The Experts below are selected from a list of 115857 Experts worldwide ranked by ideXlab platform
Rolf Kemler - One of the best experts on this subject based on the ideXlab platform.
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inactivation of the beta catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:beta-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of beta-catenin during brain morphogenesis, by specifically inactivating the beta-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of beta-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. beta-Catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(-/-)), suggesting that WNT1 acts through beta-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for beta-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (beta-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of beta-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of beta-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the β catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:beta-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of beta-catenin during brain morphogenesis, by specifically inactivating the beta-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of beta-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. beta-Catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(-/-)), suggesting that WNT1 acts through beta-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for beta-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (beta-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of beta-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of beta-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the β catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(−)(/)(−)), suggesting that WNT1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the beta catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(−)(/)(−)), suggesting that WNT1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.
Veronique Brault - One of the best experts on this subject based on the ideXlab platform.
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inactivation of the beta catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:beta-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of beta-catenin during brain morphogenesis, by specifically inactivating the beta-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of beta-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. beta-Catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(-/-)), suggesting that WNT1 acts through beta-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for beta-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (beta-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of beta-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of beta-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the β catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:beta-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of beta-catenin during brain morphogenesis, by specifically inactivating the beta-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of beta-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. beta-Catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(-/-)), suggesting that WNT1 acts through beta-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for beta-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (beta-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of beta-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of beta-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the β catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(−)(/)(−)), suggesting that WNT1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the beta catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(−)(/)(−)), suggesting that WNT1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.
David H Rowitch - One of the best experts on this subject based on the ideXlab platform.
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loss of emx2 function leads to ectopic expression of WNT1 in the developing telencephalon and cortical dysplasia
Development, 2003Co-Authors: Keith L Ligon, Stavroula Assimacopoulos, Elizabeth A. Grove, Yann Echelard, Paul S Danielian, Sovann Kaing, Andrew P Mcmahon, David H RowitchAbstract:Leptomeningeal glioneuronal heterotopias are a focal type of cortical dysplasia in which neural cells migrate aberrantly into superficial layers of the cerebral cortex and meninges. These heterotopias are frequently observed as microscopic abnormalities in the brains of individuals with central nervous system (CNS) malformations and epilepsy. Previous work has demonstrated that the function of Emx2, which encodes a homeodomain transcription factor, is essential for development of the cortical preplate, which gives rise to the marginal zone and subplate. However, transcriptional targets of EMX2 during CNS development are unknown. We report that leptomeningeal glioneuronal heterotopias form in Emx2(-/-) mice that are equivalent to human lesions. Additionally, we observed ectopic expression of WNT1 in the embryonic roofplate organizer region and dorsal telencephalon. To determine the phenotypic consequences of such WNT1 misexpression, we deleted a putative EMX2 DNA-binding site from the WNT1 enhancer and used this to misexpress WNT1 in the developing murine CNS. Heterotopias were detected in transgenic mice as early as 13.5 days postcoitum, consistent with a defect of preplate development during early phases of radial neuronal migration. Furthermore, we observed diffuse abnormalities of reelin- and calretinin-positive cell populations in the marginal zone and subplate similar to those observed in Emx2-null animals. Taken together, these findings indicate that EMX2 is a direct repressor of WNT1 expression in the developing mammalian telencephalon. They further suggest that EMX2-WNT1 interactions are essential for normal development of preplate derivatives in the mammalian cerebral cortex.
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inactivation of the beta catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:beta-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of beta-catenin during brain morphogenesis, by specifically inactivating the beta-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of beta-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. beta-Catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(-/-)), suggesting that WNT1 acts through beta-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for beta-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (beta-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of beta-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of beta-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the β catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:beta-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of beta-catenin during brain morphogenesis, by specifically inactivating the beta-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of beta-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. beta-Catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(-/-)), suggesting that WNT1 acts through beta-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for beta-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (beta-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of beta-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of beta-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the β catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(−)(/)(−)), suggesting that WNT1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the beta catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(−)(/)(−)), suggesting that WNT1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.
Andrew P Mcmahon - One of the best experts on this subject based on the ideXlab platform.
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loss of emx2 function leads to ectopic expression of WNT1 in the developing telencephalon and cortical dysplasia
Development, 2003Co-Authors: Keith L Ligon, Stavroula Assimacopoulos, Elizabeth A. Grove, Yann Echelard, Paul S Danielian, Sovann Kaing, Andrew P Mcmahon, David H RowitchAbstract:Leptomeningeal glioneuronal heterotopias are a focal type of cortical dysplasia in which neural cells migrate aberrantly into superficial layers of the cerebral cortex and meninges. These heterotopias are frequently observed as microscopic abnormalities in the brains of individuals with central nervous system (CNS) malformations and epilepsy. Previous work has demonstrated that the function of Emx2, which encodes a homeodomain transcription factor, is essential for development of the cortical preplate, which gives rise to the marginal zone and subplate. However, transcriptional targets of EMX2 during CNS development are unknown. We report that leptomeningeal glioneuronal heterotopias form in Emx2(-/-) mice that are equivalent to human lesions. Additionally, we observed ectopic expression of WNT1 in the embryonic roofplate organizer region and dorsal telencephalon. To determine the phenotypic consequences of such WNT1 misexpression, we deleted a putative EMX2 DNA-binding site from the WNT1 enhancer and used this to misexpress WNT1 in the developing murine CNS. Heterotopias were detected in transgenic mice as early as 13.5 days postcoitum, consistent with a defect of preplate development during early phases of radial neuronal migration. Furthermore, we observed diffuse abnormalities of reelin- and calretinin-positive cell populations in the marginal zone and subplate similar to those observed in Emx2-null animals. Taken together, these findings indicate that EMX2 is a direct repressor of WNT1 expression in the developing mammalian telencephalon. They further suggest that EMX2-WNT1 interactions are essential for normal development of preplate derivatives in the mammalian cerebral cortex.
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inactivation of the beta catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:beta-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of beta-catenin during brain morphogenesis, by specifically inactivating the beta-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of beta-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. beta-Catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(-/-)), suggesting that WNT1 acts through beta-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for beta-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (beta-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of beta-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of beta-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the β catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:beta-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of beta-catenin during brain morphogenesis, by specifically inactivating the beta-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of beta-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. beta-Catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(-/-)), suggesting that WNT1 acts through beta-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for beta-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (beta-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of beta-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of beta-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the β catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(−)(/)(−)), suggesting that WNT1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the beta catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(−)(/)(−)), suggesting that WNT1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.
Robert Moore - One of the best experts on this subject based on the ideXlab platform.
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inactivation of the beta catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:beta-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of beta-catenin during brain morphogenesis, by specifically inactivating the beta-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of beta-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. beta-Catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(-/-)), suggesting that WNT1 acts through beta-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for beta-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (beta-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of beta-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of beta-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the β catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:beta-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of beta-catenin during brain morphogenesis, by specifically inactivating the beta-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of beta-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. beta-Catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(-/-)), suggesting that WNT1 acts through beta-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for beta-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (beta-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of beta-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of beta-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the β catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(−)(/)(−)), suggesting that WNT1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.
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inactivation of the beta catenin gene by WNT1 cre mediated deletion results in dramatic brain malformation and failure of craniofacial development
Development, 2001Co-Authors: Veronique Brault, Andrew P Mcmahon, David H Rowitch, Robert Moore, Stefanie Kutsch, Makoto Ishibashi, Lukas Sommer, Oreda Boussadia, Rolf KemlerAbstract:('bgr;)-Catenin is a central component of both the cadherin-catenin cell adhesion complex and the Wnt signaling pathway. We have investigated the role of (β)-catenin during brain morphogenesis, by specifically inactivating the (β)-catenin gene in the region of WNT1 expression. To achieve this, mice with a conditional ('floxed') allele of (β)-catenin with required exons flanked by loxP recombination sequences were intercrossed with transgenic mice that expressed Cre recombinase under control of WNT1 regulatory sequences. (β)-catenin gene deletion resulted in dramatic brain malformation and failure of craniofacial development. Absence of part of the midbrain and all of the cerebellum is reminiscent of the conventional WNT1 knockout (WNT1(−)(/)(−)), suggesting that WNT1 acts through (β)-catenin in controlling midbrain-hindbrain development. The craniofacial phenotype, not observed in embryos that lack WNT1, indicates a role for (β)-catenin in the fate of neural crest cells. Analysis of neural tube explants shows that (β)-catenin is efficiently deleted in migrating neural crest cell precursors. This, together with an increased apoptosis in cells migrating to the cranial ganglia and in areas of prechondrogenic condensations, suggests that removal of (β)-catenin affects neural crest cell survival and/or differentiation. Our results demonstrate the pivotal role of (β)-catenin in morphogenetic processes during brain and craniofacial development.
