprey SoxE1 enhancer activity, mediating homologous expression in jawed vertebrates. Our data provide insight into the core GRN elements conserved to the base of the vertebrates and expose others that are unique to lampreys."

	* '''Migratory Neural Crest Cells Phagocytose Dead Cells in the Developing Nervous System{'''{#pmid:31495570\|PMID31495570}} "During neural tube closure and spinal cord development, many cells die in both the central and peripheral nervous systems (CNS and PNS, respectively). However, myeloid-derived professional phagocytes have not yet colonized the trunk region during early neurogenesis. How apoptotic cells are removed from this region during these stages remains largely unknown. Using live imaging in zebrafish, we demonstrate that neural crest cells (NCCs) respond rapidly to dying cells and phagocytose cellular debris around the neural tube. Additionally, NCCs have the ability to enter the CNS through motor exit point transition zones and clear debris in the spinal cord. Surprisingly, NCCs phagocytosis mechanistically resembles macrophage phagocytosis and their recruitment toward cellular debris is mediated by interleukin-1β. Taken together, our results reveal a role for NCCs in phagocytosis of debris in the developing nervous system before the presence of professional phagocytes." {{apoptosis}}
	\|}		\|}

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	\| {{Older papers}}		\| {{Older papers}}
			* '''A genome-wide assessment of the ancestral {{neural crest}} gene regulatory network'''{{#pmid:31619682\|PMID31619682}} "The {{neural crest}} (NC) is an embryonic cell population that contributes to key vertebrate-specific features including the craniofacial skeleton and peripheral nervous system. Here we examine the transcriptional and epigenomic profiles of NC cells in the sea lamprey, in order to gain insight into the ancestral state of the NC gene regulatory network (GRN). Transcriptome analyses identify clusters of co-regulated genes during NC specification and migration that show high conservation across vertebrates but also identify transcription factors (TFs) and cell-adhesion molecules not previously implicated in NC migration. ATAC-seq analysis uncovers an ensemble of cis-regulatory elements, including enhancers of Tfap2B, {{}}SoxE1 and {{Hox}}-α2 validated in the embryo. Cross-species deployment of lamprey elements identifies the deep conservation of lamprey SoxE1 enhancer activity, mediating homologous expression in jawed vertebrates. Our data provide insight into the core GRN elements conserved to the base of the vertebrates and expose others that are unique to lampreys."

			* '''Migratory Neural Crest Cells Phagocytose Dead Cells in the Developing Nervous System{'''{#pmid:31495570\|PMID31495570}} "During neural tube closure and spinal cord development, many cells die in both the central and peripheral nervous systems (CNS and PNS, respectively). However, myeloid-derived professional phagocytes have not yet colonized the trunk region during early neurogenesis. How apoptotic cells are removed from this region during these stages remains largely unknown. Using live imaging in zebrafish, we demonstrate that neural crest cells (NCCs) respond rapidly to dying cells and phagocytose cellular debris around the neural tube. Additionally, NCCs have the ability to enter the CNS through motor exit point transition zones and clear debris in the spinal cord. Surprisingly, NCCs phagocytosis mechanistically resembles macrophage phagocytosis and their recruitment toward cellular debris is mediated by interleukin-1β. Taken together, our results reveal a role for NCCs in phagocytosis of debris in the developing nervous system before the presence of professional phagocytes." {{apoptosis}}

	* '''Krox20 defines a subpopulation of cardiac neural crest cells contributing to arterial valves and bicuspid aortic valve Development'''{{#pmid:29158447\|PMID29158447}} "Although cardiac neural crest cells are required at early stages of arterial valve development, their contribution during valvular leaflet maturation remains poorly understood. Here, we show in mouse that neural crest cells from pre-otic and post-otic regions make distinct contributions to the arterial valve leaflets.... Our findings demonstrate a crucial role for Krox20 in arterial valve development and reveal that an excess of neural crest cells may be associated with bicuspid aortic valve." {{heart}}		* '''Krox20 defines a subpopulation of cardiac neural crest cells contributing to arterial valves and bicuspid aortic valve Development'''{{#pmid:29158447\|PMID29158447}} "Although cardiac neural crest cells are required at early stages of arterial valve development, their contribution during valvular leaflet maturation remains poorly understood. Here, we show in mouse that neural crest cells from pre-otic and post-otic regions make distinct contributions to the arterial valve leaflets.... Our findings demonstrate a crucial role for Krox20 in arterial valve development and reveal that an excess of neural crest cells may be associated with bicuspid aortic valve." {{heart}}

Z8600021 at 07:09, 1 December 2021

2021-12-01T07:09:17Z

← Older revision		Revision as of 17:09, 1 December 2021
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	* '''Migratory Neural Crest Cells Phagocytose Dead Cells in the Developing Nervous System{'''{#pmid:31495570\|PMID31495570}} "During neural tube closure and spinal cord development, many cells die in both the central and peripheral nervous systems (CNS and PNS, respectively). However, myeloid-derived professional phagocytes have not yet colonized the trunk region during early neurogenesis. How apoptotic cells are removed from this region during these stages remains largely unknown. Using live imaging in zebrafish, we demonstrate that neural crest cells (NCCs) respond rapidly to dying cells and phagocytose cellular debris around the neural tube. Additionally, NCCs have the ability to enter the CNS through motor exit point transition zones and clear debris in the spinal cord. Surprisingly, NCCs phagocytosis mechanistically resembles macrophage phagocytosis and their recruitment toward cellular debris is mediated by interleukin-1β. Taken together, our results reveal a role for NCCs in phagocytosis of debris in the developing nervous system before the presence of professional phagocytes." {{apoptosis}}		* '''Migratory Neural Crest Cells Phagocytose Dead Cells in the Developing Nervous System{'''{#pmid:31495570\|PMID31495570}} "During neural tube closure and spinal cord development, many cells die in both the central and peripheral nervous systems (CNS and PNS, respectively). However, myeloid-derived professional phagocytes have not yet colonized the trunk region during early neurogenesis. How apoptotic cells are removed from this region during these stages remains largely unknown. Using live imaging in zebrafish, we demonstrate that neural crest cells (NCCs) respond rapidly to dying cells and phagocytose cellular debris around the neural tube. Additionally, NCCs have the ability to enter the CNS through motor exit point transition zones and clear debris in the spinal cord. Surprisingly, NCCs phagocytosis mechanistically resembles macrophage phagocytosis and their recruitment toward cellular debris is mediated by interleukin-1β. Taken together, our results reveal a role for NCCs in phagocytosis of debris in the developing nervous system before the presence of professional phagocytes." {{apoptosis}}

	* '''Krox20 defines a subpopulation of cardiac neural crest cells contributing to arterial valves and bicuspid aortic valve Development'''{{#pmid:29158447\|PMID29158447}} "Although cardiac neural crest cells are required at early stages of arterial valve development, their contribution during valvular leaflet maturation remains poorly understood. Here, we show in mouse that neural crest cells from pre-otic and post-otic regions make distinct contributions to the arterial valve leaflets.... Our findings demonstrate a crucial role for Krox20 in arterial valve development and reveal that an excess of neural crest cells may be associated with bicuspid aortic valve." {{heart}}

	* '''The neural border: Induction, specification and maturation of the territory that generates neural crest cells'''{{#pmid:29852131\|PMID29852131}} "The neural crest is induced at the edge between the neural plate and the nonneural ectoderm, in an area called the neural (plate) border, during gastrulation and neurulation. In recent years, many studies have explored how this domain is patterned, and how the neural crest is induced within this territory, that also participates to the prospective dorsal neural tube, the dorsalmost nonneural ectoderm, as well as {{placode}} derivatives in the anterior area. This review highlights the tissue interactions, the cell-cell signaling and the molecular mechanisms involved in this dynamic spatiotemporal patterning, resulting in the induction of the premigratory neural crest. Collectively, these studies allow building a complex neural border and early neural crest gene regulatory network, mostly composed by transcriptional regulations but also, more recently, including novel signaling interactions."

	* '''Review - Development of interstitial cells of Cajal in the human digestive tract as the result of reciprocal induction of mesenchymal and neural crest cells'''{{#pmid:29193736\|PMID29193736}} "Neural crest cells (NCC) can migrate into different parts of the body and express their strong inductive potential. In addition, they are multipotent and are able to differentiate into various cell types with diverse functions. In the primitive gut, NCC induce differentiation of muscular structures and interstitial cells of Cajal (ICC), and they themselves differentiate into the elements of the enteric nervous system (ENS), neurons and glial cells. ICC develop by way of mesenchymal cell differentiation in the outer parts of the primitive gut wall around the myenteric plexus (MP) ganglia, with the exception of colon, where they appear simultaneously also at the submucosal border of the circular muscular layer around the submucosal plexus (SMP) ganglia. ...Under the impact of stem cell factor (SCF), a portion of c-kit positive precursors lying immediately around the ganglia differentiate into ICC, while the rest differentiate into SMC." [[Neural Crest - Enteric Nervous System\|Enteric Nervous System]]
	\|}		\|}

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	\|-		\|-
	\| {{Older papers}}		\| {{Older papers}}
			* '''Krox20 defines a subpopulation of cardiac neural crest cells contributing to arterial valves and bicuspid aortic valve Development'''{{#pmid:29158447\|PMID29158447}} "Although cardiac neural crest cells are required at early stages of arterial valve development, their contribution during valvular leaflet maturation remains poorly understood. Here, we show in mouse that neural crest cells from pre-otic and post-otic regions make distinct contributions to the arterial valve leaflets.... Our findings demonstrate a crucial role for Krox20 in arterial valve development and reveal that an excess of neural crest cells may be associated with bicuspid aortic valve." {{heart}}

			* '''The neural border: Induction, specification and maturation of the territory that generates neural crest cells'''{{#pmid:29852131\|PMID29852131}} "The neural crest is induced at the edge between the neural plate and the nonneural ectoderm, in an area called the neural (plate) border, during gastrulation and neurulation. In recent years, many studies have explored how this domain is patterned, and how the neural crest is induced within this territory, that also participates to the prospective dorsal neural tube, the dorsalmost nonneural ectoderm, as well as {{placode}} derivatives in the anterior area. This review highlights the tissue interactions, the cell-cell signaling and the molecular mechanisms involved in this dynamic spatiotemporal patterning, resulting in the induction of the premigratory neural crest. Collectively, these studies allow building a complex neural border and early neural crest gene regulatory network, mostly composed by transcriptional regulations but also, more recently, including novel signaling interactions."

			* '''Review - Development of interstitial cells of Cajal in the human digestive tract as the result of reciprocal induction of mesenchymal and neural crest cells'''{{#pmid:29193736\|PMID29193736}} "Neural crest cells (NCC) can migrate into different parts of the body and express their strong inductive potential. In addition, they are multipotent and are able to differentiate into various cell types with diverse functions. In the primitive gut, NCC induce differentiation of muscular structures and interstitial cells of Cajal (ICC), and they themselves differentiate into the elements of the enteric nervous system (ENS), neurons and glial cells. ICC develop by way of mesenchymal cell differentiation in the outer parts of the primitive gut wall around the myenteric plexus (MP) ganglia, with the exception of colon, where they appear simultaneously also at the submucosal border of the circular muscular layer around the submucosal plexus (SMP) ganglia. ...Under the impact of stem cell factor (SCF), a portion of c-kit positive precursors lying immediately around the ganglia differentiate into ICC, while the rest differentiate into SMC." [[Neural Crest - Enteric Nervous System\|Enteric Nervous System]]

	* '''Retinoic acid temporally orchestrates colonization of the gut by vagal neural crest cells'''{{#pmid:29108781\|PMID29108781}} "The enteric nervous system arises from neural crest cells that migrate as chains into and along the primitive gut, subsequently differentiating into enteric neurons and glia. Little is known about the mechanisms governing neural crest migration en route to and along the gut in vivo. Here, we report that Retinoic Acid (RA) temporally controls zebrafish enteric neural crest cell chain migration. In vivo imaging reveals that RA loss severely compromises the integrity and migration of the chain of neural crest cells during the window of time window when they are moving along the foregut. After loss of RA, enteric progenitors accumulate in the foregut and differentiate into enteric neurons, but subsequently undergo apoptosis resulting in a striking neuronal deficit. Moreover, ectopic expression of the transcription factor meis3 and/or the receptor ret, partially rescues enteric neuron colonization after RA attenuation. Collectively, our findings suggest that retinoic acid plays a critical temporal role in promoting enteric neural crest chain migration and neuronal survival upstream of Meis3 and RET in vivo." [[Developmental Signals - Retinoic acid\|Retinoic acid]] \| {{Zebrafish}}		* '''Retinoic acid temporally orchestrates colonization of the gut by vagal neural crest cells'''{{#pmid:29108781\|PMID29108781}} "The enteric nervous system arises from neural crest cells that migrate as chains into and along the primitive gut, subsequently differentiating into enteric neurons and glia. Little is known about the mechanisms governing neural crest migration en route to and along the gut in vivo. Here, we report that Retinoic Acid (RA) temporally controls zebrafish enteric neural crest cell chain migration. In vivo imaging reveals that RA loss severely compromises the integrity and migration of the chain of neural crest cells during the window of time window when they are moving along the foregut. After loss of RA, enteric progenitors accumulate in the foregut and differentiate into enteric neurons, but subsequently undergo apoptosis resulting in a striking neuronal deficit. Moreover, ectopic expression of the transcription factor meis3 and/or the receptor ret, partially rescues enteric neuron colonization after RA attenuation. Collectively, our findings suggest that retinoic acid plays a critical temporal role in promoting enteric neural crest chain migration and neuronal survival upstream of Meis3 and RET in vivo." [[Developmental Signals - Retinoic acid\|Retinoic acid]] \| {{Zebrafish}}

Z8600021 at 03:51, 7 December 2020

2020-12-07T03:51:26Z

← Older revision		Revision as of 13:51, 7 December 2020
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	* '''Nubp2 is required for cranial neural crest survival in the mouse'''{{#pmid:31733190\|PMID31733190}} "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 ([https://omim.org/entry/610779 Nubp2]) to be causative. This finding was confirmed by a complementation assay with the dorothy allele and an independent Nubp2 null allele (Nubp2null). 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 {{Wnt}}1-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."		* '''Nubp2 is required for cranial neural crest survival in the mouse'''{{#pmid:31733190\|PMID31733190}} "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 ([https://omim.org/entry/610779 Nubp2]) to be causative. This finding was confirmed by a complementation assay with the dorothy allele and an independent Nubp2 null allele (Nubp2null). 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 {{Wnt}}1-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."

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	* '''A genome-wide assessment of the ancestral {{neural crest}} gene regulatory network'''{{#pmid:31619682\|PMID31619682}} "The {{neural crest}} (NC) is an embryonic cell population that contributes to key vertebrate-specific features including the craniofacial skeleton and peripheral nervous system. Here we examine the transcriptional and epigenomic profiles of NC cells in the sea lamprey, in order to gain insight into the ancestral state of the NC gene regulatory network (GRN). Transcriptome analyses identify clusters of co-regulated genes during NC specification and migration that show high conservation across vertebrates but also identify transcription factors (TFs) and cell-adhesion molecules not previously implicated in NC migration. ATAC-seq analysis uncovers an ensemble of cis-regulatory elements, including enhancers of Tfap2B, {{}}SoxE1 and {{Hox}}-α2 validated in the embryo. Cross-species deployment of lamprey elements identifies the deep conservation of lamprey SoxE1 enhancer activity, mediating homologous expression in jawed vertebrates. Our data provide insight into the core GRN elements conserved to the base of the vertebrates and expose others that are unique to lampreys."		* '''A genome-wide assessment of the ancestral {{neural crest}} gene regulatory network'''{{#pmid:31619682\|PMID31619682}} "The {{neural crest}} (NC) is an embryonic cell population that contributes to key vertebrate-specific features including the craniofacial skeleton and peripheral nervous system. Here we examine the transcriptional and epigenomic profiles of NC cells in the sea lamprey, in order to gain insight into the ancestral state of the NC gene regulatory network (GRN). Transcriptome analyses identify clusters of co-regulated genes during NC specification and migration that show high conservation across vertebrates but also identify transcription factors (TFs) and cell-adhesion molecules not previously implicated in NC migration. ATAC-seq analysis uncovers an ensemble of cis-regulatory elements, including enhancers of Tfap2B, {{}}SoxE1 and {{Hox}}-α2 validated in the embryo. Cross-species deployment of lamprey elements identifies the deep conservation of lamprey SoxE1 enhancer activity, mediating homologous expression in jawed vertebrates. Our data provide insight into the core GRN elements conserved to the base of the vertebrates and expose others that are unique to lampreys."

			* '''Migratory Neural Crest Cells Phagocytose Dead Cells in the Developing Nervous System{'''{#pmid:31495570\|PMID31495570}} "During neural tube closure and spinal cord development, many cells die in both the central and peripheral nervous systems (CNS and PNS, respectively). However, myeloid-derived professional phagocytes have not yet colonized the trunk region during early neurogenesis. How apoptotic cells are removed from this region during these stages remains largely unknown. Using live imaging in zebrafish, we demonstrate that neural crest cells (NCCs) respond rapidly to dying cells and phagocytose cellular debris around the neural tube. Additionally, NCCs have the ability to enter the CNS through motor exit point transition zones and clear debris in the spinal cord. Surprisingly, NCCs phagocytosis mechanistically resembles macrophage phagocytosis and their recruitment toward cellular debris is mediated by interleukin-1β. Taken together, our results reveal a role for NCCs in phagocytosis of debris in the developing nervous system before the presence of professional phagocytes." {{apoptosis}}

	* '''Krox20 defines a subpopulation of cardiac neural crest cells contributing to arterial valves and bicuspid aortic valve Development'''{{#pmid:29158447\|PMID29158447}} "Although cardiac neural crest cells are required at early stages of arterial valve development, their contribution during valvular leaflet maturation remains poorly understood. Here, we show in mouse that neural crest cells from pre-otic and post-otic regions make distinct contributions to the arterial valve leaflets.... Our findings demonstrate a crucial role for Krox20 in arterial valve development and reveal that an excess of neural crest cells may be associated with bicuspid aortic valve." {{heart}}		* '''Krox20 defines a subpopulation of cardiac neural crest cells contributing to arterial valves and bicuspid aortic valve Development'''{{#pmid:29158447\|PMID29158447}} "Although cardiac neural crest cells are required at early stages of arterial valve development, their contribution during valvular leaflet maturation remains poorly understood. Here, we show in mouse that neural crest cells from pre-otic and post-otic regions make distinct contributions to the arterial valve leaflets.... Our findings demonstrate a crucial role for Krox20 in arterial valve development and reveal that an excess of neural crest cells may be associated with bicuspid aortic valve." {{heart}}

Z8600021 at 00:43, 3 December 2019

2019-12-03T00:43:30Z

← Older revision		Revision as of 10:43, 3 December 2019
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	In the head region, {{neural crest}} cells migrate into the pharyngeal arches (as shown in movie below) forming ectomesenchyme contributing tissues which in the body region are typically derived from mesoderm (cartilage, bone, and connective tissue). General neural development is also covered in {{Neural}} Notes.		In the head region, {{neural crest}} cells migrate into the pharyngeal arches (as shown in movie below) forming ectomesenchyme contributing tissues which in the body region are typically derived from mesoderm (cartilage, bone, and connective tissue). General neural development is also covered in {{Neural}} Notes.

	Nicole Le Douarin has a long research career, ~~her research area has been~~ mainly on the development of neural crest cells using originally a Chicken-Quail chimera model she had developed{{#pmid:29616728\|PMID29616728}}, see also her recent review paper on the "beginnings" of the neural crest.{{#pmid:30048640\|PMID30048640}}		Nicole Le Douarin has had a long research career, mainly on the development of neural crest cells using originally a Chicken-Quail chimera model she had developed{{#pmid:29616728\|PMID29616728}}, see also her recent review paper on the "beginnings" of the neural crest.{{#pmid:30048640\|PMID30048640}}

	{{Neural Crest Vignette‎‎}}		{{Neural Crest Vignette‎‎}}

Z8600021 at 00:42, 3 December 2019

2019-12-03T00:42:24Z

← Older revision		Revision as of 10:42, 3 December 2019
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	[[File:Stage11 sem21.jpg\|thumb\|300px\|alt=Human embryo week 4 neural crest cells\|Human embryo neural crest cells ([[Week 4]], Carnegie stage {{CS11}})]]		[[File:Stage11 sem21.jpg\|thumb\|300px\|alt=Human embryo week 4 neural crest cells\|Human embryo neural crest cells ([[Week 4]], Carnegie stage {{CS11}})]]
	[[File:LeDouarin.jpg\|thumb\|alt=Nicole Le Douarin\|link=Embryology History - Nicole Le Douarin\|Nicole Le Douarin]]		[[File:LeDouarin.jpg\|thumb\|alt=Nicole Le Douarin\|link=Embryology History - Nicole Le Douarin\|Nicole Le Douarin]]
	Nicole Le Douarin has a long research career, her research area has been mainly on the development of neural crest cells using originally a Chicken-Quail chimera model she had developed{{#pmid:29616728\|PMID29616728}}, see also her recent review paper on the "beginnings" of the neural crest.{{#pmid:30048640\|PMID30048640}}

	The {{neural crest}} are bilaterally paired strips of cells arising in the ectoderm at the margins of the neural tube. These cells migrate to many different locations and differentiate into many cell types within the embryo. This means that many different systems (neural, skin, teeth, head, face, heart, adrenal glands, gastrointestinal tract) will also have a contribution fron the neural crest cells. An in vitro study{{#pmid:18689800\|PMID18689800}} has shown neural crest cell migration occurs at different rates along the embryo axis between Carnegie stage 11 to 13 in week 4.		The {{neural crest}} are bilaterally paired strips of cells arising in the ectoderm at the margins of the neural tube. These cells migrate to many different locations and differentiate into many cell types within the embryo. This means that many different systems (neural, skin, teeth, head, face, heart, adrenal glands, gastrointestinal tract) will also have a contribution fron the neural crest cells. An in vitro study{{#pmid:18689800\|PMID18689800}} has shown neural crest cell migration occurs at different rates along the embryo axis between Carnegie stage 11 to 13 in week 4.

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	In the head region, {{neural crest}} cells migrate into the pharyngeal arches (as shown in movie below) forming ~~[[E#~~ectomesenchyme~~\|ectomesenchyme]]~~ contributing tissues which in the body region are typically derived from mesoderm (cartilage, bone, and connective tissue). General neural development is also covered in ~~[[Neural System Development\|~~Neural Notes]].		In the head region, {{neural crest}} cells migrate into the pharyngeal arches (as shown in movie below) forming ectomesenchyme contributing tissues which in the body region are typically derived from mesoderm (cartilage, bone, and connective tissue). General neural development is also covered in {{Neural}} Notes.

			Nicole Le Douarin has a long research career, her research area has been mainly on the development of neural crest cells using originally a Chicken-Quail chimera model she had developed{{#pmid:29616728\|PMID29616728}}, see also her recent review paper on the "beginnings" of the neural crest.{{#pmid:30048640\|PMID30048640}}

	{{Neural Crest Vignette‎‎}}		{{Neural Crest Vignette‎‎}}

Z8600021 at 00:41, 3 December 2019

2019-12-03T00:41:23Z

← Older revision		Revision as of 10:41, 3 December 2019
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	== Introduction ==		== Introduction ==
	[[File:Stage11 sem21.jpg\|thumb\|300px\|alt=Human embryo week 4 neural crest cells\|Human embryo neural crest cells ([[Week 4]], Carnegie stage {{CS11}})]]		[[File:Stage11 sem21.jpg\|thumb\|300px\|alt=Human embryo week 4 neural crest cells\|Human embryo neural crest cells ([[Week 4]], Carnegie stage {{CS11}})]]
			[[File:LeDouarin.jpg\|thumb\|alt=Nicole Le Douarin\|link=Embryology History - Nicole Le Douarin\|Nicole Le Douarin]]
			Nicole Le Douarin has a long research career, her research area has been mainly on the development of neural crest cells using originally a Chicken-Quail chimera model she had developed{{#pmid:29616728\|PMID29616728}}, see also her recent review paper on the "beginnings" of the neural crest.{{#pmid:30048640\|PMID30048640}}

	The {{neural crest}} are bilaterally paired strips of cells arising in the ectoderm at the margins of the neural tube. These cells migrate to many different locations and differentiate into many cell types within the embryo. This means that many different systems (neural, skin, teeth, head, face, heart, adrenal glands, gastrointestinal tract) will also have a contribution fron the neural crest cells. An in vitro study{{#pmid:18689800\|PMID18689800}} has shown neural crest cell migration occurs at different rates along the embryo axis between Carnegie stage 11 to 13 in week 4.		The {{neural crest}} are bilaterally paired strips of cells arising in the ectoderm at the margins of the neural tube. These cells migrate to many different locations and differentiate into many cell types within the embryo. This means that many different systems (neural, skin, teeth, head, face, heart, adrenal glands, gastrointestinal tract) will also have a contribution fron the neural crest cells. An in vitro study{{#pmid:18689800\|PMID18689800}} has shown neural crest cell migration occurs at different rates along the embryo axis between Carnegie stage 11 to 13 in week 4.