Base de dados : MEDLINE
Pesquisa : A16.629 [Categoria DeCS]
Referências encontradas : 391 [refinar]
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[PMID]:28941984
[Au] Autor:Schock EN; Brugmann SA
[Ad] Endereço:Division of Plastic Surgery, Department of Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA; Division of Developmental Biology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
[Ti] Título:Neural crest cells utilize primary cilia to regulate ventral forebrain morphogenesis via Hedgehog-dependent regulation of oriented cell division.
[So] Source:Dev Biol;431(2):168-178, 2017 11 15.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Development of the brain directly influences the development of the face via both physical growth and Sonic hedgehog (SHH) activity; however, little is known about how neural crest cells (NCCs), the mesenchymal population that comprise the developing facial prominences, influence the development of the brain. We utilized the conditional ciliary mutant Wnt1-Cre;Kif3a to demonstrate that loss of primary cilia on NCCs resulted in a widened ventral forebrain. We found that neuroectodermal Shh expression, dorsal/ventral patterning, and amount of proliferation in the ventral neuroectoderm was not changed in Wnt1-Cre;Kif3a mutants; however, tissue polarity and directional cell division were disrupted. Furthermore, NCCs of Wnt1-Cre;Kif3a mutants failed to respond to a SHH signal emanating from the ventral forebrain. We were able to recapitulate the ventral forebrain phenotype by removing Smoothened from NCCs (Wnt1-Cre;Smo ) indicating that changes in the ventral forebrain were mediated through a Hedgehog-dependent mechanism. Together, these data suggest a novel, cilia-dependent mechanism for NCCs during forebrain development.
[Mh] Termos MeSH primário: Divisão Celular
Cílios/metabolismo
Proteínas Hedgehog/metabolismo
Morfogênese
Crista Neural/citologia
Prosencéfalo/citologia
Prosencéfalo/embriologia
[Mh] Termos MeSH secundário: Animais
Padronização Corporal/genética
Polaridade Celular
Face/embriologia
Regulação da Expressão Gênica no Desenvolvimento
Integrases/metabolismo
Cinesina/metabolismo
Camundongos
Modelos Biológicos
Morfogênese/genética
Mutação/genética
Crista Neural/metabolismo
Placa Neural/citologia
Placa Neural/embriologia
Placa Neural/metabolismo
Fenótipo
Prosencéfalo/metabolismo
Recombinação Genética/genética
Fatores de Transcrição SOXE/metabolismo
Telencéfalo/embriologia
Telencéfalo/metabolismo
Proteínas Wnt/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hedgehog Proteins); 0 (Kif3a protein, mouse); 0 (SOXE Transcription Factors); 0 (Shh protein, mouse); 0 (Wnt Proteins); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases); EC 3.6.4.4 (Kinesin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170925
[St] Status:MEDLINE


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[PMID]:28663133
[Au] Autor:Marchak A; Grant PA; Neilson KM; Datta Majumdar H; Yaklichkin S; Johnson D; Moody SA
[Ad] Endereço:Department of Anatomy and Regenerative Biology, George Washington University School of Medicine and Health Sciences, Washington DC, USA.
[Ti] Título:Wbp2nl has a developmental role in establishing neural and non-neural ectodermal fates.
[So] Source:Dev Biol;429(1):213-224, 2017 09 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In many animals, maternally synthesized mRNAs are critical for primary germ layer formation. In Xenopus, several maternal mRNAs are enriched in the animal blastomere progenitors of the embryonic ectoderm. We previously identified one of these, WW-domain binding protein 2 N-terminal like (wbp2nl), that others previously characterized as a sperm protein (PAWP) that promotes meiotic resumption. Herein we demonstrate that it has an additional developmental role in regionalizing the embryonic ectoderm. Knock-down of Wbp2nl in the dorsal ectoderm reduced cranial placode and neural crest gene expression domains and expanded neural plate domains; knock-down in ventral ectoderm reduced epidermal gene expression. Conversely, increasing levels of Wbp2nl in the neural plate induced ectopic epidermal and neural crest gene expression and repressed many neural plate and cranial placode genes. The effects in the neural plate appear to be mediated, at least in part, by down-regulating chd, a BMP antagonist. Because the cellular function of Wbp2nl is not known, we mutated several predicted motifs. Expressing mutated proteins in embryos showed that a putative phosphorylation site at Thr45 and an α-helix in the PH-G domain are required to ectopically induce epidermal and neural crest genes in the neural plate. An intact YAP-binding motif also is required for ectopic epidermal gene expression as well as for down-regulating chd. This work reveals novel developmental roles for a cytoplasmic protein that promotes epidermal and neural crest formation at the expense of neural ectoderm.
[Mh] Termos MeSH primário: Proteínas de Transporte/metabolismo
Ectoderma/embriologia
Ectoderma/metabolismo
Sistema Nervoso/embriologia
Sistema Nervoso/metabolismo
Proteínas de Plasma Seminal/metabolismo
Proteínas de Xenopus/metabolismo
Xenopus laevis/embriologia
Xenopus laevis/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Proteínas Morfogenéticas Ósseas/metabolismo
Proteínas de Transporte/química
Proteínas de Transporte/genética
Epiderme/embriologia
Epiderme/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Mesoderma/embriologia
Mesoderma/metabolismo
Mutação/genética
Crista Neural/embriologia
Crista Neural/metabolismo
Placa Neural/embriologia
Placa Neural/metabolismo
Fenótipo
Domínios Proteicos
Transporte Proteico
Proteínas de Plasma Seminal/química
Proteínas de Plasma Seminal/genética
Alinhamento de Sequência
Proteínas de Xenopus/química
Proteínas de Xenopus/genética
Xenopus laevis/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Carrier Proteins); 0 (Seminal Plasma Proteins); 0 (Wbp2nl protein, Xenopus); 0 (Xenopus Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE


  3 / 391 MEDLINE  
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[PMID]:28623229
[Au] Autor:Dong X; Li J; He L; Gu C; Jia W; Yue Y; Li J; Zhang Q; Chu L; Zhao Q
[Ad] Endereço:From the Ministry of Education Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing 210061, China.
[Ti] Título:Zebrafish Znfl1 proteins control the expression of gene in the posterior neuroectoderm by acting upstream of and genes.
[So] Source:J Biol Chem;292(31):13045-13055, 2017 Aug 04.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transcription factors play crucial roles in patterning posterior neuroectoderm. Previously, zinc finger transcription factor was reported to be expressed in the posterior neuroectoderm of zebrafish embryos. However, its roles remain unknown. Here, we report that there are 13 copies of in the zebrafish genome, and all the paralogues share highly identical protein sequences and cDNA sequences. When are knocked down using a morpholino to inhibit their translation or dCas9-Eve to inhibit their transcription, the zebrafish gastrula displays reduced expression of , the marker gene for the posterior neuroectoderm. Further analyses reveal that diminishing produces the decreased expressions of , whereas overexpression of effectively rescues the reduced expression of in the posterior neuroectoderm. Additionally, knocking down causes the reduced expression of , a direct regulator of , in the posterior neuroectoderm, and overexpression of rescues the expression of in the knockdown embryos. In contrast, knocking down either or does not affect the expressions of Taken together, our results demonstrate that zebrafish control the expression of in the posterior neuroectoderm by acting upstream of and .
[Mh] Termos MeSH primário: Regulação da Expressão Gênica no Desenvolvimento
Proteínas de Homeodomínio/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Placa Neural/metabolismo
Fator 3 de Transcrição de Octâmero/metabolismo
Fatores de Transcrição/metabolismo
Proteínas de Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Biologia Computacional
Gástrula/efeitos dos fármacos
Gástrula/metabolismo
Dosagem de Genes
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Proteínas de Homeodomínio/genética
Hibridização In Situ
Microinjeções
Morfolinos/farmacologia
Proteínas do Tecido Nervoso/antagonistas & inibidores
Proteínas do Tecido Nervoso/genética
Placa Neural/efeitos dos fármacos
Placa Neural/embriologia
Neurogênese/efeitos dos fármacos
Fator 3 de Transcrição de Octâmero/antagonistas & inibidores
Fator 3 de Transcrição de Octâmero/genética
Interferência de RNA
RNA Antissenso/farmacologia
RNA Mensageiro/antagonistas & inibidores
RNA Mensageiro/metabolismo
Fatores de Transcrição/química
Fatores de Transcrição/genética
Peixe-Zebra
Proteínas de Peixe-Zebra/antagonistas & inibidores
Proteínas de Peixe-Zebra/química
Proteínas de Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (HOXB1 homeodomain protein); 0 (Homeodomain Proteins); 0 (Morpholinos); 0 (Nerve Tissue Proteins); 0 (Octamer Transcription Factor-3); 0 (RNA, Antisense); 0 (RNA, Messenger); 0 (Sall4 protein, zebrafish); 0 (Transcription Factors); 0 (Zebrafish Proteins); 0 (Znfl1 protein, zebrafish); 0 (pou5f1 protein, zebrafish)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170618
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.777094


  4 / 391 MEDLINE  
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[PMID]:28545845
[Au] Autor:Baumholtz AI; Simard A; Nikolopoulou E; Oosenbrug M; Collins MM; Piontek A; Krause G; Piontek J; Greene NDE; Ryan AK
[Ad] Endereço:Department of Human Genetics, McGill University, Canada; The Research Institute of the McGill University Health Centre, Montréal, Québec, Canada. Electronic address: amanda.baumholtz@mail.mcgill.ca.
[Ti] Título:Claudins are essential for cell shape changes and convergent extension movements during neural tube closure.
[So] Source:Dev Biol;428(1):25-38, 2017 08 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During neural tube closure, regulated changes at the level of individual cells are translated into large-scale morphogenetic movements to facilitate conversion of the flat neural plate into a closed tube. Throughout this process, the integrity of the neural epithelium is maintained via cell interactions through intercellular junctions, including apical tight junctions. Members of the claudin family of tight junction proteins regulate paracellular permeability, apical-basal cell polarity and link the tight junction to the actin cytoskeleton. Here, we show that claudins are essential for neural tube closure: the simultaneous removal of Cldn3, -4 and -8 from tight junctions caused folate-resistant open neural tube defects. Their removal did not affect cell type differentiation, neural ectoderm patterning nor overall apical-basal polarity. However, apical accumulation of Vangl2, RhoA, and pMLC were reduced, and Par3 and Cdc42 were mislocalized at the apical cell surface. Our data showed that claudins act upstream of planar cell polarity and RhoA/ROCK signaling to regulate cell intercalation and actin-myosin contraction, which are required for convergent extension and apical constriction during neural tube closure, respectively.
[Mh] Termos MeSH primário: Polaridade Celular/fisiologia
Forma Celular/fisiologia
Placa Neural/embriologia
Tubo Neural/embriologia
Neurulação/fisiologia
Junções Íntimas/fisiologia
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/metabolismo
Animais
Moléculas de Adesão Celular/metabolismo
Embrião de Galinha
Claudina-3/genética
Claudina-3/metabolismo
Claudina-4/genética
Claudina-4/metabolismo
Claudinas/genética
Claudinas/metabolismo
Técnicas de Cultura Embrionária
Camundongos
Morfogênese/fisiologia
Proteínas do Tecido Nervoso/metabolismo
Defeitos do Tubo Neural/genética
Transdução de Sinais/fisiologia
Proteína cdc42 de Ligação ao GTP/metabolismo
Proteínas rho de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cdc42 protein, mouse); 0 (Cell Adhesion Molecules); 0 (Claudin-3); 0 (Claudin-4); 0 (Claudins); 0 (Cldn3 protein, mouse); 0 (Cldn4 protein, mouse); 0 (Ltap protein, mouse); 0 (Nerve Tissue Proteins); 0 (Pard3 protein, mouse); 0 (claudin 8); EC 3.6.5.2 (RhoA protein, mouse); EC 3.6.5.2 (cdc42 GTP-Binding Protein); EC 3.6.5.2 (rho GTP-Binding Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE


  5 / 391 MEDLINE  
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[PMID]:28346501
[Au] Autor:Schock EN; Struve JN; Chang CF; Williams TJ; Snedeker J; Attia AC; Stottmann RW; Brugmann SA
[Ad] Endereço:Division of Plastic Surgery, Department of Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States of America.
[Ti] Título:A tissue-specific role for intraflagellar transport genes during craniofacial development.
[So] Source:PLoS One;12(3):e0174206, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Primary cilia are nearly ubiquitous, cellular projections that function to transduce molecular signals during development. Loss of functional primary cilia has a particularly profound effect on the developing craniofacial complex, causing several anomalies including craniosynostosis, micrognathia, midfacial dysplasia, cleft lip/palate and oral/dental defects. Development of the craniofacial complex is an intricate process that requires interactions between several different tissues including neural crest cells, neuroectoderm and surface ectoderm. To understand the tissue-specific requirements for primary cilia during craniofacial development we conditionally deleted three separate intraflagellar transport genes, Kif3a, Ift88 and Ttc21b with three distinct drivers, Wnt1-Cre, Crect and AP2-Cre which drive recombination in neural crest, surface ectoderm alone, and neural crest, surface ectoderm and neuroectoderm, respectively. We found that tissue-specific conditional loss of ciliary genes with different functions produces profoundly different facial phenotypes. Furthermore, analysis of basic cellular behaviors in these mutants suggests that loss of primary cilia in a distinct tissue has unique effects on development of adjacent tissues. Together, these data suggest specific spatiotemporal roles for intraflagellar transport genes and the primary cilium during craniofacial development.
[Mh] Termos MeSH primário: Anormalidades Craniofaciais/genética
Face/embriologia
Regulação da Expressão Gênica no Desenvolvimento
Crânio/embriologia
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Animais
Cílios/genética
Face/anormalidades
Feminino
Deleção de Genes
Cinesina/genética
Masculino
Camundongos
Crista Neural/embriologia
Crista Neural/metabolismo
Placa Neural/embriologia
Placa Neural/metabolismo
Crânio/anormalidades
Crânio/metabolismo
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Kif3a protein, mouse); 0 (THM1 protein, mouse); 0 (Tg737Rpw protein, mouse); 0 (Tumor Suppressor Proteins); EC 3.6.4.4 (Kinesin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174206


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[PMID]:28346437
[Au] Autor:Smutny M; Ákos Z; Grigolon S; Shamipour S; Ruprecht V; Capek D; Behrndt M; Papusheva E; Tada M; Hof B; Vicsek T; Salbreux G; Heisenberg CP
[Ad] Endereço:Institute of Science and Technology Austria, Am Campus 1, A-3400 Klosterneuburg, Austria.
[Ti] Título:Friction forces position the neural anlage.
[So] Source:Nat Cell Biol;19(4):306-317, 2017 Apr.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:During embryonic development, mechanical forces are essential for cellular rearrangements driving tissue morphogenesis. Here, we show that in the early zebrafish embryo, friction forces are generated at the interface between anterior axial mesoderm (prechordal plate, ppl) progenitors migrating towards the animal pole and neurectoderm progenitors moving in the opposite direction towards the vegetal pole of the embryo. These friction forces lead to global rearrangement of cells within the neurectoderm and determine the position of the neural anlage. Using a combination of experiments and simulations, we show that this process depends on hydrodynamic coupling between neurectoderm and ppl as a result of E-cadherin-mediated adhesion between those tissues. Our data thus establish the emergence of friction forces at the interface between moving tissues as a critical force-generating process shaping the embryo.
[Mh] Termos MeSH primário: Fricção
Sistema Nervoso/embriologia
Peixe-Zebra/embriologia
[Mh] Termos MeSH secundário: Animais
Fenômenos Biomecânicos
Caderinas/metabolismo
Comunicação Celular
Movimento Celular
Embrião não Mamífero/citologia
Endoderma/citologia
Endoderma/embriologia
Gastrulação
Hidrodinâmica
Mesoderma/citologia
Mesoderma/embriologia
Modelos Biológicos
Morfogênese
Mutação/genética
Placa Neural/citologia
Placa Neural/embriologia
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (Zebrafish Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3492


  7 / 391 MEDLINE  
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[PMID]:28322736
[Au] Autor:Exner CRT; Kim AY; Mardjuki SM; Harland RM
[Ad] Endereço:Department of Molecular & Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA.
[Ti] Título:sall1 and sall4 repress pou5f3 family expression to allow neural patterning, differentiation, and morphogenesis in Xenopus laevis.
[So] Source:Dev Biol;425(1):33-43, 2017 05 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The embryonic precursor of the vertebrate central nervous system, the neural plate, is patterned along the anterior-posterior axis and shaped by morphogenetic movements early in development. We previously identified the genes sall1 and sall4, known regulators of pluripotency in other contexts, as transcriptional targets of developmental signaling pathways that regulate neural development. Here, we demonstrate that these two genes are required for induction of posterior neural fates, the cell shape changes that contribute to neural tube closure, and later neurogenesis. Upon sall1 or sall4 knockdown, defects are associated with the failure of the neural plate to differentiate. Consistent with this, sall-deficient neural tissue exhibits an aberrant upregulation of pou5f3 family genes, the Xenopus homologs of the mammalian stem cell maintenance factor Pou5f1 (Oct4). Furthermore, overexpression of pou5f3 genes in Xenopus causes defects in neural patterning, morphogenesis, and differentiation that phenocopy those observed in sall1 and sall4 morphants. In all, this work shows that both sall1 and sall4 act to repress pou5f3 family gene expression in the neural plate, thereby allowing vertebrate neural development to proceed.
[Mh] Termos MeSH primário: Placa Neural/metabolismo
Fator 3 de Transcrição de Octâmero/genética
Fatores de Transcrição/genética
Proteínas de Xenopus/genética
Xenopus laevis/genética
[Mh] Termos MeSH secundário: Animais
Padronização Corporal/genética
Diferenciação Celular/genética
Embrião não Mamífero/embriologia
Embrião não Mamífero/metabolismo
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Técnicas de Silenciamento de Genes
Hibridização In Situ
Microscopia Confocal
Morfogênese/genética
Placa Neural/embriologia
Neurulação/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Xenopus laevis/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Octamer Transcription Factor-3); 0 (SALL4 protein, Xenopus); 0 (Sall1 protein, Xenopus); 0 (Transcription Factors); 0 (Xenopus Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE


  8 / 391 MEDLINE  
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[PMID]:28316121
[Au] Autor:Sherman JH; Karpinski BA; Fralish MS; Cappuzzo JM; Dhindsa DS; Thal AG; Moody SA; LaMantia AS; Maynard TM
[Ad] Endereço:Department of Neurological Surgery, George Washington University Hospital, Washington, District of Columbia.
[Ti] Título:Foxd4 is essential for establishing neural cell fate and for neuronal differentiation.
[So] Source:Genesis;55(6), 2017 Jun.
[Is] ISSN:1526-968X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many molecular factors required for later stages of neuronal differentiation have been identified; however, much less is known about the early events that regulate the initial establishment of the neuroectoderm. We have used an in vitro embryonic stem cell (ESC) differentiation model to investigate early events of neuronal differentiation and to define the role of mouse Foxd4, an ortholog of a forkhead-family transcription factor central to Xenopus neural plate/neuroectodermal precursor development. We found that Foxd4 is a necessary regulator of the transition from pluripotent ESC to neuroectodermal stem cell, and its expression is necessary for neuronal differentiation. Mouse Foxd4 expression is not only limited to the neural plate but it is also expressed and apparently functions to regulate neurogenesis in the olfactory placode. These in vitro results suggest that mouse Foxd4 has a similar function to its Xenopus ortholog; this was confirmed by successfully substituting murine Foxd4 for its amphibian counterpart in overexpression experiments. Thus, Foxd4 appears to regulate the initial steps in establishing neuroectodermal precursors during initial development of the nervous system.
[Mh] Termos MeSH primário: Células-Tronco Embrionárias/metabolismo
Fatores de Transcrição Forkhead/genética
Células-Tronco Neurais/metabolismo
Neurogênese
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Células-Tronco Embrionárias/citologia
Fatores de Transcrição Forkhead/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Camundongos
Placa Neural/citologia
Placa Neural/metabolismo
Células-Tronco Neurais/citologia
Xenopus
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Forkhead Transcription Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170320
[St] Status:MEDLINE
[do] DOI:10.1002/dvg.23031


  9 / 391 MEDLINE  
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[PMID]:28259755
[Au] Autor:Tanaka S; Hosokawa H; Weinberg ES; Maegawa S
[Ad] Endereço:Graduate School of Biostudies, Kyoto University, Kyoto 606-8501, Japan.
[Ti] Título:Chordin and dickkopf-1b are essential for the formation of head structures through activation of the FGF signaling pathway in zebrafish.
[So] Source:Dev Biol;424(2):189-197, 2017 04 15.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The ability of the Spemann organizer to induce dorsal axis formation is dependent on downstream factors of the maternal Wnt/ß-catenin signaling pathway. The fibroblast growth factor (FGF) signaling pathway has been identified as one of the downstream components of the maternal Wnt/ß-catenin signaling pathway. The ability of the FGF signaling pathway to induce the formation of a dorsal axis with a complete head structure requires chordin (chd) expression; however, the molecular mechanisms involved in this developmental process, due to activation of FGF signaling, remain unclear. In this study, we showed that activation of the FGF signaling pathway induced the formation of complete head structures through the expression of chd and dickkopf-1b (dkk1b). Using the organizer-deficient maternal mutant, ichabod, we identified dkk1b as a novel downstream factor in the FGF signaling pathway. We also demonstrate that dkk1b expression is necessary, after activation of the FGF signaling pathway, to induce neuroectoderm patterning along the anteroposterior (AP) axis and for formation of complete head structures. Co-injection of chd and dkk1b mRNA resulted in the formation of a dorsal axis with a complete head structure in ichabod embryos, confirming the role of these factors in this developmental process. Unexpectedly, we found that chd induced dkk1b expression in ichabod embryos at the shield stage. However, chd failed to maintain dkk1b expression levels in cells of the shield and, subsequently, in the cells of the prechordal plate after mid-gastrula stage. In contrast, activation of the FGF signaling pathway maintained the dkk1b expression from the beginning of gastrulation to early somitogenesis. In conclusion, activation of the FGF signaling pathway induces the formation of a dorsal axis with a complete head structure through the expression of chd and subsequent maintenance of dkk1b expression levels.
[Mh] Termos MeSH primário: Fatores de Crescimento de Fibroblastos/metabolismo
Glicoproteínas/metabolismo
Cabeça/embriologia
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Transdução de Sinais
Proteínas de Peixe-Zebra/metabolismo
Peixe-Zebra/embriologia
[Mh] Termos MeSH secundário: Animais
Padronização Corporal
Embrião não Mamífero/metabolismo
Gastrulação
Regulação da Expressão Gênica no Desenvolvimento
Peptídeos e Proteínas de Sinalização Intercelular/genética
Modelos Biológicos
Placa Neural/embriologia
Placa Neural/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Somitos/embriologia
Somitos/metabolismo
Peixe-Zebra/genética
Proteínas de Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Glycoproteins); 0 (Intercellular Signaling Peptides and Proteins); 0 (RNA, Messenger); 0 (Zebrafish Proteins); 0 (dkk1 protein, zebrafish); 62031-54-3 (Fibroblast Growth Factors); 93586-27-7 (chordin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170306
[St] Status:MEDLINE


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[PMID]:28255006
[Au] Autor:Balashova OA; Visina O; Borodinsky LN
[Ad] Endereço:Department of Physiology & Membrane Biology and Institute for Pediatric Regenerative Medicine, Shriners Hospital for Children, University of California Davis School of Medicine, Sacramento, CA 95817, USA.
[Ti] Título:Folate receptor 1 is necessary for neural plate cell apical constriction during neural tube formation.
[So] Source:Development;144(8):1518-1530, 2017 04 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Folate supplementation prevents up to 70% of neural tube defects (NTDs), which result from a failure of neural tube closure during embryogenesis. The elucidation of the mechanisms underlying folate action has been challenging. This study introduces as a model to determine the cellular and molecular mechanisms involved in folate action during neural tube formation. We show that knockdown of folate receptor 1 (Folr1; also known as FRα) impairs neural tube formation and leads to NTDs. Folr1 knockdown in neural plate cells only is necessary and sufficient to induce NTDs. Folr1-deficient neural plate cells fail to constrict, resulting in widening of the neural plate midline and defective neural tube closure. Pharmacological inhibition of folate action by methotrexate during neurulation induces NTDs by inhibiting folate interaction with its uptake systems. Our findings support a model in which the folate receptor interacts with cell adhesion molecules, thus regulating the apical cell membrane remodeling and cytoskeletal dynamics necessary for neural plate folding. Further studies in this organism could unveil novel cellular and molecular events mediated by folate and lead to new ways of preventing NTDs.
[Mh] Termos MeSH primário: Polaridade Celular
Receptor 1 de Folato/metabolismo
Placa Neural/citologia
Placa Neural/metabolismo
Tubo Neural/citologia
Tubo Neural/embriologia
Organogênese
Proteínas de Xenopus/metabolismo
Xenopus laevis/embriologia
[Mh] Termos MeSH secundário: Animais
Caderinas/metabolismo
Polaridade Celular/efeitos dos fármacos
Forma Celular/efeitos dos fármacos
Embrião não Mamífero/citologia
Embrião não Mamífero/metabolismo
Endocitose/efeitos dos fármacos
Feminino
Receptor 1 de Folato/genética
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Marcação de Genes
Seres Humanos
Morfolinos/farmacologia
Tubo Neural/metabolismo
Neurulação/efeitos dos fármacos
Organogênese/efeitos dos fármacos
Proteínas de Xenopus/genética
Xenopus laevis/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Cadherins); 0 (Folate Receptor 1); 0 (Morpholinos); 0 (Xenopus Proteins)
[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:170304
[St] Status:MEDLINE
[do] DOI:10.1242/dev.137315



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