The Experts below are selected from a list of 300 Experts worldwide ranked by ideXlab platform
Kathryn V. Anderson - One of the best experts on this subject based on the ideXlab platform.
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β-Pix-dependent cellular protrusions propel collective Mesoderm migration in the mouse embryo.
Nature communications, 2020Co-Authors: Tatiana Omelchenko, Alan Hall, Kathryn V. AndersonAbstract:Coordinated directional migration of cells in the Mesoderm layer of the early embryo is essential for organization of the body plan. Here we show that Mesoderm organization in mouse embryos depends on β-Pix (Arhgef7), a guanine nucleotide exchange factor for Rac1 and Cdc42. As early as E7.5, β-Pix mutants have an abnormally thick Mesoderm layer; later, paraxial Mesoderm fails to organize into somites. To define the mechanism of action of β-Pix in vivo, we optimize single-cell live-embryo imaging, cell tracking, and volumetric analysis of individual and groups of Mesoderm cells. Use of these methods shows that wild-type cells move in the same direction as their neighbors, whereas adjacent β-Pix mutant cells move in random directions. Wild-type Mesoderm cells have long polarized filopodia-like protrusions, which are absent in β-Pix mutants. The data indicate that β-Pix-dependent cellular protrusions drive and coordinate collective migration of the Mesoderm in vivo.
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β pix dependent cellular protrusions propel collective Mesoderm migration in the mouse embryo
Nature Communications, 2020Co-Authors: Tatiana Omelchenko, Alan Hall, Kathryn V. AndersonAbstract:Coordinated directional migration of cells in the Mesoderm layer of the early embryo is essential for organization of the body plan. Here we show that Mesoderm organization in mouse embryos depends on β-Pix (Arhgef7), a guanine nucleotide exchange factor for Rac1 and Cdc42. As early as E7.5, β-Pix mutants have an abnormally thick Mesoderm layer; later, paraxial Mesoderm fails to organize into somites. To define the mechanism of action of β-Pix in vivo, we optimize single-cell live-embryo imaging, cell tracking, and volumetric analysis of individual and groups of Mesoderm cells. Use of these methods shows that wild-type cells move in the same direction as their neighbors, whereas adjacent β-Pix mutant cells move in random directions. Wild-type Mesoderm cells have long polarized filopodia-like protrusions, which are absent in β-Pix mutants. The data indicate that β-Pix-dependent cellular protrusions drive and coordinate collective migration of the Mesoderm in vivo. Mesodermal directional cell migration is needed to establish body plan but how this is regulated is unclear. Here, the authors show that loss of the guanine nucleotide exchange factor for Rac1 and Cdc42, β-Pix, at mouse gastrulation disrupts the orderly, collective anterior migration of Mesoderm cells due to defective cell protrusions.
Rudolf Winklbauer - One of the best experts on this subject based on the ideXlab platform.
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Mesoderm layer formation in Xenopus and Drosophila gastrulation.
Physical biology, 2011Co-Authors: Rudolf Winklbauer, H-arno J MüllerAbstract:During gastrulation, the Mesoderm spreads out between ectoderm and endoderm to form a mesenchymal cell layer. Surprisingly the underlying principles of Mesoderm layer formation are very similar in evolutionarily distant species like the fruit fly, Drosophila melanogaster, and the frog, Xenopus laevis, in which the molecular and the cellular basis of Mesoderm layer formation have been extensively studied. Complementary expression of growth factors in the ectoderm and their receptors in the Mesoderm act to orient cellular protrusive activities and direct cell movement, leading to radial cell intercalation and the spreading of the Mesoderm layer. This mechanism is contrasted with generic physical mechanisms of tissue spreading that consider the adhesive and physical properties of the cells and tissues. Both mechanisms need to be integrated to orchestrate mesenchymal morphogenesis.
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Fibronectin, Mesoderm migration, and gastrulation in Xenopus.
Developmental biology, 1996Co-Authors: Rudolf Winklbauer, Ray KellerAbstract:The role of fibronectin in Mesoderm cell migration and and the importance of Mesoderm migration for gastrulation in Xenopus are examined. To allow for migration, a stable interface must exist between migrating Mesoderm cells and the cells of the substrate layer, the blastocoel roof. We show that maintenance of this interface does not depend on fibronectin. We further demonstrate that fibronectin contributes to, but is not essential for, Mesoderm cell adhesion to the blastocoel roof. However, interaction with fibronectin is necessary for cell spreading and the formation of lamelliform cytoplasmic protrusions. Apparently, the specific role of fibronectin in Mesoderm migration is to control cell protrusive activity. Consequently, when fibronectin function is blocked by GRGDSP peptide or antibodies, Mesoderm cell migration is inhibited. Nevertheless, gastrulation proceeds nearly normally in inhibitor-treated embryos. It appears that in Xenopus, Mesoderm migration is not essential for gastrulation.
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Mesoderm migration in the Xenopus gastrula.
The International journal of developmental biology, 1996Co-Authors: Rudolf Winklbauer, M Nagel, A Selchow, S WackerAbstract:During Xenopus gastrulation, the Mesoderm involutes at the blastopore lip and moves on the inner surface of the BCR toward the animal pole of the embryo. Active cell migration is involved in this Mesoderm translocation. In vitro, Mesoderm cells migrate non-persistently and intermittently by extending and retracting multiple lamellipodia, which pull the cell body in their direction. Lamellipodia formation is induced by FN. FN fibrils are present on the BCR as part of the in vivo substrate of Mesoderm migration. Mesoderm cells can attach to the BCR independently of FN, but interaction with FN is required for lamellipodia extension and cell migration on the BCR. In contrast to preinvolution Mesoderm, involuted migrating Mesoderm always stays on the surface of the BCR cell layer: migrating Mesoderm cells do not mix with BCR cells, and a stable interface between tissues is maintained. A corresponding change in cell sorting behavior occurs during Mesoderm involution. In Xenopus, the Mesoderm moves as a multilayered coherent cell mass held together by cadherin-mediated cell adhesion. Aggregate formation changes Mesoderm cell behavior, rendering it more continuous, persistent and directional, i.e. more efficient. The Mesoderm possesses an intrinsic tissue polarity which biases the direction of its movement. In addition, the fibrillar FN matrix of the BCR contains guidance cues which also direct the Mesoderm toward the animal pole. Haptotaxis is most likely not involved in this substrate-dependent guidance of the Mesoderm, but intact FN fibrils seem to be required. A polarity of the BCR cell layer which underlies this anisotropy of the BCR matrix develops under the influence of the marginal zone in the late blastula. Although in other amphibian species, gastrulation depends critically on Mesoderm cell migration, in Xenopus, convergent extension of the axial Mesoderm seems to provide the main driving force for gastrulation.
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Mesoderm cell migration in the vertebrate gastrula
Seminars in Developmental Biology, 1994Co-Authors: Rudolf WinklbauerAbstract:Abstract Mesoderm migration across the inner surface of the outer embryonic layer is an essential morphogenetic mechanism in vertebrate gastrulation. Conserved traits of this process are (1) cadherin-dependent cohesion of the Mesoderm, and (2) a predominant role for fibronectin in mediating Mesoderm cell-substrate interactions. Compared to lower vertebrates, differentiation of the outer substrate-forming cell layer is accelerated in amniotes, providing Mesoderm cells with a basement membrane substrate instead of a loose network of extracellular matrix fibrils. Guidance cues which determine the direction of Mesoderm migration have been demonstrated in the fibrillar matrix of the amphibian gastrula.
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Directional Mesoderm cell migration in the Xenopus gastrula.
Developmental biology, 1991Co-Authors: Rudolf Winklbauer, M NagelAbstract:The movement of the dorsal Mesoderm across the blastocoel roof of the Xenopus gastrula is examined. We show that different parts of the Mesoderm which can be distinguished by their morphogenetic behavior in the embryo are all able to migrate independently on the inner surface of the blastocoel roof. The direction of Mesoderm cell migration is determined by guidance cues in the extracellular matrix of the blastocoel roof and by an intrinsic tissue polarity of the Mesoderm. The Mesodermal polarity shows the same orientation as the external guidance cues and is strongly expressed in the more posterior Mesoderm. The guidance cues of the extracellular matrix are recognized by all parts of the dorsal Mesoderm and even by nonMesodermal cells from other regions of the embryo. The extracellular matrix consists of a network of fibronectin-containing fibrils. The adhesiveness of this matrix does not vary along the axis of Mesoderm movement, excluding haptotaxis as a guidance mechanism in this system. However, an intact fibronectin fibril structure is necessary for directional Mesoderm cell migration. When the assembly of fibronectin into fibrils is inhibited, Mesoderm explants still migrate on the amorphous extracellular matrix, but no longer directionally. It is proposed that polarized extracellular matrix fibrils may normally guide the migrating Mesoderm to its target region.
Tatiana Omelchenko - One of the best experts on this subject based on the ideXlab platform.
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β-Pix-dependent cellular protrusions propel collective Mesoderm migration in the mouse embryo.
Nature communications, 2020Co-Authors: Tatiana Omelchenko, Alan Hall, Kathryn V. AndersonAbstract:Coordinated directional migration of cells in the Mesoderm layer of the early embryo is essential for organization of the body plan. Here we show that Mesoderm organization in mouse embryos depends on β-Pix (Arhgef7), a guanine nucleotide exchange factor for Rac1 and Cdc42. As early as E7.5, β-Pix mutants have an abnormally thick Mesoderm layer; later, paraxial Mesoderm fails to organize into somites. To define the mechanism of action of β-Pix in vivo, we optimize single-cell live-embryo imaging, cell tracking, and volumetric analysis of individual and groups of Mesoderm cells. Use of these methods shows that wild-type cells move in the same direction as their neighbors, whereas adjacent β-Pix mutant cells move in random directions. Wild-type Mesoderm cells have long polarized filopodia-like protrusions, which are absent in β-Pix mutants. The data indicate that β-Pix-dependent cellular protrusions drive and coordinate collective migration of the Mesoderm in vivo.
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β pix dependent cellular protrusions propel collective Mesoderm migration in the mouse embryo
Nature Communications, 2020Co-Authors: Tatiana Omelchenko, Alan Hall, Kathryn V. AndersonAbstract:Coordinated directional migration of cells in the Mesoderm layer of the early embryo is essential for organization of the body plan. Here we show that Mesoderm organization in mouse embryos depends on β-Pix (Arhgef7), a guanine nucleotide exchange factor for Rac1 and Cdc42. As early as E7.5, β-Pix mutants have an abnormally thick Mesoderm layer; later, paraxial Mesoderm fails to organize into somites. To define the mechanism of action of β-Pix in vivo, we optimize single-cell live-embryo imaging, cell tracking, and volumetric analysis of individual and groups of Mesoderm cells. Use of these methods shows that wild-type cells move in the same direction as their neighbors, whereas adjacent β-Pix mutant cells move in random directions. Wild-type Mesoderm cells have long polarized filopodia-like protrusions, which are absent in β-Pix mutants. The data indicate that β-Pix-dependent cellular protrusions drive and coordinate collective migration of the Mesoderm in vivo. Mesodermal directional cell migration is needed to establish body plan but how this is regulated is unclear. Here, the authors show that loss of the guanine nucleotide exchange factor for Rac1 and Cdc42, β-Pix, at mouse gastrulation disrupts the orderly, collective anterior migration of Mesoderm cells due to defective cell protrusions.
Alan Hall - One of the best experts on this subject based on the ideXlab platform.
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β-Pix-dependent cellular protrusions propel collective Mesoderm migration in the mouse embryo.
Nature communications, 2020Co-Authors: Tatiana Omelchenko, Alan Hall, Kathryn V. AndersonAbstract:Coordinated directional migration of cells in the Mesoderm layer of the early embryo is essential for organization of the body plan. Here we show that Mesoderm organization in mouse embryos depends on β-Pix (Arhgef7), a guanine nucleotide exchange factor for Rac1 and Cdc42. As early as E7.5, β-Pix mutants have an abnormally thick Mesoderm layer; later, paraxial Mesoderm fails to organize into somites. To define the mechanism of action of β-Pix in vivo, we optimize single-cell live-embryo imaging, cell tracking, and volumetric analysis of individual and groups of Mesoderm cells. Use of these methods shows that wild-type cells move in the same direction as their neighbors, whereas adjacent β-Pix mutant cells move in random directions. Wild-type Mesoderm cells have long polarized filopodia-like protrusions, which are absent in β-Pix mutants. The data indicate that β-Pix-dependent cellular protrusions drive and coordinate collective migration of the Mesoderm in vivo.
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β pix dependent cellular protrusions propel collective Mesoderm migration in the mouse embryo
Nature Communications, 2020Co-Authors: Tatiana Omelchenko, Alan Hall, Kathryn V. AndersonAbstract:Coordinated directional migration of cells in the Mesoderm layer of the early embryo is essential for organization of the body plan. Here we show that Mesoderm organization in mouse embryos depends on β-Pix (Arhgef7), a guanine nucleotide exchange factor for Rac1 and Cdc42. As early as E7.5, β-Pix mutants have an abnormally thick Mesoderm layer; later, paraxial Mesoderm fails to organize into somites. To define the mechanism of action of β-Pix in vivo, we optimize single-cell live-embryo imaging, cell tracking, and volumetric analysis of individual and groups of Mesoderm cells. Use of these methods shows that wild-type cells move in the same direction as their neighbors, whereas adjacent β-Pix mutant cells move in random directions. Wild-type Mesoderm cells have long polarized filopodia-like protrusions, which are absent in β-Pix mutants. The data indicate that β-Pix-dependent cellular protrusions drive and coordinate collective migration of the Mesoderm in vivo. Mesodermal directional cell migration is needed to establish body plan but how this is regulated is unclear. Here, the authors show that loss of the guanine nucleotide exchange factor for Rac1 and Cdc42, β-Pix, at mouse gastrulation disrupts the orderly, collective anterior migration of Mesoderm cells due to defective cell protrusions.
François Fagotto - One of the best experts on this subject based on the ideXlab platform.
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Ectoderm to Mesoderm transition by down-regulation of actomyosin contractility.
PLoS biology, 2021Co-Authors: Leily Kashkooli, David Rozema, Lina Espejo-ramirez, Paul Lasko, François FagottoAbstract:Collective migration of cohesive tissues is a fundamental process in morphogenesis and is particularly well illustrated during gastrulation by the rapid and massive internalization of the Mesoderm, which contrasts with the much more modest movements of the ectoderm. In the Xenopus embryo, the differences in morphogenetic capabilities of ectoderm and Mesoderm can be connected to the intrinsic motility of individual cells, very low for ectoderm, high for Mesoderm. Surprisingly, we find that these seemingly deep differences can be accounted for simply by differences in Rho-kinases (Rock)-dependent actomyosin contractility. We show that Rock inhibition is sufficient to rapidly unleash motility in the ectoderm and confer it with Mesoderm-like properties. In the Mesoderm, this motility is dependent on two negative regulators of RhoA, the small GTPase Rnd1 and the RhoGAP Shirin/Dlc2/ArhGAP37. Both are absolutely essential for gastrulation. At the cellular and tissue level, the two regulators show overlapping yet distinct functions. They both contribute to decrease cortical tension and confer motility, but Shirin tends to increase tissue fluidity and stimulate dispersion, while Rnd1 tends to favor more compact collective migration. Thus, each is able to contribute to a specific property of the migratory behavior of the Mesoderm. We propose that the "ectoderm to Mesoderm transition" is a prototypic case of collective migration driven by a down-regulation of cellular tension, without the need for the complex changes traditionally associated with the epithelial-to-mesenchymal transition.
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Ectoderm to Mesoderm transition by downregulation of actomyosin contractility
2019Co-Authors: Leily Kashkooli, David Rozema, Lina Espejo-ramirez, Paul Lasko, François FagottoAbstract:Collective migration of cohesive tissues is a fundamental process in morphogenesis, and is particularly well illustrated during gastrulation by the rapid and massive internalization of the Mesoderm, which contrasts with the much more modest movements of the ectoderm. In the Xenopus embryo, the differences in morphogenetic capabilities of ectoderm and Mesoderm can be connected to the properties of individual cells, which, when studied in vitro, show opposite intrinsic organizations, cohesive for ectoderm, dispersive for Mesoderm. Surprisingly, we find these seemingly deep differences can be accounted for simply by differences in Rock-dependent actomyosin contractility. We show that Rock inhibition is sufficient to rapidly unleash motility in the ectoderm and confer it with Mesoderm-like properties. In the Mesoderm, this motility is dependent on two RhoA negative regulators, the small GTPase Rnd1 and the RhoGAP Shirin/Dlc2/ArhGAP37. Both are absolutely essential for gastrulation. At the cellular and tissue level, the two regulators show overlapping yet distinct functions. They both contribute to decrease cortical tension and confer motility, but Shirin tends to increase tissue fluidity and stimulate dispersion, while Rnd1 tends to favour more compact collective migration. Thus, each is able to contribute to a specific property of the migratory behaviour of the Mesoderm.
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A role for maternal β-catenin in early Mesoderm induction in Xenopus
The EMBO journal, 2003Co-Authors: Anne Schohl, François FagottoAbstract:Mesoderm formation results from an inducing process that requires maternal and zygotic FGF/MAPK and TGFβ activities, while maternal activation of the Wnt/β-catenin pathway determines the anterior–dorsal axis. Here, we show a new role of Wnt/β-catenin signaling in Mesoderm induction. We find that maternal β-catenin signaling is not only active dorsally but also all around the equatorial region, coinciding with the prospective Mesoderm. Maternal β-catenin function is required both for expression of dorsal genes and for activation of MAPK and the Mesodermal markers Xbra and eoMesodermin. β-catenin acts in a non- cell-autonomous manner upstream of zygotic FGF and nodal signals. The Wnt/β-catenin activity in the equatorial region of the early embryo is the first example of a maternally provided Mesoderm inducer restricted to the prospective Mesoderm.
