The Experts below are selected from a list of 4008 Experts worldwide ranked by ideXlab platform
Olivier Pourquié - One of the best experts on this subject based on the ideXlab platform.
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The WHHERE coactivator complex is required for retinoic acid-dependent regulation of embryonic symmetry
Nature Publishing Group, 2017Co-Authors: Gonçalo C. Vilhais-neto, Marjorie Fournier, Jean-luc Plassat, Mihaela E. Sardiu, Anita Saraf, Jean-marie Garnier, Mitsuji Maruhashi, Laurence Florens, Michael P. Washburn, Olivier PourquiéAbstract:Retinoic acid (RA) regulates the maintenance of Somitogenesis symmetry. Here, the authors use a proteomic approach to identify a protein complex of Wdr5, Hdac1, Hdac2 that act together with RA and coactivator Rere/Atrophin2 and a histone methyltransferase Ehmt2 to regulate embryonic symmetry
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On periodicity and directionality of Somitogenesis
Anatomy and Embryology, 2006Co-Authors: Alexander Aulehla, Olivier PourquiéAbstract:It is currently thought that the mechanism underlying Somitogenesis is linked to a molecular oscillator, the segmentation clock, and to gradients of signaling molecules within the paraxial mesoderm. Here, we review the current picture of this segmentation clock and gradients, and use this knowledge to critically ask: What is the basis for periodicity and directionality of Somitogenesis?
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Retinoic acid coordinates Somitogenesis and left–right patterning in vertebrate embryos
Nature, 2005Co-Authors: Julien Vermot, Olivier PourquiéAbstract:A striking feature of the body plan of a majority of animals is bilateral symmetry. Almost nothing is known about the mechanisms controlling the symmetrical arrangement of the left and right body sides during development. Here we report that blocking the production of retinoic acid (RA) in chicken embryos leads to a desynchronization of somite formation between the two embryonic sides, demonstrated by a shortened left segmented region. This defect is linked to a loss of coordination of the segmentation clock oscillations. The lateralization of this defect led us to investigate the relation between Somitogenesis and the left-right asymmetry machinery in RA-deficient embryos. Reversal of the situs in chick or mouse embryos lacking RA results in a reversal of the Somitogenesis laterality defect. Our data indicate that RA is important in buffering the lateralizing influence of the left-right machinery, thus permitting synchronization of the development of the two embryonic sides.
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retinoic acid coordinates Somitogenesis and left right patterning in vertebrate embryos
Nature, 2005Co-Authors: Julien Vermot, Olivier PourquiéAbstract:A striking feature of the body plan of a majority of animals is bilateral symmetry. Almost nothing is known about the mechanisms controlling the symmetrical arrangement of the left and right body sides during development. Here we report that blocking the production of retinoic acid (RA) in chicken embryos leads to a desynchronization of somite formation between the two embryonic sides, demonstrated by a shortened left segmented region. This defect is linked to a loss of coordination of the segmentation clock oscillations. The lateralization of this defect led us to investigate the relation between Somitogenesis and the left-right asymmetry machinery in RA-deficient embryos. Reversal of the situs in chick or mouse embryos lacking RA results in a reversal of the Somitogenesis laterality defect. Our data indicate that RA is important in buffering the lateralizing influence of the left-right machinery, thus permitting synchronization of the development of the two embryonic sides.
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The chick embryo: a leading model in Somitogenesis studies.
Mechanisms of development, 2004Co-Authors: Olivier PourquiéAbstract:The vertebrate body is built on a metameric organization which consists of a repetition of functionally equivalent units, each comprising a vertebra, its associated muscles, peripheral nerves and blood vessels. This periodic pattern is established during embryogenesis by the Somitogenesis process. Somites are generated in a rhythmic fashion from the presomitic mesoderm and they subsequently differentiate to give rise to the vertebrae and skeletal muscles of the body. Somitogenesis has been very actively studied in the chick embryo since the 19th century and many of the landmark experiments that led to our current understanding of the vertebrate segmentation process have been performed in this organism. Somite formation involves an oscillator, the segmentation clock whose periodic signal is converted into the periodic array of somite boundaries by a spacing mechanism relying on a traveling threshold of FGF signaling regressing in concert with body axis extension.
Jeffrey R. Miller - One of the best experts on this subject based on the ideXlab platform.
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regulation of Somitogenesis by ena vasp proteins and fak during xenopus development
Development, 2006Co-Authors: Katherine A. Kragtorp, Jeffrey R. MillerAbstract:The metameric organization of the vertebrate body plan is established during Somitogenesis as somite pairs sequentially form along the anteroposterior axis. Coordinated regulation of cell shape, motility and adhesion are crucial for directing the morphological segmentation of somites. We show that members of the Ena/VASP family of actin regulatory proteins are required for Somitogenesis in Xenopus. Xenopus Ena (Xena) localizes to the cell periphery in the presomitic mesoderm (PSM), and is enriched at intersomitic junctions and at myotendinous junctions in somites and the myotome, where it co-localizes with beta1-integrin, vinculin and FAK. Inhibition of Ena/VASP function with dominant-negative mutants results in abnormal somite formation that correlates with later defects in intermyotomal junctions. Neutralization of Ena/VASP activity disrupts cell rearrangements during somite rotation and leads to defects in the fibronectin (FN) matrix surrounding somites. Furthermore, inhibition of Ena/VASP function impairs FN matrix assembly, spreading of somitic cells on FN and autophosphorylation of FAK, suggesting a role for Ena/VASP proteins in the modulation of integrin-mediated processes. We also show that inhibition of FAK results in defects in somite formation, blocks FN matrix deposition and alters Xena localization. Together, these results provide evidence that Ena/VASP proteins and FAK are required for somite formation in Xenopus and support the idea that Ena/VASP and FAK function in a common pathway to regulate integrin-dependent migration and adhesion during Somitogenesis.
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Regulation of Somitogenesis by Ena/VASP proteins and FAK during Xenopus development.
Development (Cambridge England), 2006Co-Authors: Katherine A. Kragtorp, Jeffrey R. MillerAbstract:The metameric organization of the vertebrate body plan is established during Somitogenesis as somite pairs sequentially form along the anteroposterior axis. Coordinated regulation of cell shape, motility and adhesion are crucial for directing the morphological segmentation of somites. We show that members of the Ena/VASP family of actin regulatory proteins are required for Somitogenesis in Xenopus. Xenopus Ena (Xena) localizes to the cell periphery in the presomitic mesoderm (PSM), and is enriched at intersomitic junctions and at myotendinous junctions in somites and the myotome, where it co-localizes with beta1-integrin, vinculin and FAK. Inhibition of Ena/VASP function with dominant-negative mutants results in abnormal somite formation that correlates with later defects in intermyotomal junctions. Neutralization of Ena/VASP activity disrupts cell rearrangements during somite rotation and leads to defects in the fibronectin (FN) matrix surrounding somites. Furthermore, inhibition of Ena/VASP function impairs FN matrix assembly, spreading of somitic cells on FN and autophosphorylation of FAK, suggesting a role for Ena/VASP proteins in the modulation of integrin-mediated processes. We also show that inhibition of FAK results in defects in somite formation, blocks FN matrix deposition and alters Xena localization. Together, these results provide evidence that Ena/VASP proteins and FAK are required for somite formation in Xenopus and support the idea that Ena/VASP and FAK function in a common pathway to regulate integrin-dependent migration and adhesion during Somitogenesis.
Xiaoyan Ding - One of the best experts on this subject based on the ideXlab platform.
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wnt β catenin signaling controls mespo expression to regulate segmentation during xenopus Somitogenesis
Developmental Biology, 2007Co-Authors: Jinhu Wang, Yuelei Chen, Xiaoyan DingAbstract:The vertebral column is derived from somites, which are transient segments of the paraxial mesoderm that are present in developing vertebrates. The strict spatial and temporal regulation of Somitogenesis is of crucial developmental importance. Signals such as Wnt and FGF play roles in Somitogenesis, but details regarding how Wnt signaling functions in this process remain unclear. In this study, we report that Wnt/beta-catenin signaling regulates the expression of Mespo, a basic-helix-loop-helix (bHLH) gene critical for segmental patterning in Xenopus Somitogenesis. Transgenic analysis of the Mespo promoter identifies Mespo as a direct downstream target of Wnt/beta-catenin signaling pathway. We also demonstrate that activity of Wnt/-catenin. signaling in Somitogenesis can be enhanced by the PI3-K/AKT pathway. Our results illustrate that Wnt/-catenin signaling in conjunction with PI3-K/AKT pathway plays a key role in controlling development of the paraxial mesoderm. (c) 2007 Published by Elsevier Inc.
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Wnt/β-catenin signaling controls Mespo expression to regulate segmentation during Xenopus Somitogenesis
Developmental biology, 2006Co-Authors: Jinhu Wang, Yuelei Chen, Xiaoyan DingAbstract:The vertebral column is derived from somites, which are transient segments of the paraxial mesoderm that are present in developing vertebrates. The strict spatial and temporal regulation of Somitogenesis is of crucial developmental importance. Signals such as Wnt and FGF play roles in Somitogenesis, but details regarding how Wnt signaling functions in this process remain unclear. In this study, we report that Wnt/beta-catenin signaling regulates the expression of Mespo, a basic-helix-loop-helix (bHLH) gene critical for segmental patterning in Xenopus Somitogenesis. Transgenic analysis of the Mespo promoter identifies Mespo as a direct downstream target of Wnt/beta-catenin signaling pathway. We also demonstrate that activity of Wnt/-catenin. signaling in Somitogenesis can be enhanced by the PI3-K/AKT pathway. Our results illustrate that Wnt/-catenin signaling in conjunction with PI3-K/AKT pathway plays a key role in controlling development of the paraxial mesoderm. (c) 2007 Published by Elsevier Inc.
Miguel Maroto - One of the best experts on this subject based on the ideXlab platform.
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The chick Somitogenesis oscillator is arrested before all paraxial mesoderm is segmented into somites
BMC developmental biology, 2010Co-Authors: Gennady Tenin, David Wright, Zoltan Ferjentsik, Robert A. Bone, Michael J. Mcgrew, Miguel MarotoAbstract:Somitogenesis is the earliest sign of segmentation in the developing vertebrate embryo. This process starts very early, soon after gastrulation has initiated and proceeds in an anterior-to-posterior direction during body axis elongation. It is widely accepted that Somitogenesis is controlled by a molecular oscillator with the same periodicity as somite formation. This periodic mechanism is repeated a specific number of times until the embryo acquires a defined specie-specific final number of somites at the end of the process of axis elongation. This final number of somites varies widely between vertebrate species. How termination of the process of Somitogenesis is determined is still unknown. Here we show that during development there is an imbalance between the speed of somite formation and growth of the presomitic mesoderm (PSM)/tail bud. This decrease in the PSM size of the chick embryo is not due to an acceleration of the speed of somite formation because it remains constant until the last stages of Somitogenesis, when it slows down. When the chick embryo reaches its final number of somites at stage HH 24-25 there is still some remaining unsegmented PSM in which expression of components of the Somitogenesis oscillator is no longer dynamic. Finally, we identify a change in expression of retinoic acid regulating factors in the tail bud at late stages of Somitogenesis, such that in the chick embryo there is a pronounced onset of Raldh2 expression while in the mouse embryo the expression of the RA inhibitor Cyp26A1 is downregulated. Our results show that the chick Somitogenesis oscillator is arrested before all paraxial mesoderm is segmented into somites. In addition, endogenous retinoic acid is probably also involved in the termination of the process of segmentation, and in tail growth in general.
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Notch is a critical component of the mouse Somitogenesis oscillator and is essential for the formation of the somites.
PLoS Genetics, 2009Co-Authors: Zoltan Ferjentsik, Shinichi Hayashi, J. Kim Dale, Yasumasa Bessho, An Herreman, Bart De Strooper, Gonzalo Del Monte, José Luis De La Pompa, Miguel MarotoAbstract:Segmentation of the vertebrate body axis is initiated through Somitogenesis, whereby epithelial somites bud off in pairs periodically from the rostral end of the unsegmented presomitic mesoderm (PSM). The periodicity of Somitogenesis is governed by a molecular oscillator that drives periodic waves of clock gene expression caudo-rostrally through the PSM with a periodicity that matches somite formation. To date the clock genes comprise components of the Notch, Wnt, and FGF pathways. The literature contains controversial reports as to the absolute role(s) of Notch signalling during the process of somite formation. Recent data in the zebrafish have suggested that the only role of Notch signalling is to synchronise clock gene oscillations across the PSM and that somite formation can continue in the absence of Notch activity. However, it is not clear in the mouse if an FGF/Wnt-based oscillator is sufficient to generate segmented structures, such as the somites, in the absence of all Notch activity. We have investigated the requirement for Notch signalling in the mouse Somitogenesis clock by analysing embryos carrying a mutation in different components of the Notch pathway, such as Lunatic fringe (Lfng), Hes7, Rbpj, and presenilin1/presenilin2 (Psen1/Psen2), and by pharmacological blocking of the Notch pathway. In contrast to the fish studies, we show that mouse embryos lacking all Notch activity do not show oscillatory activity, as evidenced by the absence of waves of clock gene expression across the PSM, and they do not develop somites. We propose that, at least in the mouse embryo, Notch activity is absolutely essential for the formation of a segmented body axis.
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A molecular clock involved in Somite segmentation
Current topics in developmental biology, 2001Co-Authors: Miguel Maroto, Olivier PourquiéAbstract:Somites are transient embryonic structures that are formed from the unsegmented presomitic mesoderm (PSM) in a highly regulated process called Somitogenesis. Somite, formation can be considered as the result of several sequential processes: generation of a basic metameric pattern, specification of the antero-posterior identity of each somite, and, finally, formation of the somitic border. Evidence for the existence of a molecular clock or oscillator linked to Somitogenesis has been provided by the discovery of the rhythmic and dynamic expression in the PSM of c-hairyl and lunatic fringe, two genes potentially related to the Notch signaling pathway. These oscillating expression patterns suggest that an important role of the molecular clock could reside in the temporal control of periodic Notch activation, ultimately resulting in the regular array of the somites. We discuss both the importance of the Notch signaling pathway in the molecular events of Somitogenesis and its relationship with the molecular clock, and, finally, in that context we review a number of other genes known to play a role in Somitogenesis.
Katherine A. Kragtorp - One of the best experts on this subject based on the ideXlab platform.
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regulation of Somitogenesis by ena vasp proteins and fak during xenopus development
Development, 2006Co-Authors: Katherine A. Kragtorp, Jeffrey R. MillerAbstract:The metameric organization of the vertebrate body plan is established during Somitogenesis as somite pairs sequentially form along the anteroposterior axis. Coordinated regulation of cell shape, motility and adhesion are crucial for directing the morphological segmentation of somites. We show that members of the Ena/VASP family of actin regulatory proteins are required for Somitogenesis in Xenopus. Xenopus Ena (Xena) localizes to the cell periphery in the presomitic mesoderm (PSM), and is enriched at intersomitic junctions and at myotendinous junctions in somites and the myotome, where it co-localizes with beta1-integrin, vinculin and FAK. Inhibition of Ena/VASP function with dominant-negative mutants results in abnormal somite formation that correlates with later defects in intermyotomal junctions. Neutralization of Ena/VASP activity disrupts cell rearrangements during somite rotation and leads to defects in the fibronectin (FN) matrix surrounding somites. Furthermore, inhibition of Ena/VASP function impairs FN matrix assembly, spreading of somitic cells on FN and autophosphorylation of FAK, suggesting a role for Ena/VASP proteins in the modulation of integrin-mediated processes. We also show that inhibition of FAK results in defects in somite formation, blocks FN matrix deposition and alters Xena localization. Together, these results provide evidence that Ena/VASP proteins and FAK are required for somite formation in Xenopus and support the idea that Ena/VASP and FAK function in a common pathway to regulate integrin-dependent migration and adhesion during Somitogenesis.
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Regulation of Somitogenesis by Ena/VASP proteins and FAK during Xenopus development.
Development (Cambridge England), 2006Co-Authors: Katherine A. Kragtorp, Jeffrey R. MillerAbstract:The metameric organization of the vertebrate body plan is established during Somitogenesis as somite pairs sequentially form along the anteroposterior axis. Coordinated regulation of cell shape, motility and adhesion are crucial for directing the morphological segmentation of somites. We show that members of the Ena/VASP family of actin regulatory proteins are required for Somitogenesis in Xenopus. Xenopus Ena (Xena) localizes to the cell periphery in the presomitic mesoderm (PSM), and is enriched at intersomitic junctions and at myotendinous junctions in somites and the myotome, where it co-localizes with beta1-integrin, vinculin and FAK. Inhibition of Ena/VASP function with dominant-negative mutants results in abnormal somite formation that correlates with later defects in intermyotomal junctions. Neutralization of Ena/VASP activity disrupts cell rearrangements during somite rotation and leads to defects in the fibronectin (FN) matrix surrounding somites. Furthermore, inhibition of Ena/VASP function impairs FN matrix assembly, spreading of somitic cells on FN and autophosphorylation of FAK, suggesting a role for Ena/VASP proteins in the modulation of integrin-mediated processes. We also show that inhibition of FAK results in defects in somite formation, blocks FN matrix deposition and alters Xena localization. Together, these results provide evidence that Ena/VASP proteins and FAK are required for somite formation in Xenopus and support the idea that Ena/VASP and FAK function in a common pathway to regulate integrin-dependent migration and adhesion during Somitogenesis.
