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  1 / 105 MEDLINE  
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[PMID]:28507001
[Au] Autor:Molina MD; Quirin M; Haillot E; Jimenez F; Chessel A; Lepage T
[Ad] Endereço:Université Côte d'Azur, CNRS, INSERM iBV, 06108 Nice cedex 2, France.
[Ti] Título:p38 MAPK as an essential regulator of dorsal-ventral axis specification and skeletogenesis during sea urchin development: a re-evaluation.
[So] Source:Development;144(12):2270-2281, 2017 06 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dorsal-ventral axis formation in the sea urchin embryo relies on the asymmetrical expression of the TGFß Nodal. The p38-MAPK pathway has been proposed to be essential for dorsal-ventral axis formation by acting upstream of expression. Here, we report that, in contrast to previous studies that used pharmacological inhibitors of p38, manipulating the activity of p38 by genetic means has no obvious impact on morphogenesis. Instead, we discovered that p38 inhibitors strongly disrupt specification of all germ layers by blocking signalling from the Nodal receptor and by interfering with the ERK pathway. Strikingly, while expression of a mutant p38 that is resistant to SB203580 did not rescue dorsal-ventral axis formation or skeletogenesis in embryos treated with this inhibitor, expression of mutant Nodal receptors that are resistant to SB203580 fully restored expression in SB203580-treated embryos. Taken together, these results establish that p38 activity is not required for dorsal-ventral axis formation through expression nor for skeletogenesis. Our results prompt a re-evaluation of the conclusions of several recent studies that linked p38 activity to dorsal-ventral axis formation and to patterning of the skeleton.
[Mh] Termos MeSH primário: Paracentrotus/embriologia
Paracentrotus/enzimologia
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Padronização Corporal/efeitos dos fármacos
Padronização Corporal/genética
Padronização Corporal/fisiologia
Regulação da Expressão Gênica no Desenvolvimento
Regulação Enzimológica da Expressão Gênica
Imidazóis/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Morfogênese/efeitos dos fármacos
Morfogênese/genética
Morfogênese/fisiologia
Mutação
Ligantes da Sinalização Nodal/genética
Ligantes da Sinalização Nodal/metabolismo
Paracentrotus/genética
Fenótipo
Inibidores de Proteínas Quinases/farmacologia
Piridinas/farmacologia
Homologia de Sequência de Aminoácidos
Transdução de Sinais/efeitos dos fármacos
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases p38 Ativadas por Mitógeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Imidazoles); 0 (Nodal Signaling Ligands); 0 (Protein Kinase Inhibitors); 0 (Pyridines); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); OU13V1EYWQ (SB 203580); PVX798P8GI (4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE
[do] DOI:10.1242/dev.152330


  2 / 105 MEDLINE  
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[PMID]:27553781
[Au] Autor:Tisler M; Wetzel F; Mantino S; Kremnyov S; Thumberger T; Schweickert A; Blum M; Vick P
[Ad] Endereço:University of Hohenheim, Institute of Zoology, 70593, Stuttgart, Germany.
[Ti] Título:Cilia are required for asymmetric nodal induction in the sea urchin embryo.
[So] Source:BMC Dev Biol;16(1):28, 2016 Aug 23.
[Is] ISSN:1471-213X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Left-right (LR) organ asymmetries are a common feature of metazoan animals. In many cases, laterality is established by a conserved asymmetric Nodal signaling cascade during embryogenesis. In most vertebrates, asymmetric nodal induction results from a cilia-driven leftward fluid flow at the left-right organizer (LRO), a ciliated epithelium present during gastrula/neurula stages. Conservation of LRO and flow beyond the vertebrates has not been reported yet. RESULTS: Here we study sea urchin embryos, which use nodal to establish larval LR asymmetry as well. Cilia were found in the archenteron of embryos undergoing gastrulation. Expression of foxj1 and dnah9 suggested that archenteron cilia were motile. Cilia were polarized to the posterior pole of cells, a prerequisite of directed flow. High-speed videography revealed rotating cilia in the archenteron slightly before asymmetric nodal induction. Removal of cilia through brief high salt treatments resulted in aberrant patterns of nodal expression. Our data demonstrate that cilia - like in vertebrates - are required for asymmetric nodal induction in sea urchin embryos. CONCLUSIONS: Based on these results we argue that the anterior archenteron represents a bona fide LRO and propose that cilia-based symmetry breakage is a synapomorphy of the deuterostomes.
[Mh] Termos MeSH primário: Embrião não Mamífero/citologia
Ouriços-do-Mar/embriologia
[Mh] Termos MeSH secundário: Animais
Dineínas do Axonema/metabolismo
Padronização Corporal
Cílios/metabolismo
Embrião não Mamífero/metabolismo
Fatores de Transcrição Forkhead/metabolismo
Gastrulação
Ligantes da Sinalização Nodal/metabolismo
Ouriços-do-Mar/citologia
Ouriços-do-Mar/metabolismo
Gravação em Vídeo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Forkhead Transcription Factors); 0 (Nodal Signaling Ligands); EC 3.6.4.2 (Axonemal Dyneins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160825
[St] Status:MEDLINE
[do] DOI:10.1186/s12861-016-0128-7


  3 / 105 MEDLINE  
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[PMID]:27101364
[Au] Autor:Wang Y; Wang X; Wohland T; Sampath K
[Ad] Endereço:Division of Biomedical Sciences, Warwick Medical School, University of Warwick, Coventry, United Kingdom.
[Ti] Título:Extracellular interactions and ligand degradation shape the nodal morphogen gradient.
[So] Source:Elife;5, 2016 Apr 21.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The correct distribution and activity of secreted signaling proteins called morphogens is required for many developmental processes. Nodal morphogens play critical roles in embryonic axis formation in many organisms. Models proposed to generate the Nodal gradient include diffusivity, ligand processing, and a temporal activation window. But how the Nodal morphogen gradient forms in vivo remains unclear. Here, we have measured in vivo for the first time, the binding affinity of Nodal ligands to their major cell surface receptor, Acvr2b, and to the Nodal inhibitor, Lefty, by fluorescence cross-correlation spectroscopy. We examined the diffusion coefficient of Nodal ligands and Lefty inhibitors in live zebrafish embryos by fluorescence correlation spectroscopy. We also investigated the contribution of ligand degradation to the Nodal gradient. We show that ligand clearance via degradation shapes the Nodal gradient and correlates with its signaling range. By computational simulations of gradient formation, we demonstrate that diffusivity, extra-cellular interactions, and selective ligand destruction collectively shape the Nodal morphogen gradient.
[Mh] Termos MeSH primário: Morfogênese
Ligantes da Sinalização Nodal/metabolismo
Peixe-Zebra/embriologia
[Mh] Termos MeSH secundário: Receptores de Activinas Tipo II/metabolismo
Animais
Fatores de Determinação Direita-Esquerda/metabolismo
Ligação Proteica
Proteólise
Espectrometria de Fluorescência
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Left-Right Determination Factors); 0 (Nodal Signaling Ligands); 0 (Zebrafish Proteins); EC 2.7.11.30 (Activin Receptors, Type II); EC 2.7.11.30 (Acvr2b protein, zebrafish)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160422
[St] Status:MEDLINE


  4 / 105 MEDLINE  
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[PMID]:27085753
[Au] Autor:Reid CD; Steiner AB; Yaklichkin S; Lu Q; Wang S; Hennessy M; Kessler DS
[Ad] Endereço:Department of Cell and Developmental Biology, University of Pennsylvania Perelman School of Medicine Smilow Center for Translational Research, Room 9-104, 3400 Civic Center Blvd Philadelphia, PA 19104, USA.
[Ti] Título:FoxH1 mediates a Grg4 and Smad2 dependent transcriptional switch in Nodal signaling during Xenopus mesoderm development.
[So] Source:Dev Biol;414(1):34-44, 2016 06 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the vertebrate blastula and gastrula the Nodal pathway is essential for formation of the primary germ layers and the organizer. Nodal autoregulatory feedback potentiates signaling activity, but mechanisms limiting embryonic Nodal ligand transcription are poorly understood. Here we describe a transcriptional switch mechanism mediated by FoxH1, the principle effector of Nodal autoregulation. FoxH1 contains a conserved engrailed homology (EH1) motif that mediates direct binding of groucho-related gene 4 (Grg4), a Groucho family corepressor. Nodal-dependent gene expression is suppressed by FoxH1, but enhanced by a FoxH1 EH1 mutant, indicating that the EH1 motif is necessary for repression. Grg4 blocks Nodal-induced mesodermal gene expression and Nodal autoregulation, suggesting that Grg4 limits Nodal pathway activity. Conversely, blocking Grg4 function in the ectoderm results in ectopic expression of Nodal target genes. FoxH1 and Grg4 occupy the Xnr1 enhancer, and Grg4 occupancy is dependent on the FoxH1 EH1 motif. Grg4 occupancy at the Xnr1 enhancer significantly decreases with Nodal activation or Smad2 overexpression, while FoxH1 occupancy is unaffected. These results suggest that Nodal-activated Smad2 physically displaces Grg4 from FoxH1, an essential feature of the transcriptional switch mechanism. In support of this model, when FoxH1 is unable to bind Smad2, Grg4 occupancy is maintained at the Xnr1 enhancer, even in the presence of Nodal signaling. Our findings reveal that FoxH1 mediates both activation and repression of Nodal gene expression. We propose that this transcriptional switch is essential to delimit Nodal pathway activity in vertebrate germ layer formation.
[Mh] Termos MeSH primário: Proteínas Correpressoras/fisiologia
Elementos Facilitadores Genéticos/genética
Fatores de Transcrição Forkhead/fisiologia
Regulação da Expressão Gênica no Desenvolvimento/fisiologia
Mesoderma/crescimento & desenvolvimento
Ligantes da Sinalização Nodal/fisiologia
Proteína Smad2/fisiologia
Transcrição Genética/genética
Proteínas de Xenopus/fisiologia
Xenopus laevis/genética
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Animais
Blástula/metabolismo
Gástrula/metabolismo
Regulação da Expressão Gênica no Desenvolvimento/genética
Microinjeções
Ligação Proteica
Mapeamento de Interação de Proteínas
RNA Mensageiro/genética
Proteínas de Xenopus/biossíntese
Proteínas de Xenopus/genética
Xenopus laevis/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Co-Repressor Proteins); 0 (FOXH1 protein, Xenopus); 0 (Forkhead Transcription Factors); 0 (Nodal Signaling Ligands); 0 (RNA, Messenger); 0 (Smad2 Protein); 0 (Smad2 protein, Xenopus); 0 (TLE4 protein, Xenopus); 0 (Xenopus Proteins); 0 (Xnr1 protein, Xenopus)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160418
[St] Status:MEDLINE
[do] DOI:10.1016/j.ydbio.2016.04.006


  5 / 105 MEDLINE  
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[PMID]:27028068
[Au] Autor:Takemoto A; Miyamoto T; Simono F; Kurogi N; Shirae-Kurabayashi M; Awazu A; Suzuki KT; Yamamoto T; Sakamoto N
[Ad] Endereço:Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Higashi-Hiroshima, 739-8526, Japan.
[Ti] Título:Cilia play a role in breaking left-right symmetry of the sea urchin embryo.
[So] Source:Genes Cells;21(6):568-78, 2016 Jun.
[Is] ISSN:1365-2443
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Left-right asymmetry of bilaterian animals is established during early development. In mice, frogs and fishes, the ciliated left-right organizer plays an essential role in establishing bilateral asymmetry, and leftward flow of extracellular fluid generated by ciliary motion results in Nodal activity on the left side. However, H(+) /K(+) -ATPase activity is also involved in the determination of left-right asymmetry in a variety of animals, and it has been thought to be an ancestral mechanism in deuterostomes. In sea urchin, the determination of the left-right asymmetry based on H(+) /K(+) -ATPase activity was already clarified, but it remains to be uncovered whether ciliary motion is involved in the left-right asymmetry of the embryo. Here, we show evidence that ciliary motion is involved in the establishment of left-right asymmetry of sea urchin embryo. Furthermore, we show that the initial cilia generated on small micromeres during the early stage of embryogenesis may be involved in this process. These results suggest that the cilia-mediated mechanism for the determination of left-right asymmetry may be acquired at the base of the deuterostomes.
[Mh] Termos MeSH primário: Ouriços-do-Mar/embriologia
[Mh] Termos MeSH secundário: Animais
Cílios
Embrião não Mamífero
Desenvolvimento Embrionário
Ligantes da Sinalização Nodal/metabolismo
Ouriços-do-Mar/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nodal Signaling Ligands)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170111
[Lr] Data última revisão:
170111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160331
[St] Status:MEDLINE
[do] DOI:10.1111/gtc.12362


  6 / 105 MEDLINE  
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[PMID]:26934886
[Au] Autor:Brown LE; Middleton AM; King JR; Loose M
[Ad] Endereço:MyCIB, School of Biosciences, University of Nottingham, Sutton Bonington, Loughborough, LE12 5RD, UK. laura.brown@slcu.cam.ac.uk.
[Ti] Título:Multicellular Mathematical Modelling of Mesendoderm Formation in Amphibians.
[So] Source:Bull Math Biol;78(3):436-67, 2016 Mar.
[Is] ISSN:1522-9602
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The earliest cell fate decisions in a developing embryo are those associated with establishing the germ layers. The specification of the mesoderm and endoderm is of particular interest as the mesoderm is induced from the endoderm, potentially from an underlying bipotential group of cells, the mesendoderm. Mesendoderm formation has been well studied in an amphibian model frog, Xenopus laevis, and its formation is driven by a gene regulatory network (GRN) induced by maternal factors deposited in the egg. We have recently demonstrated that the axolotl, a urodele amphibian, utilises a different topology in its GRN to specify the mesendoderm. In this paper, we develop spatially structured mathematical models of the GRNs governing mesendoderm formation in a line of cells. We explore several versions of the model of mesendoderm formation in both Xenopus and the axolotl, incorporating the key differences between these two systems. Model simulations are able to reproduce known experimental data, such as Nodal expression domains in Xenopus, and also make predictions about how the positional information derived from maternal factors may be interpreted to drive cell fate decisions. We find that whilst cell-cell signalling plays a minor role in Xenopus, it is crucial for correct patterning domains in axolotl.
[Mh] Termos MeSH primário: Anfíbios/embriologia
Modelos Biológicos
[Mh] Termos MeSH secundário: Ambystoma mexicanum/embriologia
Ambystoma mexicanum/genética
Proteínas de Anfíbios/genética
Anfíbios/genética
Animais
Simulação por Computador
Endoderma/embriologia
Regulação da Expressão Gênica no Desenvolvimento
Redes Reguladoras de Genes
Conceitos Matemáticos
Mesoderma/embriologia
Ligantes da Sinalização Nodal/genética
Xenopus laevis/embriologia
Xenopus laevis/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amphibian Proteins); 0 (Nodal Signaling Ligands)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170123
[Lr] Data última revisão:
170123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160304
[St] Status:MEDLINE
[do] DOI:10.1007/s11538-016-0150-8


  7 / 105 MEDLINE  
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[PMID]:26664104
[Au] Autor:Yarygin KN; Lupatov AY; Kholodenko IV
[Ad] Endereço:Laboratory of Cell Biology, Institute of Biomedical Chemistry, Moscow, Russia.
[Ti] Título:Cell-based therapies of liver diseases: age-related challenges.
[So] Source:Clin Interv Aging;10:1909-24, 2015.
[Is] ISSN:1178-1998
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:The scope of this review is to revise recent advances of the cell-based therapies of liver diseases with an emphasis on cell donor's and patient's age. Regenerative medicine with cell-based technologies as its integral part is focused on the structural and functional restoration of tissues impaired by sickness or aging. Unlike drug-based medicine directed primarily at alleviation of symptoms, regenerative medicine offers a more holistic approach to disease and senescence management aimed to achieve restoration of homeostasis. Hepatocyte transplantation and organ engineering are very probable forthcoming options of liver disease treatment in people of different ages and vigorous research and technological innovations in this area are in progress. Accordingly, availability of sufficient amounts of functional human hepatocytes is crucial. Direct isolation of autologous hepatocytes from liver biopsy is problematic due to related discomfort and difficulties with further expansion of cells, particularly those derived from aging people. Allogeneic primary human hepatocytes meeting quality standards are also in short supply. Alternatively, autologous hepatocytes can be produced by reprogramming of differentiated cells through the stage of induced pluripotent stem cells. In addition, fibroblasts and mesenchymal stromal cells can be directly induced to undergo advanced stage hepatogenic differentiation. Reprogramming of cells derived from elderly people is accompanied by the reversal of age-associated changes at the cellular level manifesting itself by telomere elongation and the U-turn of DNA methylation. Cell reprogramming can provide high quality rejuvenated hepatocytes for cell therapy and liver tissue engineering. Further technological advancements and establishment of national and global registries of induced pluripotent stem cell lines homozygous for HLA haplotypes can allow industry-style production of livers for immunosuppression-free transplantation.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Terapia Baseada em Transplante de Células e Tecidos/métodos
Hepatopatias/terapia
Regeneração Hepática/fisiologia
Engenharia Tecidual/métodos
[Mh] Termos MeSH secundário: Ativinas/metabolismo
Fatores Etários
Técnicas de Reprogramação Celular/métodos
Metilação de DNA
Fibroblastos/metabolismo
Hepatócitos/metabolismo
Seres Humanos
Células-Tronco Pluripotentes Induzidas/metabolismo
Células Mesenquimais Estromais/metabolismo
Ligantes da Sinalização Nodal/metabolismo
Homeostase do Telômero
Proteínas Wnt/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Nodal Signaling Ligands); 0 (Wnt Proteins); 0 (activin A); 104625-48-1 (Activins)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151215
[St] Status:MEDLINE
[do] DOI:10.2147/CIA.S97926


  8 / 105 MEDLINE  
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[PMID]:26013826
[Au] Autor:Sun G; Hu Z; Min Z; Yan X; Guan Z; Su H; Fu Y; Ma X; Chen YG; Zhang MQ; Tao Q; Wu W
[Ad] Endereço:From the MOE Key Laboratory of Protein Science, School of Life Sciences, Tsinghua University, Beijing 100084, China.
[Ti] Título:Small C-terminal Domain Phosphatase 3 Dephosphorylates the Linker Sites of Receptor-regulated Smads (R-Smads) to Ensure Transforming Growth Factor ß (TGFß)-mediated Germ Layer Induction in Xenopus Embryos.
[So] Source:J Biol Chem;290(28):17239-49, 2015 Jul 10.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Germ layer induction is one of the earliest events shortly after fertilization that initiates body formation of vertebrate embryos. In Xenopus, the maternally deposited transcriptional factor VegT promotes the expression of zygotic Nodal/Activin ligands that further form a morphogen gradient along the vegetal-animal axis and trigger the induction of the three germ layers. Here we found that SCP3 (small C-terminal domain phosphatase 3) is maternally expressed and vegetally enriched in Xenopus embryos and is essential for the timely induction of germ layers. SCP3 is required for the full activation of Nodal/Activin and bone morphogenetic protein signals and functions via dephosphorylation in the linker regions of receptor-regulated Smads. Consistently, the linker regions of receptor-regulated Smads are heavily phosphorylated in fertilized eggs, and this phosphorylation is gradually removed when embryos approach the midblastula transition. Knockdown of maternal SCP3 attenuates these dephosphorylation events and the activation of Nodal/Activin and bone morphogenetic protein signals after midblastula transition. This study thus suggested that the maternal SCP3 serves as a vegetally enriched, intrinsic factor to ensure a prepared status of Smads for their activation by the upcoming ligands during germ layer induction of Xenopus embryos.
[Mh] Termos MeSH primário: Fosfoproteínas Fosfatases/metabolismo
Proteínas Smad Reguladas por Receptor/metabolismo
Fator de Crescimento Transformador beta/metabolismo
Proteínas de Xenopus/metabolismo
Xenopus laevis/embriologia
Xenopus laevis/metabolismo
[Mh] Termos MeSH secundário: Ativinas/metabolismo
Animais
Sítios de Ligação
Blástula/embriologia
Blástula/metabolismo
Proteínas Morfogenéticas Ósseas/metabolismo
Feminino
Gástrula/embriologia
Gástrula/metabolismo
Técnicas de Silenciamento de Genes
Camadas Germinativas/embriologia
Camadas Germinativas/metabolismo
Ligantes
Ligantes da Sinalização Nodal/metabolismo
Fosfoproteínas Fosfatases/antagonistas & inibidores
Fosfoproteínas Fosfatases/genética
Fosforilação
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/genética
Transdução de Sinais
Proteínas Smad Reguladas por Receptor/química
Proteínas de Xenopus/antagonistas & inibidores
Proteínas de Xenopus/genética
Xenopus laevis/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Ligands); 0 (Nodal Signaling Ligands); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (Smad Proteins, Receptor-Regulated); 0 (Transforming Growth Factor beta); 0 (Xenopus Proteins); 104625-48-1 (Activins); EC 3.1.3.16 (Phosphoprotein Phosphatases)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:160710
[Lr] Data última revisão:
160710
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150528
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M115.655605


  9 / 105 MEDLINE  
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[PMID]:25819227
[Au] Autor:Lagadec R; Laguerre L; Menuet A; Amara A; Rocancourt C; Péricard P; Godard BG; Rodicio MC; Rodriguez-Moldes I; Mayeur H; Rougemont Q; Mazan S; Boutet A
[Ad] Endereço:CNRS, Sorbonne Universités, UPMC Univ Paris 06, FR2424, Development and Evolution of Vertebrates Group, Station Biologique, F-29688 Roscoff, France.
[Ti] Título:The ancestral role of nodal signalling in breaking L/R symmetry in the vertebrate forebrain.
[So] Source:Nat Commun;6:6686, 2015 Mar 30.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Left-right asymmetries in the epithalamic region of the brain are widespread across vertebrates, but their magnitude and laterality varies among species. Whether these differences reflect independent origins of forebrain asymmetries or taxa-specific diversifications of an ancient vertebrate feature remains unknown. Here we show that the catshark Scyliorhinus canicula and the lampreys Petromyzon marinus and Lampetra planeri exhibit conserved molecular asymmetries between the left and right developing habenulae. Long-term pharmacological treatments in these species show that nodal signalling is essential to their generation, rather than their directionality as in teleosts. Moreover, in contrast to zebrafish, habenular left-right differences are observed in the absence of overt asymmetry of the adjacent pineal field. These data support an ancient origin of epithalamic asymmetry, and suggest that a nodal-dependent asymmetry programme operated in the forebrain of ancestral vertebrates before evolving into a variable trait in bony fish.
[Mh] Termos MeSH primário: Lateralidade Funcional/genética
Regulação da Expressão Gênica no Desenvolvimento
Ligantes da Sinalização Nodal/genética
Petromyzon/genética
Prosencéfalo/embriologia
Tubarões/genética
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Diencéfalo/embriologia
Diencéfalo/metabolismo
Embrião não Mamífero
Fatores de Crescimento de Fibroblastos/genética
Fatores de Crescimento de Fibroblastos/metabolismo
Proteínas de Homeodomínio/genética
Proteínas de Homeodomínio/metabolismo
Lampreias/genética
Fatores de Determinação Direita-Esquerda/genética
Fatores de Determinação Direita-Esquerda/metabolismo
Dados de Sequência Molecular
Proteína Nodal/genética
Proteína Nodal/metabolismo
Ligantes da Sinalização Nodal/metabolismo
Prosencéfalo/metabolismo
Transdução de Sinais
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (Left-Right Determination Factors); 0 (Nodal Protein); 0 (Nodal Signaling Ligands); 0 (Transforming Growth Factor beta); 62031-54-3 (Fibroblast Growth Factors)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150331
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms7686


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[PMID]:25665164
[Au] Autor:Gu W; Monteiro R; Zuo J; Simões FC; Martella A; Andrieu-Soler C; Grosveld F; Sauka-Spengler T; Patient R
[Ad] Endereço:Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom.
[Ti] Título:A novel TGFß modulator that uncouples R-Smad/I-Smad-mediated negative feedback from R-Smad/ligand-driven positive feedback.
[So] Source:PLoS Biol;13(2):e1002051, 2015 Feb.
[Is] ISSN:1545-7885
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:As some of the most widely utilised intercellular signalling molecules, transforming growth factor ß (TGFß) superfamily members play critical roles in normal development and become disrupted in human disease. Establishing appropriate levels of TGFß signalling involves positive and negative feedback, which are coupled and driven by the same signal transduction components (R-Smad transcription factor complexes), but whether and how the regulation of the two can be distinguished are unknown. Genome-wide comparison of published ChIP-seq datasets suggests that LIM domain binding proteins (Ldbs) co-localise with R-Smads at a substantial subset of R-Smad target genes including the locus of inhibitory Smad7 (I-Smad7), which mediates negative feedback for TGFß signalling. We present evidence suggesting that zebrafish Ldb2a binds and directly activates the I-Smad7 gene, whereas it binds and represses the ligand gene, Squint (Sqt), which drives positive feedback. Thus, the fine tuning of TGFß signalling derives from positive and negative control by Ldb2a. Expression of ldb2a is itself activated by TGFß signals, suggesting potential feed-forward loops that might delay the negative input of Ldb2a to the positive feedback, as well as the positive input of Ldb2a to the negative feedback. In this way, precise gene expression control by Ldb2a enables an initial build-up of signalling via a fully active positive feedback in the absence of buffering by the negative feedback. In Ldb2a-deficient zebrafish embryos, homeostasis of TGFß signalling is perturbed and signalling is stably enhanced, giving rise to excess mesoderm and endoderm, an effect that can be rescued by reducing signalling by the TGFß family members, Nodal and BMP. Thus, Ldb2a is critical to the homeostatic control of TGFß signalling and thereby embryonic patterning.
[Mh] Termos MeSH primário: Padronização Corporal/genética
Retroalimentação Fisiológica
Proteínas com Domínio LIM/genética
Ligantes da Sinalização Nodal/metabolismo
Proteína Smad7/metabolismo
Fator de Crescimento Transformador beta/metabolismo
Proteínas de Peixe-Zebra/genética
Proteínas de Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Embrião não Mamífero
Endoderma/citologia
Endoderma/embriologia
Endoderma/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Seres Humanos
Proteínas com Domínio LIM/antagonistas & inibidores
Proteínas com Domínio LIM/deficiência
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Mesoderma/citologia
Mesoderma/embriologia
Mesoderma/metabolismo
Camundongos
Microinjeções
Dados de Sequência Molecular
Morfolinos/genética
Morfolinos/metabolismo
Ligantes da Sinalização Nodal/genética
Alinhamento de Sequência
Transdução de Sinais
Proteína Smad7/genética
Transcrição Genética
Fator de Crescimento Transformador beta/genética
Peixe-Zebra
Proteínas de Peixe-Zebra/antagonistas & inibidores
Proteínas de Peixe-Zebra/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (LIM Domain Proteins); 0 (Membrane Proteins); 0 (Morpholinos); 0 (Nodal Signaling Ligands); 0 (Smad7 Protein); 0 (Transforming Growth Factor beta); 0 (Zebrafish Proteins); 0 (ldb2a protein, zebrafish); 0 (ndr1 protein, zebrafish); 0 (nomo protein, zebrafish); 0 (smad7 protein, zebrafish)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150210
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.1002051



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