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Pesquisa : A16.627 [Categoria DeCS]
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  1 / 5554 MEDLINE  
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[PMID]:29237533
[Au] Autor:Wang J; Wang F; Gui YH
[Ad] Endereço:Department of Cardiovascular Medicine, Children's Hospital of Fudan University, Shanghai 200023, China. yhgui@shmu.edu.cn.
[Ti] Título:[Research advances in the mechanism of congenital heart disease induced by pregestational diabetes mellitus].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;19(12):1297-1300, 2017 Dec.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Congenital heart disease (CHD) is the most common birth defect at present and has a complex etiology which involves the combined effect of genetic and environmental factors. Pregestational diabetes mellitus is significantly associated with the development of CHD, but the detailed mechanism remains unknown. This article reviews the research advances in the molecular mechanism of CHD caused by pregestational diabetes mellitus.
[Mh] Termos MeSH primário: Cardiopatias Congênitas/etiologia
Gravidez em Diabéticas
[Mh] Termos MeSH secundário: Animais
Apoptose
Movimento Celular
Feminino
Seres Humanos
Crista Neural/fisiologia
Gravidez
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Reactive Oxygen Species)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE


  2 / 5554 MEDLINE  
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[PMID]:28463847
[Au] Autor:Benítez-Burraco A; Di Pietro L; Barba M; Lattanzi W
[Ad] Endereço:Department of Philology, Faculty of Humanities, University of Huelva, Huelva, Spain.
[Ti] Título:Schizophrenia and Human Self-Domestication: An Evolutionary Linguistics Approach.
[So] Source:Brain Behav Evol;89(3):162-184, 2017.
[Is] ISSN:1421-9743
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Schizophrenia (SZ) is a pervasive neurodevelopmental disorder that entails social and cognitive deficits, including marked language problems. Its complex multifactorial etiopathogenesis, including genetic and environmental factors, is still widely uncertain. SZ incidence has always been high and quite stable in human populations, across time and regardless of cultural implications, for unclear reasons. It has been hypothesized that SZ pathophysiology may involve the biological components that changed during the recent human evolutionary history, and led to our distinctive mode of cognition, which includes language skills. In this paper we explore this hypothesis, focusing on the self-domestication of the human species. This has been claimed to account for many human-specific distinctive traits, including aspects of our behavior and cognition, and to favor the emergence of complex languages through cultural evolution. The "domestication syndrome" in mammals comprises the constellation of traits exhibited by domesticated strains, seemingly resulting from the hypofunction of the neural crest. It is our intention to show that people with SZ exhibit more marked domesticated traits at the morphological, physiological, and behavioral levels. We also show that genes involved in domestication and neural crest development and function comprise nearly 20% of SZ candidates, most of which exhibit altered expression profiles in the brain of SZ patients, specifically in areas involved in language processing. Based on these observations, we conclude that SZ may represent an abnormal ontogenetic itinerary for the human faculty of language, resulting, at least in part, from changes in genes important for the domestication syndrome and primarily involving the neural crest.
[Mh] Termos MeSH primário: Esquizofrenia/genética
Esquizofrenia/fisiopatologia
[Mh] Termos MeSH secundário: Evolução Biológica
Encéfalo/patologia
Cognição/fisiologia
Transtornos Cognitivos/fisiopatologia
Bases de Dados Genéticas
Regulação da Expressão Gênica no Desenvolvimento/genética
Seres Humanos
Linguagem
Linguística/métodos
Crista Neural/fisiologia
Psicologia do Esquizofrênico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1159/000468506


  3 / 5554 MEDLINE  
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[PMID]:27776507
[Au] Autor:Konstantinidou C; Taraviras S; Pachnis V
[Ad] Endereço:The Francis Crick Institute, Mill Hill Laboratory, The Ridgeway, Mill Hill, London, NW7 1AA, UK.
[Ti] Título:Geminin prevents DNA damage in vagal neural crest cells to ensure normal enteric neurogenesis.
[So] Source:BMC Biol;14(1):94, 2016 10 24.
[Is] ISSN:1741-7007
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In vertebrate organisms, the neural crest (NC) gives rise to multipotential and highly migratory progenitors which are distributed throughout the embryo and generate, among other structures, the peripheral nervous system, including the intrinsic neuroglial networks of the gut, i.e. the enteric nervous system (ENS). The majority of enteric neurons and glia originate from vagal NC-derived progenitors which invade the foregut mesenchyme and migrate rostro-caudally to colonise the entire length of the gut. Although the migratory behaviour of NC cells has been studied extensively, it remains unclear how their properties and response to microenvironment change as they navigate through complex cellular terrains to reach their target embryonic sites. RESULTS: Using conditional gene inactivation in mice we demonstrate here that the cell cycle-dependent protein Geminin (Gem) is critical for the survival of ENS progenitors in a stage-dependent manner. Gem deletion in early ENS progenitors (prior to foregut invasion) resulted in cell-autonomous activation of DNA damage response and p53-dependent apoptosis, leading to severe intestinal aganglionosis. In contrast, ablation of Gem shortly after ENS progenitors had invaded the embryonic gut did not result in discernible survival or migratory deficits. In contrast to other developmental systems, we obtained no evidence for a role of Gem in commitment or differentiation of ENS lineages. The stage-dependent resistance of ENS progenitors to mutation-induced genotoxic stress was further supported by the enhanced survival of post gut invasion ENS lineages to γ-irradiation relative to their predecessors. CONCLUSIONS: Our experiments demonstrate that, in mammals, NC-derived ENS lineages are sensitive to genotoxic stress in a stage-specific manner. Following gut invasion, ENS progenitors are distinctly resistant to Gem ablation and irradiation in comparison to their pre-enteric counterparts. These studies suggest that the microenvironment of the embryonic gut protects ENS progenitors and their progeny from genotoxic stress.
[Mh] Termos MeSH primário: Dano ao DNA/efeitos dos fármacos
Sistema Nervoso Entérico/citologia
Geminina/farmacologia
Crista Neural/citologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Diferenciação Celular/genética
Células Cultivadas
Sistema Nervoso Entérico/efeitos dos fármacos
Feminino
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Camundongos
Neurogênese/efeitos dos fármacos
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Geminin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  4 / 5554 MEDLINE  
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[PMID]:29190819
[Au] Autor:Mathavan K; Khedgikar V; Bartolo V; Alfandari D
[Ad] Endereço:Department of Veterinary and Animal Sciences, University of Massachusetts Amherst, Amherst, Massachusetts, United States of America.
[Ti] Título:The ectodomain of cadherin-11 binds to erbB2 and stimulates Akt phosphorylation to promote cranial neural crest cell migration.
[So] Source:PLoS One;12(11):e0188963, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During development, a multi-potent group of cells known as the cranial neural crest (CNC) migrate to form craniofacial structures. Proper migration of these cells requires proteolysis of cell adhesion molecules, such as cadherins. In Xenopus laevis, preventing extracellular cleavage of cadherin-11 impairs CNC migration. However, overexpression of the soluble cleavage product (EC1-3) is capable of rescuing this phenotype. The mechanism by which EC1-3 promotes CNC migration has not been investigated until now. Here we show that EC1-3 stimulates phosphorylation of Akt, a target of PI3K, in X.laevis CNC. Through immunoprecipitation experiments, we determined that EC1-3 interacts with all ErbB receptors, PDGFRα, and FGFR1. Of these receptors, only ErbB2 was able to produce an increase in Akt phosphorylation upon treatment with a recombinant EC1-3. This increase was abrogated by mubritinib, an inhibitor of ErbB2. We were able to recapitulate this decrease in Akt phosphorylation in vivo by knocking down ErbB2 in CNC cells. Knockdown of the receptor also significantly reduced CNC migration in vivo. We confirmed the importance of ErbB2 and ErbB receptor signaling in CNC migration using mubritinib and canertinib, respectively. Mubritinib and the PI3K inhibitor LY294002 significantly decreased cell migration while canertinib nearly prevented it altogether. These data show that ErbB2 and Akt are important for CNC migration and implicate other ErbB receptors and Akt-independent signaling pathways. Our findings provide the first example of a functional interaction between the extracellular domain of a type II classical cadherin and growth factor receptors.
[Mh] Termos MeSH primário: Encéfalo/citologia
Caderinas/metabolismo
Movimento Celular
Crista Neural/citologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptor ErbB-2/metabolismo
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Caderinas/química
Células HEK293
Seres Humanos
Fosforilação
Ligação Proteica
Xenopus laevis/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 156621-71-5 (osteoblast cadherin); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188963


  5 / 5554 MEDLINE  
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[PMID]:29277616
[Au] Autor:Bae CJ; Hong CS; Saint-Jeannet JP
[Ad] Endereço:Department of Basic Science & Craniofacial Biology, College of Dentistry, New York University, New York, USA.
[Ti] Título:Anosmin-1 is essential for neural crest and cranial placodes formation in Xenopus.
[So] Source:Biochem Biophys Res Commun;495(3):2257-2263, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During embryogenesis vertebrates develop a complex craniofacial skeleton associated with sensory organs. These structures are primarily derived from two embryonic cell populations the neural crest and cranial placodes, respectively. Neural crest cells and cranial placodes are specified through the integrated action of several families of signaling molecules, and the subsequent activation of a complex network of transcription factors. Here we describe the expression and function of Anosmin-1 (Anos1), an extracellular matrix protein, during neural crest and cranial placodes development in Xenopus laevis. Anos1 was identified as a target of Pax3 and Zic1, two transcription factors necessary and sufficient to generate neural crest and cranial placodes. Anos1 is expressed in cranial neural crest progenitors at early neurula stage and in cranial placode derivatives later in development. We show that Anos1 function is required for neural crest and sensory organs development in Xenopus, consistent with the defects observed in Kallmann syndrome patients carrying a mutation in ANOS1. These findings indicate that anos1 has a conserved function in the development of craniofacial structures, and indicate that anos1-depleted Xenopus embryos represent a useful model to analyze the pathogenesis of Kallmann syndrome.
[Mh] Termos MeSH primário: Desenvolvimento Embrionário/fisiologia
Proteínas da Matriz Extracelular/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Crista Neural/embriologia
Crista Neural/metabolismo
Neurogênese/fisiologia
Crânio/embriologia
Crânio/metabolismo
Proteínas de Xenopus/metabolismo
[Mh] Termos MeSH secundário: Animais
Xenopus
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Extracellular Matrix Proteins); 0 (Nerve Tissue Proteins); 0 (Xenopus Proteins); 0 (anosmin-1 protein, Xenopus)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


  6 / 5554 MEDLINE  
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[PMID]:29196262
[Au] Autor:Nishida S; Yoshizaki H; Yasui Y; Kuwahara T; Kiyokawa E; Kohno M
[Ad] Endereço:Department of Pediatric Surgery, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku-gun, Ishikawa 920-0293, Japan.
[Ti] Título:Collagen VI suppresses fibronectin-induced enteric neural crest cell migration by downregulation of focal adhesion proteins.
[So] Source:Biochem Biophys Res Commun;495(1):1461-1467, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The enteric nervous system (ENS) is a network of neurons and glia that are derived from enteric neural crest cells (ENCCs) and essential for regulating peristaltic activity of the colon. ENCCs migrate along the gastrointestinal tract to form the ENS, and disruption of ENCC motility leads to ENS disorders, such as Hirschsprung's disease. Previous ENCC-transplant experiments show that ENCCs can invade into isolated mouse intestines by age E13.5, but not after E15.5. We hypothesized that altered age-specific micro-environments in the intestine are responsible for ENCC invasion/migration. Here, we compared gene expression in the intestine between at E11.5 and E15.5 and identified 1355 differentially expressed transcripts. Among these, we found that genes encoding extracellular matrix (ECM) proteins were enriched. Notably, collagen VI (ColVI) family members were upregulated in the E15.5 mouse intestine at the mRNA and protein levels, whereas fibronectin (FN) was downregulated; however, both proteins showed colocalization at E15.5. To understand the mechanisms of ColVI and FN in ENCC migration, we examined neurosphere or individual ENCC-adherence capabilities toward the ECM. ColVI suppressed FN-induced ENCC spreading/migration, whereas ColVI induced morphologically narrow ENCC spreading and weak stress-fiber formation as compared with those with FN. Additionally, in ENCCs cultured on plates containing ColVI, the expression and phosphorylation of p130 , a members of focal adhesion complexes, was reduced. These data indicated an inhibitory role of ColVI in ENCC migration and suggested that ColVI suppression in the intestine might represent a novel therapeutic strategy for aganglionic colonic diseases.
[Mh] Termos MeSH primário: Movimento Celular/fisiologia
Colágeno Tipo VI/metabolismo
Sistema Nervoso Entérico/metabolismo
Proteínas da Matriz Extracelular/metabolismo
Fibronectinas/metabolismo
Adesões Focais/metabolismo
Crista Neural/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Regulação para Baixo/fisiologia
Sistema Nervoso Entérico/citologia
Camundongos
Camundongos Endogâmicos C57BL
Crista Neural/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Collagen Type VI); 0 (Extracellular Matrix Proteins); 0 (Fibronectins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171203
[St] Status:MEDLINE


  7 / 5554 MEDLINE  
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[PMID]:28450643
[Au] Autor:Librado P; Gamba C; Gaunitz C; Der Sarkissian C; Pruvost M; Albrechtsen A; Fages A; Khan N; Schubert M; Jagannathan V; Serres-Armero A; Kuderna LFK; Povolotskaya IS; Seguin-Orlando A; Lepetz S; Neuditschko M; Thèves C; Alquraishi S; Alfarhan AH; Al-Rasheid K; Rieder S; Samashev Z; Francfort HP; Benecke N; Hofreiter M; Ludwig A; Keyser C; Marques-Bonet T; Ludes B; Crubézy E; Leeb T; Willerslev E; Orlando L
[Ad] Endereço:Centre for GeoGenetics, Natural History Museum of Denmark, Øster Voldgade 5-7, 1350K Copenhagen, Denmark.
[Ti] Título:Ancient genomic changes associated with domestication of the horse.
[So] Source:Science;356(6336):442-445, 2017 04 28.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The genomic changes underlying both early and late stages of horse domestication remain largely unknown. We examined the genomes of 14 early domestic horses from the Bronze and Iron Ages, dating to between ~4.1 and 2.3 thousand years before present. We find early domestication selection patterns supporting the neural crest hypothesis, which provides a unified developmental origin for common domestic traits. Within the past 2.3 thousand years, horses lost genetic diversity and archaic DNA tracts introgressed from a now-extinct lineage. They accumulated deleterious mutations later than expected under the cost-of-domestication hypothesis, probably because of breeding from limited numbers of stallions. We also reveal that Iron Age Scythian steppe nomads implemented breeding strategies involving no detectable inbreeding and selection for coat-color variation and robust forelimbs.
[Mh] Termos MeSH primário: Cruzamento
Domesticação
Cavalos/genética
[Mh] Termos MeSH secundário: Animais
DNA Antigo
DNA Mitocondrial/genética
Variação Genética
Genoma
Crista Neural
Característica Quantitativa Herdável
Seleção Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Ancient); 0 (DNA, Mitochondrial)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1126/science.aam5298


  8 / 5554 MEDLINE  
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[PMID]:28455376
[Au] Autor:Tavares ALP; Cox TC; Maxson RM; Ford HL; Clouthier DE
[Ad] Endereço:Department of Craniofacial Biology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
[Ti] Título:Negative regulation of endothelin signaling by SIX1 is required for proper maxillary development.
[So] Source:Development;144(11):2021-2031, 2017 06 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Jaw morphogenesis is a complex event mediated by inductive signals that establish and maintain the distinct developmental domains required for formation of hinged jaws, the defining feature of gnathostomes. The mandibular portion of pharyngeal arch 1 is patterned dorsally by Jagged-Notch signaling and ventrally by endothelin receptor A (EDNRA) signaling. Loss of EDNRA signaling disrupts normal ventral gene expression, the result of which is homeotic transformation of the mandible into a maxilla-like structure. However, loss of Jagged-Notch signaling does not result in significant changes in maxillary development. Here we show in mouse that the transcription factor SIX1 regulates dorsal arch development not only by inducing dorsal expression but also by inhibiting endothelin 1 ( ) expression in the pharyngeal endoderm of the dorsal arch, thus preventing dorsal EDNRA signaling. In the absence of SIX1, but not JAG1, aberrant EDNRA signaling in the dorsal domain results in partial duplication of the mandible. Together, our results illustrate that SIX1 is the central mediator of dorsal mandibular arch identity, thus ensuring separation of bone development between the upper and lower jaws.
[Mh] Termos MeSH primário: Endotelina-1/metabolismo
Proteínas de Homeodomínio/metabolismo
Maxila/embriologia
Maxila/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Padronização Corporal/genética
Região Branquial/metabolismo
Anormalidades Craniofaciais/embriologia
Anormalidades Craniofaciais/genética
Anormalidades Craniofaciais/patologia
Embrião de Mamíferos/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Integrases/metabolismo
Camundongos
Modelos Biológicos
Crista Neural/metabolismo
Receptor de Endotelina A/metabolismo
Receptores Notch/metabolismo
Proteínas Serrate-Jagged/metabolismo
Fator de Transcrição Sp7
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Regulação para Cima/genética
Zigoma/embriologia
Zigoma/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 (Endothelin-1); 0 (Homeodomain Proteins); 0 (Receptor, Endothelin A); 0 (Receptors, Notch); 0 (Serrate-Jagged Proteins); 0 (Six1 protein, mouse); 0 (Sp7 Transcription Factor); 0 (Sp7 protein, mouse); 0 (Transcription Factors); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases)
[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:170430
[St] Status:MEDLINE
[do] DOI:10.1242/dev.145144


  9 / 5554 MEDLINE  
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[PMID]:29049289
[Au] Autor:Plouhinec JL; Medina-Ruiz S; Borday C; Bernard E; Vert JP; Eisen MB; Harland RM; Monsoro-Burq AH
[Ad] Endereço:Université Paris Sud, Université Paris Saclay, CNRS UMR 3347, INSERM U1021, Orsay, France.
[Ti] Título:A molecular atlas of the developing ectoderm defines neural, neural crest, placode, and nonneural progenitor identity in vertebrates.
[So] Source:PLoS Biol;15(10):e2004045, 2017 Oct.
[Is] ISSN:1545-7885
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During vertebrate neurulation, the embryonic ectoderm is patterned into lineage progenitors for neural plate, neural crest, placodes and epidermis. Here, we use Xenopus laevis embryos to analyze the spatial and temporal transcriptome of distinct ectodermal domains in the course of neurulation, during the establishment of cell lineages. In order to define the transcriptome of small groups of cells from a single germ layer and to retain spatial information, dorsal and ventral ectoderm was subdivided along the anterior-posterior and medial-lateral axes by microdissections. Principal component analysis on the transcriptomes of these ectoderm fragments primarily identifies embryonic axes and temporal dynamics. This provides a genetic code to define positional information of any ectoderm sample along the anterior-posterior and dorsal-ventral axes directly from its transcriptome. In parallel, we use nonnegative matrix factorization to predict enhanced gene expression maps onto early and mid-neurula embryos, and specific signatures for each ectoderm area. The clustering of spatial and temporal datasets allowed detection of multiple biologically relevant groups (e.g., Wnt signaling, neural crest development, sensory placode specification, ciliogenesis, germ layer specification). We provide an interactive network interface, EctoMap, for exploring synexpression relationships among genes expressed in the neurula, and suggest several strategies to use this comprehensive dataset to address questions in developmental biology as well as stem cell or cancer research.
[Mh] Termos MeSH primário: Ectoderma/embriologia
Crista Neural/embriologia
Neurônios/citologia
Células-Tronco/metabolismo
Xenopus laevis/embriologia
[Mh] Termos MeSH secundário: Algoritmos
Animais
Análise por Conglomerados
Bases de Dados Genéticas
Ectoderma/metabolismo
Gastrulação/genética
Perfilação da Expressão Gênica
Regulação da Expressão Gênica no Desenvolvimento
Ontologia Genética
Redes Reguladoras de Genes
Seres Humanos
Internet
Microdissecção
Neoplasias/genética
Crista Neural/metabolismo
Neurulação/genética
Análise de Componente Principal
Fatores de Tempo
Transcriptoma/genética
Proteínas Wnt/metabolismo
Xenopus laevis/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Wnt Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.2004045


  10 / 5554 MEDLINE  
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[PMID]:29028795
[Au] Autor:Garg A; Bansal M; Gotoh N; Feng GS; Zhong J; Wang F; Kariminejad A; Brooks S; Zhang X
[Ad] Endereço:Departments of Ophthalmology, Pathology and Cell Biology, Columbia University, New York, NY, United States of America.
[Ti] Título:Alx4 relays sequential FGF signaling to induce lacrimal gland morphogenesis.
[So] Source:PLoS Genet;13(10):e1007047, 2017 Oct.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The sequential use of signaling pathways is essential for the guidance of pluripotent progenitors into diverse cell fates. Here, we show that Shp2 exclusively mediates FGF but not PDGF signaling in the neural crest to control lacrimal gland development. In addition to preventing p53-independent apoptosis and promoting the migration of Sox10-expressing neural crests, Shp2 is also required for expression of the homeodomain transcription factor Alx4, which directly controls Fgf10 expression in the periocular mesenchyme that is necessary for lacrimal gland induction. We show that Alx4 binds an Fgf10 intronic element conserved in terrestrial but not aquatic animals, underlying the evolutionary emergence of the lacrimal gland system in response to an airy environment. Inactivation of ALX4/Alx4 causes lacrimal gland aplasia in both human and mouse. These results reveal a key role of Alx4 in mediating FGF-Shp2-FGF signaling in the neural crest for lacrimal gland development.
[Mh] Termos MeSH primário: Fator 10 de Crescimento de Fibroblastos/genética
Proteínas de Homeodomínio/genética
Aparelho Lacrimal/crescimento & desenvolvimento
Morfogênese/genética
Crista Neural/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Diferenciação Celular/genética
Linhagem da Célula/genética
Regulação da Expressão Gênica no Desenvolvimento
Seres Humanos
Aparelho Lacrimal/metabolismo
Mesoderma/crescimento & desenvolvimento
Camundongos
Células-Tronco Pluripotentes/metabolismo
Ligação Proteica
Fatores de Transcrição SOXE/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alx4 protein, mouse); 0 (Fgf10 protein, mouse); 0 (Fibroblast Growth Factor 10); 0 (Homeodomain Proteins); 0 (SOXE Transcription Factors); 0 (Sox10 protein, mouse)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007047



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