The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform
Paul D Henion - One of the best experts on this subject based on the ideXlab platform.
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zebrafish colgate hdac1 functions in the non canonical wnt pathway during Axial Extension and in wnt independent branchiomotor neuron migration
Mechanisms of Development, 2007Co-Authors: Roopa M Nambiar, Myron S Ignatius, Paul D HenionAbstract:Vertebrate gastrulation involves the coordinated movements of populations of cells. These movements include cellular rearrangements in which cells polarize along their medio-lateral axes leading to cell intercalations that result in elongation of the body axis. Molecular analysis of this process has implicated the non-canonical Wnt/Frizzled signaling pathway that is similar to the planar cell polarity pathway (PCP) in Drosophila. Here we describe a zebrafish mutant, colgate (col), which displays defects in the Extension of the body axis and the migration of branchiomotor neurons. Activation of the non-canonical Wnt/PCP pathway in these mutant embryos by overexpressing ΔNdishevelled, rho kinase2 and van gogh-like protein 2 (vangl2) rescues the Extension defects suggesting that col acts as a positive regulator of the non-canonical Wnt/PCP pathway. Further, we show that col normally regulates the caudal migration of nVII facial hindbrain branchiomotor neurons and that the mutant phenotype can be rescued by misexpression of vangl2 independent of the Wnt/PCP pathway. We cloned the col locus and found that it encodes histone deacetylase1 (hdac1). Our previous results and studies by others have implicated hdac1 in repressing the canonical Wnt pathway. Here, we demonstrate novel roles for zebrafish hdac1 in activating non-canonical Wnt/PCP signaling underlying Axial Extension and in promoting Wnt-independent caudal migration of a subset of hindbrain branchiomotor neurons.
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Zebrafish colgate/hdac1 functions in the non-canonical Wnt pathway during Axial Extension and in Wnt-independent branchiomotor neuron migration.
Mechanisms of development, 2007Co-Authors: Roopa M Nambiar, Myron S Ignatius, Paul D HenionAbstract:Vertebrate gastrulation involves the coordinated movements of populations of cells. These movements include cellular rearrangements in which cells polarize along their medio-lateral axes leading to cell intercalations that result in elongation of the body axis. Molecular analysis of this process has implicated the non-canonical Wnt/Frizzled signaling pathway that is similar to the planar cell polarity pathway (PCP) in Drosophila. Here we describe a zebrafish mutant, colgate (col), which displays defects in the Extension of the body axis and the migration of branchiomotor neurons. Activation of the non-canonical Wnt/PCP pathway in these mutant embryos by overexpressing DeltaNdishevelled, rho kinase2 and van gogh-like protein 2 (vangl2) rescues the Extension defects suggesting that col acts as a positive regulator of the non-canonical Wnt/PCP pathway. Further, we show that col normally regulates the caudal migration of nVII facial hindbrain branchiomotor neurons and that the mutant phenotype can be rescued by misexpression of vangl2 independent of the Wnt/PCP pathway. We cloned the col locus and found that it encodes histone deacetylase1 (hdac1). Our previous results and studies by others have implicated hdac1 in repressing the canonical Wnt pathway. Here, we demonstrate novel roles for zebrafish hdac1 in activating non-canonical Wnt/PCP signaling underlying Axial Extension and in promoting Wnt-independent caudal migration of a subset of hindbrain branchiomotor neurons.
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Zebrafish colgate/hdac1 functions in the non-canonical Wnt pathway during Axial Extension and in Wnt-independent branchiomotor neuron migration
Mechanisms of Development, 2007Co-Authors: Roopa M Nambiar, Myron S Ignatius, Paul D HenionAbstract:Vertebrate gastrulation involves the coordinated movements of populations of cells. These movements include cellular rearrangements in which cells polarize along their medio-lateral axes leading to cell intercalations that result in elongation of the body axis. Molecular analysis of this process has implicated the non-canonical Wnt/Frizzled signaling pathway that is similar to the planar cell polarity pathway (PCP) in Drosophila. Here we describe a zebrafish mutant, colgate (col), which displays defects in the Extension of the body axis and the migration of branchiomotor neurons. Activation of the non-canonical Wnt/PCP pathway in these mutant embryos by overexpressing ΔNdishevelled, rho kinase2 and van gogh-like protein 2 (vangl2) rescues the Extension defects suggesting that col acts as a positive regulator of the non-canonical Wnt/PCP pathway. Further, we show that col normally regulates the caudal migration of nVII facial hindbrain branchiomotor neurons and that the mutant phenotype can be rescued by misexpression of vangl2 independent of the Wnt/PCP pathway. We cloned the col locus and found that it encodes histone deacetylase1 (hdac1). Our previous results and studies by others have implicated hdac1 in repressing the canonical Wnt pathway. Here, we demonstrate novel roles for zebrafish hdac1 in activating non-canonical Wnt/PCP signaling underlying Axial Extension and in promoting Wnt-independent caudal migration of a subset of hindbrain branchiomotor neurons.
Roopa M Nambiar - One of the best experts on this subject based on the ideXlab platform.
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zebrafish colgate hdac1 functions in the non canonical wnt pathway during Axial Extension and in wnt independent branchiomotor neuron migration
Mechanisms of Development, 2007Co-Authors: Roopa M Nambiar, Myron S Ignatius, Paul D HenionAbstract:Vertebrate gastrulation involves the coordinated movements of populations of cells. These movements include cellular rearrangements in which cells polarize along their medio-lateral axes leading to cell intercalations that result in elongation of the body axis. Molecular analysis of this process has implicated the non-canonical Wnt/Frizzled signaling pathway that is similar to the planar cell polarity pathway (PCP) in Drosophila. Here we describe a zebrafish mutant, colgate (col), which displays defects in the Extension of the body axis and the migration of branchiomotor neurons. Activation of the non-canonical Wnt/PCP pathway in these mutant embryos by overexpressing ΔNdishevelled, rho kinase2 and van gogh-like protein 2 (vangl2) rescues the Extension defects suggesting that col acts as a positive regulator of the non-canonical Wnt/PCP pathway. Further, we show that col normally regulates the caudal migration of nVII facial hindbrain branchiomotor neurons and that the mutant phenotype can be rescued by misexpression of vangl2 independent of the Wnt/PCP pathway. We cloned the col locus and found that it encodes histone deacetylase1 (hdac1). Our previous results and studies by others have implicated hdac1 in repressing the canonical Wnt pathway. Here, we demonstrate novel roles for zebrafish hdac1 in activating non-canonical Wnt/PCP signaling underlying Axial Extension and in promoting Wnt-independent caudal migration of a subset of hindbrain branchiomotor neurons.
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Zebrafish colgate/hdac1 functions in the non-canonical Wnt pathway during Axial Extension and in Wnt-independent branchiomotor neuron migration.
Mechanisms of development, 2007Co-Authors: Roopa M Nambiar, Myron S Ignatius, Paul D HenionAbstract:Vertebrate gastrulation involves the coordinated movements of populations of cells. These movements include cellular rearrangements in which cells polarize along their medio-lateral axes leading to cell intercalations that result in elongation of the body axis. Molecular analysis of this process has implicated the non-canonical Wnt/Frizzled signaling pathway that is similar to the planar cell polarity pathway (PCP) in Drosophila. Here we describe a zebrafish mutant, colgate (col), which displays defects in the Extension of the body axis and the migration of branchiomotor neurons. Activation of the non-canonical Wnt/PCP pathway in these mutant embryos by overexpressing DeltaNdishevelled, rho kinase2 and van gogh-like protein 2 (vangl2) rescues the Extension defects suggesting that col acts as a positive regulator of the non-canonical Wnt/PCP pathway. Further, we show that col normally regulates the caudal migration of nVII facial hindbrain branchiomotor neurons and that the mutant phenotype can be rescued by misexpression of vangl2 independent of the Wnt/PCP pathway. We cloned the col locus and found that it encodes histone deacetylase1 (hdac1). Our previous results and studies by others have implicated hdac1 in repressing the canonical Wnt pathway. Here, we demonstrate novel roles for zebrafish hdac1 in activating non-canonical Wnt/PCP signaling underlying Axial Extension and in promoting Wnt-independent caudal migration of a subset of hindbrain branchiomotor neurons.
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Zebrafish colgate/hdac1 functions in the non-canonical Wnt pathway during Axial Extension and in Wnt-independent branchiomotor neuron migration
Mechanisms of Development, 2007Co-Authors: Roopa M Nambiar, Myron S Ignatius, Paul D HenionAbstract:Vertebrate gastrulation involves the coordinated movements of populations of cells. These movements include cellular rearrangements in which cells polarize along their medio-lateral axes leading to cell intercalations that result in elongation of the body axis. Molecular analysis of this process has implicated the non-canonical Wnt/Frizzled signaling pathway that is similar to the planar cell polarity pathway (PCP) in Drosophila. Here we describe a zebrafish mutant, colgate (col), which displays defects in the Extension of the body axis and the migration of branchiomotor neurons. Activation of the non-canonical Wnt/PCP pathway in these mutant embryos by overexpressing ΔNdishevelled, rho kinase2 and van gogh-like protein 2 (vangl2) rescues the Extension defects suggesting that col acts as a positive regulator of the non-canonical Wnt/PCP pathway. Further, we show that col normally regulates the caudal migration of nVII facial hindbrain branchiomotor neurons and that the mutant phenotype can be rescued by misexpression of vangl2 independent of the Wnt/PCP pathway. We cloned the col locus and found that it encodes histone deacetylase1 (hdac1). Our previous results and studies by others have implicated hdac1 in repressing the canonical Wnt pathway. Here, we demonstrate novel roles for zebrafish hdac1 in activating non-canonical Wnt/PCP signaling underlying Axial Extension and in promoting Wnt-independent caudal migration of a subset of hindbrain branchiomotor neurons.
Myron S Ignatius - One of the best experts on this subject based on the ideXlab platform.
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zebrafish colgate hdac1 functions in the non canonical wnt pathway during Axial Extension and in wnt independent branchiomotor neuron migration
Mechanisms of Development, 2007Co-Authors: Roopa M Nambiar, Myron S Ignatius, Paul D HenionAbstract:Vertebrate gastrulation involves the coordinated movements of populations of cells. These movements include cellular rearrangements in which cells polarize along their medio-lateral axes leading to cell intercalations that result in elongation of the body axis. Molecular analysis of this process has implicated the non-canonical Wnt/Frizzled signaling pathway that is similar to the planar cell polarity pathway (PCP) in Drosophila. Here we describe a zebrafish mutant, colgate (col), which displays defects in the Extension of the body axis and the migration of branchiomotor neurons. Activation of the non-canonical Wnt/PCP pathway in these mutant embryos by overexpressing ΔNdishevelled, rho kinase2 and van gogh-like protein 2 (vangl2) rescues the Extension defects suggesting that col acts as a positive regulator of the non-canonical Wnt/PCP pathway. Further, we show that col normally regulates the caudal migration of nVII facial hindbrain branchiomotor neurons and that the mutant phenotype can be rescued by misexpression of vangl2 independent of the Wnt/PCP pathway. We cloned the col locus and found that it encodes histone deacetylase1 (hdac1). Our previous results and studies by others have implicated hdac1 in repressing the canonical Wnt pathway. Here, we demonstrate novel roles for zebrafish hdac1 in activating non-canonical Wnt/PCP signaling underlying Axial Extension and in promoting Wnt-independent caudal migration of a subset of hindbrain branchiomotor neurons.
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Zebrafish colgate/hdac1 functions in the non-canonical Wnt pathway during Axial Extension and in Wnt-independent branchiomotor neuron migration.
Mechanisms of development, 2007Co-Authors: Roopa M Nambiar, Myron S Ignatius, Paul D HenionAbstract:Vertebrate gastrulation involves the coordinated movements of populations of cells. These movements include cellular rearrangements in which cells polarize along their medio-lateral axes leading to cell intercalations that result in elongation of the body axis. Molecular analysis of this process has implicated the non-canonical Wnt/Frizzled signaling pathway that is similar to the planar cell polarity pathway (PCP) in Drosophila. Here we describe a zebrafish mutant, colgate (col), which displays defects in the Extension of the body axis and the migration of branchiomotor neurons. Activation of the non-canonical Wnt/PCP pathway in these mutant embryos by overexpressing DeltaNdishevelled, rho kinase2 and van gogh-like protein 2 (vangl2) rescues the Extension defects suggesting that col acts as a positive regulator of the non-canonical Wnt/PCP pathway. Further, we show that col normally regulates the caudal migration of nVII facial hindbrain branchiomotor neurons and that the mutant phenotype can be rescued by misexpression of vangl2 independent of the Wnt/PCP pathway. We cloned the col locus and found that it encodes histone deacetylase1 (hdac1). Our previous results and studies by others have implicated hdac1 in repressing the canonical Wnt pathway. Here, we demonstrate novel roles for zebrafish hdac1 in activating non-canonical Wnt/PCP signaling underlying Axial Extension and in promoting Wnt-independent caudal migration of a subset of hindbrain branchiomotor neurons.
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Zebrafish colgate/hdac1 functions in the non-canonical Wnt pathway during Axial Extension and in Wnt-independent branchiomotor neuron migration
Mechanisms of Development, 2007Co-Authors: Roopa M Nambiar, Myron S Ignatius, Paul D HenionAbstract:Vertebrate gastrulation involves the coordinated movements of populations of cells. These movements include cellular rearrangements in which cells polarize along their medio-lateral axes leading to cell intercalations that result in elongation of the body axis. Molecular analysis of this process has implicated the non-canonical Wnt/Frizzled signaling pathway that is similar to the planar cell polarity pathway (PCP) in Drosophila. Here we describe a zebrafish mutant, colgate (col), which displays defects in the Extension of the body axis and the migration of branchiomotor neurons. Activation of the non-canonical Wnt/PCP pathway in these mutant embryos by overexpressing ΔNdishevelled, rho kinase2 and van gogh-like protein 2 (vangl2) rescues the Extension defects suggesting that col acts as a positive regulator of the non-canonical Wnt/PCP pathway. Further, we show that col normally regulates the caudal migration of nVII facial hindbrain branchiomotor neurons and that the mutant phenotype can be rescued by misexpression of vangl2 independent of the Wnt/PCP pathway. We cloned the col locus and found that it encodes histone deacetylase1 (hdac1). Our previous results and studies by others have implicated hdac1 in repressing the canonical Wnt pathway. Here, we demonstrate novel roles for zebrafish hdac1 in activating non-canonical Wnt/PCP signaling underlying Axial Extension and in promoting Wnt-independent caudal migration of a subset of hindbrain branchiomotor neurons.
Moisés Mallo - One of the best experts on this subject based on the ideXlab platform.
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Three and Four-Dimensional Visualization and Analysis Approaches to Study Vertebrate Axial Elongation and Segmentation
Journal of visualized experiments : JoVE, 2021Co-Authors: André Dias, Gabriel G. Martins, Alexandre Lopes, Moisés MalloAbstract:Somitogenesis is a hallmark of vertebrate embryonic development. For years, researchers have been studying this process in a variety of organisms using a wide range of techniques encompassing ex vivo and in vitro approaches. However, most studies still rely on the analysis of two-dimensional (2D) imaging data, which limits proper evaluation of a developmental process like Axial Extension and somitogenesis involving highly dynamic interactions in a complex 3D space. Here we describe techniques that allow mouse live imaging acquisition, dataset processing, visualization and analysis in 3D and 4D to study the cells (e.g., neuromesodermal progenitors) involved in these developmental processes. We also provide a step-by-step protocol for optical projection tomography and whole-mount immunofluorescence microscopy in mouse embryos (from sample preparation to image acquisition) and show a pipeline that we developed to process and visualize 3D image data. We extend the use of some of these techniques and highlight specific features of different available software (e.g., Fiji/ImageJ, Drishti, Amira and Imaris) that can be used to improve our current understanding of Axial Extension and somite formation (e.g., 3D reconstructions). Altogether, the techniques here described emphasize the importance of 3D data visualization and analysis in developmental biology, and might help other researchers to better address 3D and 4D image data in the context of vertebrate Axial Extension and segmentation. Finally, the work also employs novel tools to facilitate teaching vertebrate embryonic development.
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compartment dependent activities of wnt3a β catenin signaling during vertebrate Axial Extension
Developmental Biology, 2014Co-Authors: Arnon Dias Jurberg, Rita Aires, Ana Nóvoa, Jennifer E. Rowland, Moisés MalloAbstract:Extension of the vertebrate body results from the concerted activity of many signals in the posterior embryonic end. Among them, Wnt3a has been shown to play relevant roles in the regulation of Axial progenitor activity, mesoderm formation and somitogenesis. However, its impact on Axial growth remains to be fully understood. Using a transgenic approach in the mouse, we found that the effect of Wnt3a signaling varies depending on the target tissue. High levels of Wnt3a in the epiblast prevented formation of neural tissues, but did not impair Axial progenitors from producing different mesodermal lineages. These mesodermal tissues maintained a remarkable degree of organization, even within a severely malformed embryo. However, from the cells that failed to take a neural fate, only those that left the epithelial layer of the epiblast activated a mesodermal program. The remaining tissue accumulated as a folded epithelium that kept some epiblast-like characteristics. Together with previously published observations, our results suggest a dose-dependent role for Wnt3a in regulating the balance between renewal and selection of differentiation fates of Axial progenitors in the epiblast. In the parAxial mesoderm, appropriate regulation of Wnt/β-catenin signaling was required not only for somitogenesis, but also for providing proper anterior-posterior polarity to the somites. Both processes seem to rely on mechanisms with different requirements for feedback modulation of Wnt/β-catenin signaling, once segmentation occurred in the presence of high levels of Wnt3a in the presomitic mesoderm, but not after permanent expression of a constitutively active form of β-catenin. Together, our findings suggest that Wnt3a/β-catenin signaling plays sequential roles during posterior Extension, which are strongly dependent on the target tissue. This provides an additional example of how much the functional output of signaling systems depends on the competence of the responding cells.
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Compartment-dependent activities of Wnt3a/β-catenin signaling during vertebrate Axial Extension.
Developmental biology, 2014Co-Authors: Arnon Dias Jurberg, Rita Aires, Ana Nóvoa, Jennifer E. Rowland, Moisés MalloAbstract:Extension of the vertebrate body results from the concerted activity of many signals in the posterior embryonic end. Among them, Wnt3a has been shown to play relevant roles in the regulation of Axial progenitor activity, mesoderm formation and somitogenesis. However, its impact on Axial growth remains to be fully understood. Using a transgenic approach in the mouse, we found that the effect of Wnt3a signaling varies depending on the target tissue. High levels of Wnt3a in the epiblast prevented formation of neural tissues, but did not impair Axial progenitors from producing different mesodermal lineages. These mesodermal tissues maintained a remarkable degree of organization, even within a severely malformed embryo. However, from the cells that failed to take a neural fate, only those that left the epithelial layer of the epiblast activated a mesodermal program. The remaining tissue accumulated as a folded epithelium that kept some epiblast-like characteristics. Together with previously published observations, our results suggest a dose-dependent role for Wnt3a in regulating the balance between renewal and selection of differentiation fates of Axial progenitors in the epiblast. In the parAxial mesoderm, appropriate regulation of Wnt/β-catenin signaling was required not only for somitogenesis, but also for providing proper anterior-posterior polarity to the somites. Both processes seem to rely on mechanisms with different requirements for feedback modulation of Wnt/β-catenin signaling, once segmentation occurred in the presence of high levels of Wnt3a in the presomitic mesoderm, but not after permanent expression of a constitutively active form of β-catenin. Together, our findings suggest that Wnt3a/β-catenin signaling plays sequential roles during posterior Extension, which are strongly dependent on the target tissue. This provides an additional example of how much the functional output of signaling systems depends on the competence of the responding cells.
Jay D. Humphrey - One of the best experts on this subject based on the ideXlab platform.
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Modeling effects of Axial Extension on arterial growth and remodeling
Medical & biological engineering & computing, 2009Co-Authors: A. Valentín, Jay D. HumphreyAbstract:Diverse mechanical perturbations elicit arterial growth and remodeling responses that appear to optimize structure and function so as to promote mechanical homeostasis. For example, it is well known that functional adaptations to sustained changes in transmural pressure and blood flow primarily affect wall thickness and caliber to restore circumferential and wall shear stresses toward normal. More recently, however, it has been shown that changes in Axial Extension similarly prompt dramatic cell and matrix reorganization and turnover, resulting in marked changes in unloaded geometry and mechanical behavior that presumably restore Axial stress toward normal. Because of the inability to infer Axial stress from in vivo measurements, simulations are needed to examine this hypothesis and to guide the design of future experiments. In this paper, we show that a constrained mixture model predicts salient features of observed responses to step increases in Axial Extension, including marked increases in fibrous constituent production, leading to a compensatory lengthening that restores original mechanical behavior. Because Axial Extension can be modified via diverse surgical procedures, including bypass operations, and exploited in tissue regeneration research, there is a need for increased attention to this important aspect of arterial biomechanics and mechanobiology.
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BiAxial biomechanical adaptations of mouse carotid arteries cultured at altered Axial Extension.
Journal of biomechanics, 2006Co-Authors: R. L. Gleason, Emily Wilson, Jay D. HumphreyAbstract:Many have studied the roles of altered blood flow and pressure on adaptive responses of blood vessels, but few have studied the role of altered Axial loads. We exposed common carotid arteries from wild-type mice to low, medium, or high Axial Extensions while maintaining the same pressure and luminal flow rate for two days in culture, and studied adaptations in vessel geometry, in vitro loads, and stresses while collecting biAxial biomechanical (pressure-diameter and Axial force-length) data on Day 0 (initial control conditions), Day 1, and Day 2. In addition, we compared vasoreactive responses to phenylephrine, carbamylcholine chloride, and sodium nitroprusside at the end of the 2-day culture period. We found significant differences in the structural (e.g., pressure-Axial force and Axial force-length) responses between groups as well as within each group over time. These adaptations seem to be aimed at restoring the mechanical state from a perturbed condition (e.g., low or high Axial Extension) toward a normal 'homeostatic' condition. Although structural responses (e.g., pressure-Axial force and Axial force-length) differed between groups on Day 2, the material behavior (e.g., circumferential and Axial stress-stretch responses) did not differ significantly between groups.
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Effects of a sustained Extension on arterial growth and remodeling: a theoretical study
Journal of biomechanics, 2004Co-Authors: R. L. Gleason, Jay D. HumphreyAbstract:Three recent studies reveal that the unloaded length of a carotid artery increases significantly and rapidly in response to sustained increases in Axial Extension. Moreover, such lengthening involves an "unprecedented" increase in the rate of turnover of cells and matrix. Although current data are not sufficient for detailed biomechanical analyses, we present general numerical simulations that are consistent with the reported observations and support the hypothesis that rates of turnover correlate with the extent that stresses are perturbed from normal. In particular, a 3-D analysis of wall stress suggests that moderate (15%) increases in Axial Extension can increase the Axial stress to a much greater extent than marked (50%) increases in blood pressure increase the circumferential stress. Furthermore, such increases in Axial stress can occur without inducing significant gradients in stress within the wall. Consequently, we use a new, 2-D constrained mixture model to study evolving changes in the geometry, structure, and properties of carotid arteries in response to a sustained increase in Axial Extension. These simulations are qualitatively similar to the reports in the literature and support the notion that the stress-free lengths of individual constituents evolve during growth and remodeling.
