Developmental Mechanism - Cell Migration - Revision history

Z8600021 at 23:26, 25 April 2020

2020-04-25T23:26:42Z

← Older revision		Revision as of 10:26, 26 April 2020
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	Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Developmental+Cell+Migration ''Developmental Cell Migration''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Neural+Crest+Cell+Migration ''Neural Crest Cell Migration'']		Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Developmental+Cell+Migration ''Developmental Cell Migration''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Neural+Crest+Cell+Migration ''Neural Crest Cell Migration'']

			\|}

			{\| class="wikitable mw-collapsible mw-collapsed"
			! Older papers
			\|-
			\| {{Older papers}}
	\|}		\|}
	==Neural Crest Development==		==Neural Crest Development==

Z8600021 at 23:19, 25 April 2020

2020-04-25T23:19:02Z

← Older revision		Revision as of 10:19, 26 April 2020
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	==Introduction==		==Introduction==
	[[File:Chicken-gastrulation2.jpg\|thumb\|300px\|Gastrulation involves both epithelial to mesenchymal transition and cell migration]]		[[File:Chicken-gastrulation2.jpg\|thumb\|300px\|Gastrulation involves both epithelial to mesenchymal transition and cell migration]]
	The process of cell migration occurs at different stages throughout embryonic development and involves other developmental mechanisms. The first key migration occurs during [[Gastrulation]]. Later key migratory events also occur during [[Somitogenesis~~\|somite dispersion]]~~ and ~~[[Neural Crest Development\|~~neural crest migration]].		The process of cell migration occurs at different stages throughout embryonic development and involves other developmental mechanisms. The first key migration occurs during {{Gastrulation}}. Later key migratory events also occur during {{Somitogenesis}} and {{neural crest}} migration.

	This mechanism involves several cellular processes including: cytoskeletal reorganisation, adhesion, extracellular matrix, and chemotactic signaling.		This mechanism involves several cellular processes including: cytoskeletal reorganisation, adhesion, extracellular matrix, and chemotactic signaling.



	<center>'''''Mechanism''' - "a process, technique, or system for achieving a result"''</center>		<center>'''''Mechanism''' - "a process, technique, or system for achieving a result"''</center>

			{{Mechanism Links}}
	:{{Mechanism Links}}

	== Some Recent Findings ==		== Some Recent Findings ==
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	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"
	\|		\|
	* '''STRIP1, a core component of STRIPAK complexes, is essential for normal mesoderm migration in the mouse embryo'''~~<ref name=~~PMID29203676~~><pubmed>29203676</pubmed></ref>~~ "Regulated mesoderm migration is necessary for the proper morphogenesis and organ formation during embryonic development. Cell migration and its dependence on the cytoskeleton and signaling machines have been studied extensively in cultured cells; in contrast, remarkably little is known about the mechanisms that regulate mesoderm cell migration in vivo. Here, we report the identification and characterization of a mouse mutation in striatin-interacting protein 1 (Strip1) that disrupts migration of the mesoderm after the gastrulation epithelial-to-mesenchymal transition (EMT). STRIP1 is a core component of the biochemically defined mammalian striatin-interacting phosphatases and kinase (STRIPAK) complexes that appear to act through regulation of protein phosphatase 2A (PP2A), but their functions in mammals in vivo have not been examined. Strip1-null mutants arrest development at midgestation with profound disruptions in the organization of the mesoderm and its derivatives, including a complete failure of the anterior extension of axial mesoderm. Analysis of cultured mesoderm explants and mouse embryonic fibroblasts from null mutants shows that the mesoderm migration defect is correlated with decreased cell spreading, abnormal focal adhesions, changes in the organization of the actin cytoskeleton, and decreased velocity of cell migration. The results show that STRIPAK complexes are essential for cell migration and tissue morphogenesis in vivo." (More? [[Mesoderm]] \| [https://www.ncbi.nlm.nih.gov/gene/85369 NCBI Gene - STRIP1])		* '''STRIP1, a core component of STRIPAK complexes, is essential for normal mesoderm migration in the mouse embryo'''{{#pmid:29203676\|PMID29203676}} "Regulated mesoderm migration is necessary for the proper morphogenesis and organ formation during embryonic development. Cell migration and its dependence on the cytoskeleton and signaling machines have been studied extensively in cultured cells; in contrast, remarkably little is known about the mechanisms that regulate mesoderm cell migration in vivo. Here, we report the identification and characterization of a mouse mutation in striatin-interacting protein 1 (Strip1) that disrupts migration of the mesoderm after the gastrulation epithelial-to-mesenchymal transition (EMT). STRIP1 is a core component of the biochemically defined mammalian striatin-interacting phosphatases and kinase (STRIPAK) complexes that appear to act through regulation of protein phosphatase 2A (PP2A), but their functions in mammals in vivo have not been examined. Strip1-null mutants arrest development at midgestation with profound disruptions in the organization of the mesoderm and its derivatives, including a complete failure of the anterior extension of axial mesoderm. Analysis of cultured mesoderm explants and mouse embryonic fibroblasts from null mutants shows that the mesoderm migration defect is correlated with decreased cell spreading, abnormal focal adhesions, changes in the organization of the actin cytoskeleton, and decreased velocity of cell migration. The results show that STRIPAK complexes are essential for cell migration and tissue morphogenesis in vivo." (More? [[Mesoderm]] \| [https://www.ncbi.nlm.nih.gov/gene/85369 NCBI Gene - STRIP1])

			* '''LKB1 signaling in cephalic neural crest cells is essential for vertebrate head development'''{{#pmid:27527806\|PMID27527806}} "Head development in vertebrates proceeds through a series of elaborate patterning mechanisms and cell-cell interactions involving cephalic neural crest cells (CNCC). These cells undergo extensive migration along stereotypical paths after their separation from the dorsal margins of the neural tube and they give rise to most of the craniofacial skeleton. Here, we report that the silencing of the LKB1 tumor suppressor affects the delamination of pre-migratory CNCC from the neural primordium as well as their polarization and survival, thus resulting in severe facial and brain defects. We further show that LKB1-mediated effects on the development of CNCC involve the sequential activation of the AMP-activated protein kinase (AMPK), the Rho-dependent kinase (ROCK) and the actin-based motor protein myosin II. Collectively, these results establish that the complex morphogenetic processes governing head formation critically depends on the activation of the LKB1 signaling network in CNCC."

	* '''LKB1 signaling in cephalic neural crest cells is essential for vertebrate head development'''<ref name=PMID27527806><pubmed>27527806</pubmed></ref> "Head development in vertebrates proceeds through a series of elaborate patterning mechanisms and cell-cell interactions involving cephalic neural crest cells (CNCC). These cells undergo extensive migration along stereotypical paths after their separation from the dorsal margins of the neural tube and they give rise to most of the craniofacial skeleton. Here, we report that the silencing of the LKB1 tumor suppressor affects the delamination of pre-migratory CNCC from the neural primordium as well as their polarization and survival, thus resulting in severe facial and brain defects. We further show that LKB1-mediated effects on the development of CNCC involve the sequential activation of the AMP-activated protein kinase (AMPK), the Rho-dependent kinase (ROCK) and the actin-based motor protein myosin II. Collectively, these results establish that the complex morphogenetic processes governing head formation critically depends on the activation of the LKB1 signaling network in CNCC."		* '''Review - Collective cell migration in development'''{{#pmid:26783298\|PMID26783298}} "During embryonic development, tissues undergo major rearrangements that lead to germ layer positioning, patterning, and organ morphogenesis. Often these morphogenetic movements are accomplished by the coordinated and cooperative migration of the constituent cells, referred to as collective cell migration. The molecular and biomechanical mechanisms underlying collective migration of developing tissues have been investigated in a variety of models, including border cell migration, tracheal branching, blood vessel sprouting, and the migration of the lateral line primordium, neural crest cells, or head mesendoderm. Here we review recent advances in understanding collective migration in these developmental models, focusing on the interaction between cells and guidance cues presented by the microenvironment and on the role of cell-cell adhesion in mechanical and behavioral coupling of cells within the collective."
	* '''Review - Collective cell migration in development'''~~<ref name=~~PMID26783298~~><pubmed>26783298</pubmed></ref>~~ "During embryonic development, tissues undergo major rearrangements that lead to germ layer positioning, patterning, and organ morphogenesis. Often these morphogenetic movements are accomplished by the coordinated and cooperative migration of the constituent cells, referred to as collective cell migration. The molecular and biomechanical mechanisms underlying collective migration of developing tissues have been investigated in a variety of models, including border cell migration, tracheal branching, blood vessel sprouting, and the migration of the lateral line primordium, neural crest cells, or head mesendoderm. Here we review recent advances in understanding collective migration in these developmental models, focusing on the interaction between cells and guidance cues presented by the microenvironment and on the role of cell-cell adhesion in mechanical and behavioral coupling of cells within the collective."
	\|}		\|}
	{\| class="wikitable mw-collapsible mw-collapsed"		{\| class="wikitable mw-collapsible mw-collapsed"
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	\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}		\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}

	Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Developmental+Cell+Migration ''Developmental Cell Migration'']		Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Developmental+Cell+Migration ''Developmental Cell Migration''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Neural+Crest+Cell+Migration ''Neural Crest Cell Migration'']

	<pubmed ~~limit~~=~~5>Developmental~~ Cell Migration~~</pubmed>~~

	~~Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Neural+Crest+Cell+Migration ''Neural Crest Cell Migration'']~~

	~~<pubmed limit=5>Neural Crest Cell Migration</pubmed>~~
	\|}		\|}
	==Neural Crest Development==		==Neural Crest Development==
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	===Reviews===		===Reviews===
	~~<pubmed></pubmed>~~
	~~<pubmed></pubmed>~~		{{#pmid:26783298}}
	~~<pubmed>26783298</pubmed>~~
	~~<pubmed>~~25733144~~</pubmed>~~		{{#pmid:25733144}}
	~~<pubmed>~~19914236~~</pubmed>~~
			{{#pmid:19914236}}

	===Articles===		===Articles===
	~~<pubmed></pubmed>~~
	~~<pubmed>~~25541234~~</pubmed>~~		{{#pmid:25541234}}
	~~<pubmed>~~21290476~~</pubmed>~~
	~~<pubmed></pubmed>~~		{{#pmid:21290476}}


	===Search PubMed===		===Search PubMed===

Z8600021 at 10:26, 10 Ocak 2018

2018-01-10T10:26:51Z

← Older revision		Revision as of 21:26, 10 Ocak 2018
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	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"
	\|		\|
	* '''STRIP1, a core component of STRIPAK complexes, is essential for normal mesoderm migration in the mouse embryo'''<ref name=PMID29203676><pubmed>29203676</pubmed></ref> "Regulated mesoderm migration is necessary for the proper morphogenesis and organ formation during embryonic development. Cell migration and its dependence on the cytoskeleton and signaling machines have been studied extensively in cultured cells; in contrast, remarkably little is known about the mechanisms that regulate mesoderm cell migration in vivo. Here, we report the identification and characterization of a mouse mutation in striatin-interacting protein 1 (Strip1) that disrupts migration of the mesoderm after the gastrulation epithelial-to-mesenchymal transition (EMT). STRIP1 is a core component of the biochemically defined mammalian striatin-interacting phosphatases and kinase (STRIPAK) complexes that appear to act through regulation of protein phosphatase 2A (PP2A), but their functions in mammals in vivo have not been examined. Strip1-null mutants arrest development at midgestation with profound disruptions in the organization of the mesoderm and its derivatives, including a complete failure of the anterior extension of axial mesoderm. Analysis of cultured mesoderm explants and mouse embryonic fibroblasts from null mutants shows that the mesoderm migration defect is correlated with decreased cell spreading, abnormal focal adhesions, changes in the organization of the actin cytoskeleton, and decreased velocity of cell migration. The results show that STRIPAK complexes are essential for cell migration and tissue morphogenesis in vivo."		* '''STRIP1, a core component of STRIPAK complexes, is essential for normal mesoderm migration in the mouse embryo'''<ref name=PMID29203676><pubmed>29203676</pubmed></ref> "Regulated mesoderm migration is necessary for the proper morphogenesis and organ formation during embryonic development. Cell migration and its dependence on the cytoskeleton and signaling machines have been studied extensively in cultured cells; in contrast, remarkably little is known about the mechanisms that regulate mesoderm cell migration in vivo. Here, we report the identification and characterization of a mouse mutation in striatin-interacting protein 1 (Strip1) that disrupts migration of the mesoderm after the gastrulation epithelial-to-mesenchymal transition (EMT). STRIP1 is a core component of the biochemically defined mammalian striatin-interacting phosphatases and kinase (STRIPAK) complexes that appear to act through regulation of protein phosphatase 2A (PP2A), but their functions in mammals in vivo have not been examined. Strip1-null mutants arrest development at midgestation with profound disruptions in the organization of the mesoderm and its derivatives, including a complete failure of the anterior extension of axial mesoderm. Analysis of cultured mesoderm explants and mouse embryonic fibroblasts from null mutants shows that the mesoderm migration defect is correlated with decreased cell spreading, abnormal focal adhesions, changes in the organization of the actin cytoskeleton, and decreased velocity of cell migration. The results show that STRIPAK complexes are essential for cell migration and tissue morphogenesis in vivo." (More? [[Mesoderm]] \| [https://www.ncbi.nlm.nih.gov/gene/85369 NCBI Gene - STRIP1])
	[https://www.ncbi.nlm.nih.gov/gene/85369 NCBI Gene - STRIP1]

	* '''LKB1 signaling in cephalic neural crest cells is essential for vertebrate head development'''<ref name=PMID27527806><pubmed>27527806</pubmed></ref> "Head development in vertebrates proceeds through a series of elaborate patterning mechanisms and cell-cell interactions involving cephalic neural crest cells (CNCC). These cells undergo extensive migration along stereotypical paths after their separation from the dorsal margins of the neural tube and they give rise to most of the craniofacial skeleton. Here, we report that the silencing of the LKB1 tumor suppressor affects the delamination of pre-migratory CNCC from the neural primordium as well as their polarization and survival, thus resulting in severe facial and brain defects. We further show that LKB1-mediated effects on the development of CNCC involve the sequential activation of the AMP-activated protein kinase (AMPK), the Rho-dependent kinase (ROCK) and the actin-based motor protein myosin II. Collectively, these results establish that the complex morphogenetic processes governing head formation critically depends on the activation of the LKB1 signaling network in CNCC."		* '''LKB1 signaling in cephalic neural crest cells is essential for vertebrate head development'''<ref name=PMID27527806><pubmed>27527806</pubmed></ref> "Head development in vertebrates proceeds through a series of elaborate patterning mechanisms and cell-cell interactions involving cephalic neural crest cells (CNCC). These cells undergo extensive migration along stereotypical paths after their separation from the dorsal margins of the neural tube and they give rise to most of the craniofacial skeleton. Here, we report that the silencing of the LKB1 tumor suppressor affects the delamination of pre-migratory CNCC from the neural primordium as well as their polarization and survival, thus resulting in severe facial and brain defects. We further show that LKB1-mediated effects on the development of CNCC involve the sequential activation of the AMP-activated protein kinase (AMPK), the Rho-dependent kinase (ROCK) and the actin-based motor protein myosin II. Collectively, these results establish that the complex morphogenetic processes governing head formation critically depends on the activation of the LKB1 signaling network in CNCC."

Z8600021 at 10:20, 10 Ocak 2018

2018-01-10T10:20:27Z

← Older revision		Revision as of 21:20, 10 Ocak 2018
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	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"
	\|		\|
			* '''STRIP1, a core component of STRIPAK complexes, is essential for normal mesoderm migration in the mouse embryo'''<ref name=PMID29203676><pubmed>29203676</pubmed></ref> "Regulated mesoderm migration is necessary for the proper morphogenesis and organ formation during embryonic development. Cell migration and its dependence on the cytoskeleton and signaling machines have been studied extensively in cultured cells; in contrast, remarkably little is known about the mechanisms that regulate mesoderm cell migration in vivo. Here, we report the identification and characterization of a mouse mutation in striatin-interacting protein 1 (Strip1) that disrupts migration of the mesoderm after the gastrulation epithelial-to-mesenchymal transition (EMT). STRIP1 is a core component of the biochemically defined mammalian striatin-interacting phosphatases and kinase (STRIPAK) complexes that appear to act through regulation of protein phosphatase 2A (PP2A), but their functions in mammals in vivo have not been examined. Strip1-null mutants arrest development at midgestation with profound disruptions in the organization of the mesoderm and its derivatives, including a complete failure of the anterior extension of axial mesoderm. Analysis of cultured mesoderm explants and mouse embryonic fibroblasts from null mutants shows that the mesoderm migration defect is correlated with decreased cell spreading, abnormal focal adhesions, changes in the organization of the actin cytoskeleton, and decreased velocity of cell migration. The results show that STRIPAK complexes are essential for cell migration and tissue morphogenesis in vivo."
			[https://www.ncbi.nlm.nih.gov/gene/85369 NCBI Gene - STRIP1]

	* '''LKB1 signaling in cephalic neural crest cells is essential for vertebrate head development'''<ref name=PMID27527806><pubmed>27527806</pubmed></ref> "Head development in vertebrates proceeds through a series of elaborate patterning mechanisms and cell-cell interactions involving cephalic neural crest cells (CNCC). These cells undergo extensive migration along stereotypical paths after their separation from the dorsal margins of the neural tube and they give rise to most of the craniofacial skeleton. Here, we report that the silencing of the LKB1 tumor suppressor affects the delamination of pre-migratory CNCC from the neural primordium as well as their polarization and survival, thus resulting in severe facial and brain defects. We further show that LKB1-mediated effects on the development of CNCC involve the sequential activation of the AMP-activated protein kinase (AMPK), the Rho-dependent kinase (ROCK) and the actin-based motor protein myosin II. Collectively, these results establish that the complex morphogenetic processes governing head formation critically depends on the activation of the LKB1 signaling network in CNCC."		* '''LKB1 signaling in cephalic neural crest cells is essential for vertebrate head development'''<ref name=PMID27527806><pubmed>27527806</pubmed></ref> "Head development in vertebrates proceeds through a series of elaborate patterning mechanisms and cell-cell interactions involving cephalic neural crest cells (CNCC). These cells undergo extensive migration along stereotypical paths after their separation from the dorsal margins of the neural tube and they give rise to most of the craniofacial skeleton. Here, we report that the silencing of the LKB1 tumor suppressor affects the delamination of pre-migratory CNCC from the neural primordium as well as their polarization and survival, thus resulting in severe facial and brain defects. We further show that LKB1-mediated effects on the development of CNCC involve the sequential activation of the AMP-activated protein kinase (AMPK), the Rho-dependent kinase (ROCK) and the actin-based motor protein myosin II. Collectively, these results establish that the complex morphogenetic processes governing head formation critically depends on the activation of the LKB1 signaling network in CNCC."
	* '''Review - Collective cell migration in development'''<ref name=PMID26783298><pubmed>26783298</pubmed></ref> "During embryonic development, tissues undergo major rearrangements that lead to germ layer positioning, patterning, and organ morphogenesis. Often these morphogenetic movements are accomplished by the coordinated and cooperative migration of the constituent cells, referred to as collective cell migration. The molecular and biomechanical mechanisms underlying collective migration of developing tissues have been investigated in a variety of models, including border cell migration, tracheal branching, blood vessel sprouting, and the migration of the lateral line primordium, neural crest cells, or head mesendoderm. Here we review recent advances in understanding collective migration in these developmental models, focusing on the interaction between cells and guidance cues presented by the microenvironment and on the role of cell-cell adhesion in mechanical and behavioral coupling of cells within the collective."		* '''Review - Collective cell migration in development'''<ref name=PMID26783298><pubmed>26783298</pubmed></ref> "During embryonic development, tissues undergo major rearrangements that lead to germ layer positioning, patterning, and organ morphogenesis. Often these morphogenetic movements are accomplished by the coordinated and cooperative migration of the constituent cells, referred to as collective cell migration. The molecular and biomechanical mechanisms underlying collective migration of developing tissues have been investigated in a variety of models, including border cell migration, tracheal branching, blood vessel sprouting, and the migration of the lateral line primordium, neural crest cells, or head mesendoderm. Here we review recent advances in understanding collective migration in these developmental models, focusing on the interaction between cells and guidance cues presented by the microenvironment and on the role of cell-cell adhesion in mechanical and behavioral coupling of cells within the collective."

Z8600021 at 00:35, 16 November 2016

2016-11-16T00:35:55Z

← Older revision		Revision as of 11:35, 16 November 2016
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	<center>'''''Mechanism''' - "a process, technique, or system for achieving a result".''</center>		<center>'''''Mechanism''' - "a process, technique, or system for achieving a result"''</center>

Z8600021 at 00:34, 16 November 2016

2016-11-16T00:34:29Z

← Older revision		Revision as of 11:34, 16 November 2016
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	{{Header}}		{{Header}}

	~~{{Template Page}}~~
	==Introduction==		==Introduction==
	[[File:Chicken-gastrulation2.jpg\|thumb\|300px\|Gastrulation involves both epithelial to mesenchymal transition and cell migration]]		[[File:Chicken-gastrulation2.jpg\|thumb\|300px\|Gastrulation involves both epithelial to mesenchymal transition and cell migration]]
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	===Articles===		===Articles===
	~~<pubmed></pubmed>~~
	<pubmed></pubmed>		<pubmed></pubmed>
	<pubmed>25541234</pubmed>		<pubmed>25541234</pubmed>
			<pubmed>21290476</pubmed>
	<pubmed></pubmed>		<pubmed></pubmed>
	===Search PubMed===		===Search PubMed===
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	{{Footer}}		{{Footer}}

	[[Category:Developmental Mechanism]]		[[Category:Developmental Mechanism]][[Category:Draft]]

Z8600021 at 00:31, 16 November 2016

2016-11-16T00:31:06Z

← Older revision		Revision as of 11:31, 16 November 2016
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	==Introduction==		==Introduction==
	[[File:Chicken-gastrulation2.jpg\|thumb\|300px\|Gastrulation involves both epithelial to mesenchymal transition and cell migration]]		[[File:Chicken-gastrulation2.jpg\|thumb\|300px\|Gastrulation involves both epithelial to mesenchymal transition and cell migration]]
	The process of cell migration occurs at different stages throughout embryonic development and involves other developmental mechanisms. The first key migration occurs during [[Gastrulation]]. Later key migratory events also occur during [[Somitogenesis\|somite dispersion]] and [[Neural Crest Development\|neural crest migration]].		The process of cell migration occurs at different stages throughout embryonic development and involves other developmental mechanisms. The first key migration occurs during [[Gastrulation]]. Later key migratory events also occur during [[Somitogenesis\|somite dispersion]] and [[Neural Crest Development\|neural crest migration]].

			This mechanism involves several cellular processes including: cytoskeletal reorganisation, adhesion, extracellular matrix, and chemotactic signaling.

Z8600021 at 02:38, 6 September 2016

2016-09-06T02:38:51Z

← Older revision		Revision as of 13:38, 6 September 2016
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	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"
	\|		\|
	* '''LKB1 signaling in cephalic neural crest cells is essential for vertebrate head development'''<ref name=PMID27527806><pubmed>27527806</pubmed></ref>		* '''LKB1 signaling in cephalic neural crest cells is essential for vertebrate head development'''<ref name=PMID27527806><pubmed>27527806</pubmed></ref> "Head development in vertebrates proceeds through a series of elaborate patterning mechanisms and cell-cell interactions involving cephalic neural crest cells (CNCC). These cells undergo extensive migration along stereotypical paths after their separation from the dorsal margins of the neural tube and they give rise to most of the craniofacial skeleton. Here, we report that the silencing of the LKB1 tumor suppressor affects the delamination of pre-migratory CNCC from the neural primordium as well as their polarization and survival, thus resulting in severe facial and brain defects. We further show that LKB1-mediated effects on the development of CNCC involve the sequential activation of the AMP-activated protein kinase (AMPK), the Rho-dependent kinase (ROCK) and the actin-based motor protein myosin II. Collectively, these results establish that the complex morphogenetic processes governing head formation critically depends on the activation of the LKB1 signaling network in CNCC."
	"Head development in vertebrates proceeds through a series of elaborate patterning mechanisms and cell-cell interactions involving cephalic neural crest cells (CNCC). These cells undergo extensive migration along stereotypical paths after their separation from the dorsal margins of the neural tube and they give rise to most of the craniofacial skeleton. Here, we report that the silencing of the LKB1 tumor suppressor affects the delamination of pre-migratory CNCC from the neural primordium as well as their polarization and survival, thus resulting in severe facial and brain defects. We further show that LKB1-mediated effects on the development of CNCC involve the sequential activation of the AMP-activated protein kinase (AMPK), the Rho-dependent kinase (ROCK) and the actin-based motor protein myosin II. Collectively, these results establish that the complex morphogenetic processes governing head formation critically depends on the activation of the LKB1 signaling network in CNCC."
	* '''Review - Collective cell migration in development'''<ref name=PMID26783298><pubmed>26783298</pubmed></ref> "During embryonic development, tissues undergo major rearrangements that lead to germ layer positioning, patterning, and organ morphogenesis. Often these morphogenetic movements are accomplished by the coordinated and cooperative migration of the constituent cells, referred to as collective cell migration. The molecular and biomechanical mechanisms underlying collective migration of developing tissues have been investigated in a variety of models, including border cell migration, tracheal branching, blood vessel sprouting, and the migration of the lateral line primordium, neural crest cells, or head mesendoderm. Here we review recent advances in understanding collective migration in these developmental models, focusing on the interaction between cells and guidance cues presented by the microenvironment and on the role of cell-cell adhesion in mechanical and behavioral coupling of cells within the collective."		* '''Review - Collective cell migration in development'''<ref name=PMID26783298><pubmed>26783298</pubmed></ref> "During embryonic development, tissues undergo major rearrangements that lead to germ layer positioning, patterning, and organ morphogenesis. Often these morphogenetic movements are accomplished by the coordinated and cooperative migration of the constituent cells, referred to as collective cell migration. The molecular and biomechanical mechanisms underlying collective migration of developing tissues have been investigated in a variety of models, including border cell migration, tracheal branching, blood vessel sprouting, and the migration of the lateral line primordium, neural crest cells, or head mesendoderm. Here we review recent advances in understanding collective migration in these developmental models, focusing on the interaction between cells and guidance cues presented by the microenvironment and on the role of cell-cell adhesion in mechanical and behavioral coupling of cells within the collective."
	\|}		\|}

Z8600021 at 02:31, 6 September 2016

2016-09-06T02:31:02Z

← Older revision		Revision as of 13:31, 6 September 2016
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	{{Template Page}}		{{Template Page}}
	==Introduction==		==Introduction==
	[[File:Chicken-gastrulation2.jpg\|thumb\|300px\|Gastrulation epithelial to mesenchymal transition]]		[[File:Chicken-gastrulation2.jpg\|thumb\|300px\|Gastrulation involves both epithelial to mesenchymal transition and cell migration]]
	The process of cell migration occurs at different stages throughout embryonic development and involves other developmental mechanisms. The first key migration occurs during [[Gastrulation]].		The process of cell migration occurs at different stages throughout embryonic development and involves other developmental mechanisms. The first key migration occurs during [[Gastrulation]]. Later key migratory events also occur during [[Somitogenesis\|somite dispersion]] and [[Neural Crest Development\|neural crest migration]].

Z8600021 at 02:28, 6 September 2016

2016-09-06T02:28:49Z

← Older revision		Revision as of 13:28, 6 September 2016
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	{{Template Page}}		{{Template Page}}
	==Introduction==		==Introduction==
			[[File:Chicken-gastrulation2.jpg\|thumb\|300px\|Gastrulation epithelial to mesenchymal transition]]
	The process of cell migration occurs at different stages throughout embryonic development and involves other developmental mechanisms. The first key migration occurs during [[Gastrulation]].		The process of cell migration occurs at different stages throughout embryonic development and involves other developmental mechanisms. The first key migration occurs during [[Gastrulation]].