The Experts below are selected from a list of 99 Experts worldwide ranked by ideXlab platform
Frank Costantini - One of the best experts on this subject based on the ideXlab platform.
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Actin Depolymerizing Factors Cofilin1 and Destrin Are Required for Ureteric Bud Branching Morphogenesis
2013Co-Authors: Satu Kuure ¤a, Christine B. Gurniak, Cristina Cebrian, Quentin Machingo ¤b, Benson Lu C. ¤c, Xuan Chi ¤d, Deborah Hyink, Walter Witke, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity
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P87. Actin depolymerizing factors Cfl1 and Dstn are required for Ureteric bud branching morphogenesis
Differentiation, 2010Co-Authors: Satu Kuure, Machingo Quentin, Benson Lu, Hyink Deborah, Vivette D. D'agati, Christine B. Gurniak, Witke Walter, Cristina Cebrian, Frank CostantiniAbstract:Branching morphogenesis is a central developmental mechanism utilized in the morphogenesis of several organs including lung, liver, salivary gland and kidney. The molecular control of the basic process of renal differentiation, the Ureteric bud (UB) branching, has been in the focus of extensive studies while the cellular events, such as migration and cell shape changes, underlying this process are poorly understood. The actin depolymerizing factors (ADFs) play important roles in actin cytoskeletal dynamics, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. Therefore we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl11 in UB epithelium, or an inactivating mutation in Dstn, has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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P87. Actin depolymerizing factors Cfl1 and Dstn are required for Ureteric bud branching morphogenesis
Differentiation, 2010Co-Authors: Satu Kuure, Machingo Quentin, Benson Lu, Hyink Deborah, Vivette D. D'agati, Christine B. Gurniak, Witke Walter, Cristina Cebrian, Frank CostantiniAbstract:Branching morphogenesis is a central developmental mechanism utilized in the morphogenesis of several organs including lung, liver, salivary gland and kidney. The molecular control of the basic process of renal differentiation, the Ureteric bud (UB) branching, has been in the focus of extensive studies while the cellular events, such as migration and cell shape changes, underlying this process are poorly understood. The actin depolymerizing factors (ADFs) play important roles in actin cytoskeletal dynamics, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. Therefore we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl11 in UB epithelium, or an inactivating mutation in Dstn, has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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Actin depolymerizing factors cofilin1 and destrin are required for Ureteric bud branching morphogenesis
PLOS Genetics, 2010Co-Authors: Satu Kuure, Benson Lu, Vivette D. D'agati, Christine B. Gurniak, Cristina Cebrian, Deborah Hyink, Walter Witke, Quentin Machingo, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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Actin depolymerizing factors cofilin1 and destrin are required for Ureteric bud branching morphogenesis
PLoS genetics, 2010Co-Authors: Satu Kuure, Vivette D. D'agati, Christine B. Gurniak, Cristina Cebrian, Deborah Hyink, Walter Witke, Quentin Machingo, Xuan Chi, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
Satu Kuure - One of the best experts on this subject based on the ideXlab platform.
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P87. Actin depolymerizing factors Cfl1 and Dstn are required for Ureteric bud branching morphogenesis
Differentiation, 2010Co-Authors: Satu Kuure, Machingo Quentin, Benson Lu, Hyink Deborah, Vivette D. D'agati, Christine B. Gurniak, Witke Walter, Cristina Cebrian, Frank CostantiniAbstract:Branching morphogenesis is a central developmental mechanism utilized in the morphogenesis of several organs including lung, liver, salivary gland and kidney. The molecular control of the basic process of renal differentiation, the Ureteric bud (UB) branching, has been in the focus of extensive studies while the cellular events, such as migration and cell shape changes, underlying this process are poorly understood. The actin depolymerizing factors (ADFs) play important roles in actin cytoskeletal dynamics, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. Therefore we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl11 in UB epithelium, or an inactivating mutation in Dstn, has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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P87. Actin depolymerizing factors Cfl1 and Dstn are required for Ureteric bud branching morphogenesis
Differentiation, 2010Co-Authors: Satu Kuure, Machingo Quentin, Benson Lu, Hyink Deborah, Vivette D. D'agati, Christine B. Gurniak, Witke Walter, Cristina Cebrian, Frank CostantiniAbstract:Branching morphogenesis is a central developmental mechanism utilized in the morphogenesis of several organs including lung, liver, salivary gland and kidney. The molecular control of the basic process of renal differentiation, the Ureteric bud (UB) branching, has been in the focus of extensive studies while the cellular events, such as migration and cell shape changes, underlying this process are poorly understood. The actin depolymerizing factors (ADFs) play important roles in actin cytoskeletal dynamics, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. Therefore we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl11 in UB epithelium, or an inactivating mutation in Dstn, has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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Actin depolymerizing factors cofilin1 and destrin are required for Ureteric bud branching morphogenesis
PLOS Genetics, 2010Co-Authors: Satu Kuure, Benson Lu, Vivette D. D'agati, Christine B. Gurniak, Cristina Cebrian, Deborah Hyink, Walter Witke, Quentin Machingo, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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Actin depolymerizing factors cofilin1 and destrin are required for Ureteric bud branching morphogenesis
PLoS genetics, 2010Co-Authors: Satu Kuure, Vivette D. D'agati, Christine B. Gurniak, Cristina Cebrian, Deborah Hyink, Walter Witke, Quentin Machingo, Xuan Chi, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
Christine B. Gurniak - One of the best experts on this subject based on the ideXlab platform.
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Actin Depolymerizing Factors Cofilin1 and Destrin Are Required for Ureteric Bud Branching Morphogenesis
2013Co-Authors: Satu Kuure ¤a, Christine B. Gurniak, Cristina Cebrian, Quentin Machingo ¤b, Benson Lu C. ¤c, Xuan Chi ¤d, Deborah Hyink, Walter Witke, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity
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P87. Actin depolymerizing factors Cfl1 and Dstn are required for Ureteric bud branching morphogenesis
Differentiation, 2010Co-Authors: Satu Kuure, Machingo Quentin, Benson Lu, Hyink Deborah, Vivette D. D'agati, Christine B. Gurniak, Witke Walter, Cristina Cebrian, Frank CostantiniAbstract:Branching morphogenesis is a central developmental mechanism utilized in the morphogenesis of several organs including lung, liver, salivary gland and kidney. The molecular control of the basic process of renal differentiation, the Ureteric bud (UB) branching, has been in the focus of extensive studies while the cellular events, such as migration and cell shape changes, underlying this process are poorly understood. The actin depolymerizing factors (ADFs) play important roles in actin cytoskeletal dynamics, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. Therefore we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl11 in UB epithelium, or an inactivating mutation in Dstn, has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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P87. Actin depolymerizing factors Cfl1 and Dstn are required for Ureteric bud branching morphogenesis
Differentiation, 2010Co-Authors: Satu Kuure, Machingo Quentin, Benson Lu, Hyink Deborah, Vivette D. D'agati, Christine B. Gurniak, Witke Walter, Cristina Cebrian, Frank CostantiniAbstract:Branching morphogenesis is a central developmental mechanism utilized in the morphogenesis of several organs including lung, liver, salivary gland and kidney. The molecular control of the basic process of renal differentiation, the Ureteric bud (UB) branching, has been in the focus of extensive studies while the cellular events, such as migration and cell shape changes, underlying this process are poorly understood. The actin depolymerizing factors (ADFs) play important roles in actin cytoskeletal dynamics, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. Therefore we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl11 in UB epithelium, or an inactivating mutation in Dstn, has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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Actin depolymerizing factors cofilin1 and destrin are required for Ureteric bud branching morphogenesis
PLOS Genetics, 2010Co-Authors: Satu Kuure, Benson Lu, Vivette D. D'agati, Christine B. Gurniak, Cristina Cebrian, Deborah Hyink, Walter Witke, Quentin Machingo, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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Actin depolymerizing factors cofilin1 and destrin are required for Ureteric bud branching morphogenesis
PLoS genetics, 2010Co-Authors: Satu Kuure, Vivette D. D'agati, Christine B. Gurniak, Cristina Cebrian, Deborah Hyink, Walter Witke, Quentin Machingo, Xuan Chi, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
Cristina Cebrian - One of the best experts on this subject based on the ideXlab platform.
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Actin Depolymerizing Factors Cofilin1 and Destrin Are Required for Ureteric Bud Branching Morphogenesis
2013Co-Authors: Satu Kuure ¤a, Christine B. Gurniak, Cristina Cebrian, Quentin Machingo ¤b, Benson Lu C. ¤c, Xuan Chi ¤d, Deborah Hyink, Walter Witke, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity
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P87. Actin depolymerizing factors Cfl1 and Dstn are required for Ureteric bud branching morphogenesis
Differentiation, 2010Co-Authors: Satu Kuure, Machingo Quentin, Benson Lu, Hyink Deborah, Vivette D. D'agati, Christine B. Gurniak, Witke Walter, Cristina Cebrian, Frank CostantiniAbstract:Branching morphogenesis is a central developmental mechanism utilized in the morphogenesis of several organs including lung, liver, salivary gland and kidney. The molecular control of the basic process of renal differentiation, the Ureteric bud (UB) branching, has been in the focus of extensive studies while the cellular events, such as migration and cell shape changes, underlying this process are poorly understood. The actin depolymerizing factors (ADFs) play important roles in actin cytoskeletal dynamics, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. Therefore we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl11 in UB epithelium, or an inactivating mutation in Dstn, has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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P87. Actin depolymerizing factors Cfl1 and Dstn are required for Ureteric bud branching morphogenesis
Differentiation, 2010Co-Authors: Satu Kuure, Machingo Quentin, Benson Lu, Hyink Deborah, Vivette D. D'agati, Christine B. Gurniak, Witke Walter, Cristina Cebrian, Frank CostantiniAbstract:Branching morphogenesis is a central developmental mechanism utilized in the morphogenesis of several organs including lung, liver, salivary gland and kidney. The molecular control of the basic process of renal differentiation, the Ureteric bud (UB) branching, has been in the focus of extensive studies while the cellular events, such as migration and cell shape changes, underlying this process are poorly understood. The actin depolymerizing factors (ADFs) play important roles in actin cytoskeletal dynamics, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. Therefore we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl11 in UB epithelium, or an inactivating mutation in Dstn, has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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Actin depolymerizing factors cofilin1 and destrin are required for Ureteric bud branching morphogenesis
PLOS Genetics, 2010Co-Authors: Satu Kuure, Benson Lu, Vivette D. D'agati, Christine B. Gurniak, Cristina Cebrian, Deborah Hyink, Walter Witke, Quentin Machingo, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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Actin depolymerizing factors cofilin1 and destrin are required for Ureteric bud branching morphogenesis
PLoS genetics, 2010Co-Authors: Satu Kuure, Vivette D. D'agati, Christine B. Gurniak, Cristina Cebrian, Deborah Hyink, Walter Witke, Quentin Machingo, Xuan Chi, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
Vivette D. D'agati - One of the best experts on this subject based on the ideXlab platform.
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P87. Actin depolymerizing factors Cfl1 and Dstn are required for Ureteric bud branching morphogenesis
Differentiation, 2010Co-Authors: Satu Kuure, Machingo Quentin, Benson Lu, Hyink Deborah, Vivette D. D'agati, Christine B. Gurniak, Witke Walter, Cristina Cebrian, Frank CostantiniAbstract:Branching morphogenesis is a central developmental mechanism utilized in the morphogenesis of several organs including lung, liver, salivary gland and kidney. The molecular control of the basic process of renal differentiation, the Ureteric bud (UB) branching, has been in the focus of extensive studies while the cellular events, such as migration and cell shape changes, underlying this process are poorly understood. The actin depolymerizing factors (ADFs) play important roles in actin cytoskeletal dynamics, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. Therefore we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl11 in UB epithelium, or an inactivating mutation in Dstn, has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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P87. Actin depolymerizing factors Cfl1 and Dstn are required for Ureteric bud branching morphogenesis
Differentiation, 2010Co-Authors: Satu Kuure, Machingo Quentin, Benson Lu, Hyink Deborah, Vivette D. D'agati, Christine B. Gurniak, Witke Walter, Cristina Cebrian, Frank CostantiniAbstract:Branching morphogenesis is a central developmental mechanism utilized in the morphogenesis of several organs including lung, liver, salivary gland and kidney. The molecular control of the basic process of renal differentiation, the Ureteric bud (UB) branching, has been in the focus of extensive studies while the cellular events, such as migration and cell shape changes, underlying this process are poorly understood. The actin depolymerizing factors (ADFs) play important roles in actin cytoskeletal dynamics, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. Therefore we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl11 in UB epithelium, or an inactivating mutation in Dstn, has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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Actin depolymerizing factors cofilin1 and destrin are required for Ureteric bud branching morphogenesis
PLOS Genetics, 2010Co-Authors: Satu Kuure, Benson Lu, Vivette D. D'agati, Christine B. Gurniak, Cristina Cebrian, Deborah Hyink, Walter Witke, Quentin Machingo, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
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Actin depolymerizing factors cofilin1 and destrin are required for Ureteric bud branching morphogenesis
PLoS genetics, 2010Co-Authors: Satu Kuure, Vivette D. D'agati, Christine B. Gurniak, Cristina Cebrian, Deborah Hyink, Walter Witke, Quentin Machingo, Xuan Chi, Frank CostantiniAbstract:The actin depolymerizing factors (ADFs) play important roles in several cellular processes that require cytoskeletal rearrangements, such as cell migration, but little is known about the in vivo functions of ADFs in developmental events like branching morphogenesis. While the molecular control of Ureteric bud (UB) branching during kidney development has been extensively studied, the detailed cellular events underlying this process remain poorly understood. To gain insight into the role of actin cytoskeletal dynamics during renal branching morphogenesis, we studied the functional requirements for the closely related ADFs cofilin1 (Cfl1) and destrin (Dstn) during mouse development. Either deletion of Cfl1 in UB epithelium or an inactivating mutation in Dstn has no effect on renal morphogenesis, but simultaneous lack of both genes arrests branching morphogenesis at an early stage, revealing considerable functional overlap between cofilin1 and destrin. Lack of Cfl1 and Dstn in the UB causes accumulation of filamentous actin, disruption of normal epithelial organization, and defects in cell migration. Animals with less severe combinations of mutant Cfl1 and Dstn alleles, which retain one wild-type Cfl1 or Dstn allele, display abnormalities including Ureter Duplication, renal hypoplasia, and abnormal kidney shape. The results indicate that ADF activity, provided by either cofilin1 or destrin, is essential in UB epithelial cells for normal growth and branching.
