The Experts below are selected from a list of 246 Experts worldwide ranked by ideXlab platform
J.a. Mcmahon - One of the best experts on this subject based on the ideXlab platform.
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The midbrain-hindbrain phenotype of Wnt-1−Wnt-1− mice results from stepwise deletion of engrailed-expressing cells by 9.5 days postcoitum
Cell, 1992Co-Authors: Andrew P. Mcmahon, A.l. Joyner, Allan Bradley, J.a. McmahonAbstract:Mice homozygous for null alleles of the putative signaling molecule Wnt-1 have a reproducible phenotype: loss of the midbrain and adjacent cerebellar component of the metencephalon. By examining embryonic expression of the mouse engrailed (En) genes, from 8.0 to 9.5 days postcoitum, we demonstrate that Wnt-1 primarily regulates midbrain development. The midbrain itself is required for normal development of the metencephalon. Thus, the observed neonatal phenotype is explained by a series of early events, within 48 hr of neural plate induction, that leads to a complete loss of En domains in the anterior central nervous system. Wnt-1 and a related gene, Wnt-3a, are coexpressed from early somite stages in dorsal aspects of the Myelencephalon and spinal cord. We suggest that functional redundancy between these two genes accounts for the lack of a caudal central nervous system phenotype.
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the midbrain hindbrain phenotype of wnt 1 wnt 1 mice results from stepwise deletion of engrailed expressing cells by 9 5 days postcoitum
Cell, 1992Co-Authors: Andrew P. Mcmahon, A.l. Joyner, Allan Bradley, J.a. McmahonAbstract:Abstract Mice homozygous for null alleles of the putative signaling molecule Wnt-1 have a reproducible phenotype: loss of the midbrain and adjacent cerebellar component of the metencephalon. By examining embryonic expression of the mouse engrailed (En) genes, from 8.0 to 9.5 days postcoitum, we demonstrate that Wnt-1 primarily regulates midbrain development. The midbrain itself is required for normal development of the metencephalon. Thus, the observed neonatal phenotype is explained by a series of early events, within 48 hr of neural plate induction, that leads to a complete loss of En domains in the anterior central nervous system. Wnt-1 and a related gene, Wnt-3a , are coexpressed from early somite stages in dorsal aspects of the Myelencephalon and spinal cord. We suggest that functional redundancy between these two genes accounts for the lack of a caudal central nervous system phenotype.
Andrew P. Mcmahon - One of the best experts on this subject based on the ideXlab platform.
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The midbrain-hindbrain phenotype of Wnt-1−Wnt-1− mice results from stepwise deletion of engrailed-expressing cells by 9.5 days postcoitum
Cell, 1992Co-Authors: Andrew P. Mcmahon, A.l. Joyner, Allan Bradley, J.a. McmahonAbstract:Mice homozygous for null alleles of the putative signaling molecule Wnt-1 have a reproducible phenotype: loss of the midbrain and adjacent cerebellar component of the metencephalon. By examining embryonic expression of the mouse engrailed (En) genes, from 8.0 to 9.5 days postcoitum, we demonstrate that Wnt-1 primarily regulates midbrain development. The midbrain itself is required for normal development of the metencephalon. Thus, the observed neonatal phenotype is explained by a series of early events, within 48 hr of neural plate induction, that leads to a complete loss of En domains in the anterior central nervous system. Wnt-1 and a related gene, Wnt-3a, are coexpressed from early somite stages in dorsal aspects of the Myelencephalon and spinal cord. We suggest that functional redundancy between these two genes accounts for the lack of a caudal central nervous system phenotype.
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the midbrain hindbrain phenotype of wnt 1 wnt 1 mice results from stepwise deletion of engrailed expressing cells by 9 5 days postcoitum
Cell, 1992Co-Authors: Andrew P. Mcmahon, A.l. Joyner, Allan Bradley, J.a. McmahonAbstract:Abstract Mice homozygous for null alleles of the putative signaling molecule Wnt-1 have a reproducible phenotype: loss of the midbrain and adjacent cerebellar component of the metencephalon. By examining embryonic expression of the mouse engrailed (En) genes, from 8.0 to 9.5 days postcoitum, we demonstrate that Wnt-1 primarily regulates midbrain development. The midbrain itself is required for normal development of the metencephalon. Thus, the observed neonatal phenotype is explained by a series of early events, within 48 hr of neural plate induction, that leads to a complete loss of En domains in the anterior central nervous system. Wnt-1 and a related gene, Wnt-3a , are coexpressed from early somite stages in dorsal aspects of the Myelencephalon and spinal cord. We suggest that functional redundancy between these two genes accounts for the lack of a caudal central nervous system phenotype.
A.l. Joyner - One of the best experts on this subject based on the ideXlab platform.
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The midbrain-hindbrain phenotype of Wnt-1−Wnt-1− mice results from stepwise deletion of engrailed-expressing cells by 9.5 days postcoitum
Cell, 1992Co-Authors: Andrew P. Mcmahon, A.l. Joyner, Allan Bradley, J.a. McmahonAbstract:Mice homozygous for null alleles of the putative signaling molecule Wnt-1 have a reproducible phenotype: loss of the midbrain and adjacent cerebellar component of the metencephalon. By examining embryonic expression of the mouse engrailed (En) genes, from 8.0 to 9.5 days postcoitum, we demonstrate that Wnt-1 primarily regulates midbrain development. The midbrain itself is required for normal development of the metencephalon. Thus, the observed neonatal phenotype is explained by a series of early events, within 48 hr of neural plate induction, that leads to a complete loss of En domains in the anterior central nervous system. Wnt-1 and a related gene, Wnt-3a, are coexpressed from early somite stages in dorsal aspects of the Myelencephalon and spinal cord. We suggest that functional redundancy between these two genes accounts for the lack of a caudal central nervous system phenotype.
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the midbrain hindbrain phenotype of wnt 1 wnt 1 mice results from stepwise deletion of engrailed expressing cells by 9 5 days postcoitum
Cell, 1992Co-Authors: Andrew P. Mcmahon, A.l. Joyner, Allan Bradley, J.a. McmahonAbstract:Abstract Mice homozygous for null alleles of the putative signaling molecule Wnt-1 have a reproducible phenotype: loss of the midbrain and adjacent cerebellar component of the metencephalon. By examining embryonic expression of the mouse engrailed (En) genes, from 8.0 to 9.5 days postcoitum, we demonstrate that Wnt-1 primarily regulates midbrain development. The midbrain itself is required for normal development of the metencephalon. Thus, the observed neonatal phenotype is explained by a series of early events, within 48 hr of neural plate induction, that leads to a complete loss of En domains in the anterior central nervous system. Wnt-1 and a related gene, Wnt-3a , are coexpressed from early somite stages in dorsal aspects of the Myelencephalon and spinal cord. We suggest that functional redundancy between these two genes accounts for the lack of a caudal central nervous system phenotype.
Allan Bradley - One of the best experts on this subject based on the ideXlab platform.
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The midbrain-hindbrain phenotype of Wnt-1−Wnt-1− mice results from stepwise deletion of engrailed-expressing cells by 9.5 days postcoitum
Cell, 1992Co-Authors: Andrew P. Mcmahon, A.l. Joyner, Allan Bradley, J.a. McmahonAbstract:Mice homozygous for null alleles of the putative signaling molecule Wnt-1 have a reproducible phenotype: loss of the midbrain and adjacent cerebellar component of the metencephalon. By examining embryonic expression of the mouse engrailed (En) genes, from 8.0 to 9.5 days postcoitum, we demonstrate that Wnt-1 primarily regulates midbrain development. The midbrain itself is required for normal development of the metencephalon. Thus, the observed neonatal phenotype is explained by a series of early events, within 48 hr of neural plate induction, that leads to a complete loss of En domains in the anterior central nervous system. Wnt-1 and a related gene, Wnt-3a, are coexpressed from early somite stages in dorsal aspects of the Myelencephalon and spinal cord. We suggest that functional redundancy between these two genes accounts for the lack of a caudal central nervous system phenotype.
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the midbrain hindbrain phenotype of wnt 1 wnt 1 mice results from stepwise deletion of engrailed expressing cells by 9 5 days postcoitum
Cell, 1992Co-Authors: Andrew P. Mcmahon, A.l. Joyner, Allan Bradley, J.a. McmahonAbstract:Abstract Mice homozygous for null alleles of the putative signaling molecule Wnt-1 have a reproducible phenotype: loss of the midbrain and adjacent cerebellar component of the metencephalon. By examining embryonic expression of the mouse engrailed (En) genes, from 8.0 to 9.5 days postcoitum, we demonstrate that Wnt-1 primarily regulates midbrain development. The midbrain itself is required for normal development of the metencephalon. Thus, the observed neonatal phenotype is explained by a series of early events, within 48 hr of neural plate induction, that leads to a complete loss of En domains in the anterior central nervous system. Wnt-1 and a related gene, Wnt-3a , are coexpressed from early somite stages in dorsal aspects of the Myelencephalon and spinal cord. We suggest that functional redundancy between these two genes accounts for the lack of a caudal central nervous system phenotype.
Mel Ziman - One of the best experts on this subject based on the ideXlab platform.
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Is requisite for maintenance of a subpopulation of superior collicular neurons and shows a diverging expression pattern to during superior collicular development-0
2011Co-Authors: Jennifer A Thompson, Andreas Zembrzycki, Ahmed Mansouri, Mel ZimanAbstract:W levels of expression compared to other regions (such as developing upper strata or ventricular zone, respectively) showing darker staining. Abbrev. , cerebral cortex; , cerebellum; , cerebellar primordium; , choroid plexus; , diencephalon; , Myelencephalon; , pons; , prosencephalon; , pretectum; , subthalamus; , superior colliculus; , tectum (mesencephalon); , 3ventricle; , 4ventricle. Illustrations are not to scale.Copyright information:Taken from "is requisite for maintenance of a subpopulation of superior collicular neurons and shows a diverging expression pattern to during superior collicular development"http://www.biomedcentral.com/1471-213X/8/62BMC Developmental Biology 2008;8():62-62.Published online 30 May 2008PMCID:PMC2430198.
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Is requisite for maintenance of a subpopulation of superior collicular neurons and shows a diverging expression pattern to during superior collicular development-5
2011Co-Authors: Jennifer A Thompson, Andreas Zembrzycki, Ahmed Mansouri, Mel ZimanAbstract:Rol indicating expression in astrocytes of the Myelencephalon. GFAP+ processes extend from cells located at the pial surface, however the dorsal half of the superior colliculus in mice, like that of wildtype, is not populated by GFAP+ cells. Therefore, cell fate switching and/or transdifferentiation towards the astrocytic lineage does not account for the reduction in Pax7cells dorsally. Immunohistochemical detection of Pax6 (e, f, [inset from e]) and Engrailed (En-1) (g, h [inset from g]) was utilised to examine mesencephalic boundary formation, which appear morphologically unaffected in mutant mice. Abbrev. , cerebral cortex; , interpeduncular fossa;, mesencephalon; , pretectum; , rhombencephalic isthmus. Scale bar: a-d,f,h 100 μm; e,g 500 μm.Copyright information:Taken from "is requisite for maintenance of a subpopulation of superior collicular neurons and shows a diverging expression pattern to during superior collicular development"http://www.biomedcentral.com/1471-213X/8/62BMC Developmental Biology 2008;8():62-62.Published online 30 May 2008PMCID:PMC2430198.
