Base de dados : MEDLINE
Pesquisa : G04.085.300 [Categoria DeCS]
Referências encontradas : 3412 [refinar]
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[PMID]:28728680
[Au] Autor:Neijts R; Deschamps J
[Ad] Endereço:Hubrecht Institute, Developmental Biology and Stem Cell Research, Uppsalalaan 8, 3584 CT Utrecht, and UMC Utrecht, The Netherlands.
[Ti] Título:At the base of colinear Hox gene expression: cis-features and trans-factors orchestrating the initial phase of Hox cluster activation.
[So] Source:Dev Biol;428(2):293-299, 2017 08 15.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hox genes are crucial players in the generation and pattering of the vertebrate trunk and posterior body during embryogenesis. Their initial expression takes place shortly after the establishment of the primitive streak, in the posterior-most part of the mouse embryo and is a determinant step for setting up the definitive Hox expression boundaries along the antero-posterior body axis. The developmental signals and epigenetic mechanisms underlying this early activation remained unsolved until recently. The development of novel embryo-derived model systems, combined with methods that examine chromatin status and chromosome conformation, led to deeper understanding of the process of Hox activation in the early embryo. Here we summarize how the early Hox cis-regulatory landscape becomes active upon receiving the appropriate developmental signal, and we discuss the importance of the local topological segmentation of the HoxA cluster during early Hox activation.
[Mh] Termos MeSH primário: Genes Homeobox
[Mh] Termos MeSH secundário: Animais
Padronização Corporal/genética
Indução Embrionária/genética
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Genes Homeobox/efeitos dos fármacos
Seres Humanos
Camundongos
Modelos Genéticos
Família Multigênica/efeitos dos fármacos
Ativação Transcricional
Tretinoína/metabolismo
Tretinoína/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
5688UTC01R (Tretinoin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE


  2 / 3412 MEDLINE  
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[PMID]:28049659
[Au] Autor:Robertson SM; Medina J; Oldenbroek M; Lin R
[Ad] Endereço:Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
[Ti] Título:Reciprocal signaling by Wnt and Notch specifies a muscle precursor in the C. elegans embryo.
[So] Source:Development;144(3):419-429, 2017 02 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The MS blastomere produces one-third of the body wall muscles (BWMs) in the C. elegans embryo. MS-derived BWMs require two distinct cell-cell interactions, the first inhibitory and the second, two cell cycles later, required to overcome this inhibition. The inductive interaction is not required if the inhibitory signal is absent. Although the Notch receptor GLP-1 was implicated in both interactions, the molecular nature of the two signals was unknown. We now show that zygotically expressed MOM-2 (Wnt) is responsible for both interactions. Both the inhibitory and the activating interactions require precise spatiotemporal expression of zygotic MOM-2, which is dependent upon two distinct Notch signals. In a Notch mutant defective only in the inductive interaction, MS-derived BWMs can be restored by preventing zygotic MOM-2 expression, which removes the inhibitory signal. Our results suggest that the inhibitory interaction ensures the differential lineage specification of MS and its sister blastomere, whereas the inductive interaction promotes the expression of muscle-specifying genes by modulating TCF and ß-catenin levels. These results highlight the complexity of cell fate specification by cell-cell interactions in a rapidly dividing embryo.
[Mh] Termos MeSH primário: Proteínas de Caenorhabditis elegans/metabolismo
Caenorhabditis elegans/embriologia
Caenorhabditis elegans/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Receptores Notch/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Blastômeros/citologia
Blastômeros/metabolismo
Caenorhabditis elegans/genética
Proteínas de Caenorhabditis elegans/genética
Linhagem da Célula/genética
Linhagem da Célula/fisiologia
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Indução Embrionária/genética
Indução Embrionária/fisiologia
Fatores de Transcrição GATA/genética
Fatores de Transcrição GATA/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Genes de Helmintos
Peptídeos e Proteínas de Sinalização Intracelular/genética
Modelos Biológicos
Músculos/embriologia
Mutação
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores Notch/genética
Transdução de Sinais/genética
Transdução de Sinais/fisiologia
Canais de Sódio/genética
Canais de Sódio/metabolismo
Proteínas com Domínio T-Box/genética
Proteínas com Domínio T-Box/metabolismo
Fatores de Transcrição TCF/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Proteínas Wnt/genética
Proteínas Wnt/metabolismo
Via de Sinalização Wnt/genética
Via de Sinalização Wnt/fisiologia
Zigoto/citologia
Zigoto/metabolismo
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Caenorhabditis elegans Proteins); 0 (DNA-Binding Proteins); 0 (END-1 protein, C elegans); 0 (GATA Transcription Factors); 0 (Glp-1 protein, C elegans); 0 (Intracellular Signaling Peptides and Proteins); 0 (MOM-2 protein, C elegans); 0 (RNA, Messenger); 0 (Receptors, Notch); 0 (Sodium Channels); 0 (T-Box Domain Proteins); 0 (TBX-35 protein, C elegans); 0 (TCF Transcription Factors); 0 (Transcription Factors); 0 (Wnt Proteins); 0 (apx-1 protein, C elegans); 0 (beta Catenin); 0 (ref-1 protein, C elegans); 148733-36-2 (skn-1 protein, C elegans)
[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:170105
[St] Status:MEDLINE
[do] DOI:10.1242/dev.145391


  3 / 3412 MEDLINE  
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[PMID]:27993985
[Au] Autor:Esposito R; Yasuo H; Sirour C; Palladino A; Spagnuolo A; Hudson C
[Ad] Endereço:Biology and Evolution of Marine Organisms, Stazione Zoologica Anton Dohrn, Napoli 80121, Italy.
[Ti] Título:Patterning of brain precursors in ascidian embryos.
[So] Source:Development;144(2):258-264, 2017 01 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In terms of their embryonic origins, the anterior and posterior parts of the ascidian central nervous system (CNS) are associated with distinct germ layers. The anterior part of the sensory vesicle, or brain, originates from ectoderm lineages following a neuro-epidermal binary fate decision. In contrast, a large part of the remaining posterior CNS is generated following neuro-mesodermal binary fate decisions. Here, we address the mechanisms that pattern the anterior brain precursors along the medial-lateral axis (future ventral-dorsal) at neural plate stages. Our functional studies show that Nodal signals are required for induction of lateral genes, including Delta-like, Snail, Msxb and Trp Delta-like/Notch signalling induces intermediate (Gsx) over medial (Meis) gene expression in intermediate cells, whereas the combinatorial action of Snail and Msxb prevents the expression of Gsx in lateral cells. We conclude that despite the distinct embryonic lineage origins within the larval CNS, the mechanisms that pattern neural precursors are remarkably similar.
[Mh] Termos MeSH primário: Padronização Corporal/fisiologia
Encéfalo/embriologia
Ciona intestinalis/embriologia
Células-Tronco Neurais/fisiologia
Urocordados/embriologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Embrião não Mamífero
Indução Embrionária/fisiologia
Placa Neural/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE
[do] DOI:10.1242/dev.142307


  4 / 3412 MEDLINE  
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[PMID]:27919666
[Au] Autor:De Almeida I; Oliveira NM; Randall RA; Hill CS; McCoy JM; Stern CD
[Ad] Endereço:Department of Cell & Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK.
[Ti] Título:Calreticulin is a secreted BMP antagonist, expressed in Hensen's node during neural induction.
[So] Source:Dev Biol;421(2):161-170, 2017 Jan 15.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hensen's node is the "organizer" of the avian and mammalian early embryo. It has many functions, including neural induction and patterning of the ectoderm and mesoderm. Some of the signals responsible for these activities are known but these do not explain the full complexity of organizer activity. Here we undertake a functional screen to discover new secreted factors expressed by the node at this time of development. Using a Signal Sequence Trap in yeast, we identify several candidates. Here we focus on Calreticulin. We show that in addition to its known functions in intracellular Calcium regulation and protein folding, Calreticulin is secreted, it can bind to BMP4 and act as a BMP antagonist in vivo and in vitro. Calreticulin is not sufficient to account for all organizer functions but may contribute to the complexity of its activity.
[Mh] Termos MeSH primário: Proteínas Morfogenéticas Ósseas/antagonistas & inibidores
Calreticulina/metabolismo
Indução Embrionária
Tecido Nervoso/embriologia
Tecido Nervoso/metabolismo
Organizadores Embrionários/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas Morfogenéticas Ósseas/metabolismo
Calnexina/metabolismo
Galinhas
Fatores de Crescimento de Fibroblastos/antagonistas & inibidores
Fatores de Crescimento de Fibroblastos/metabolismo
Células HEK293
Seres Humanos
Placa Neural/embriologia
Placa Neural/metabolismo
Transdução de Sinais
Solubilidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Calreticulin); 139873-08-8 (Calnexin); 62031-54-3 (Fibroblast Growth Factors)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161207
[St] Status:MEDLINE


  5 / 3412 MEDLINE  
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[PMID]:27692744
[Au] Autor:Suzuki A; Yoshida H; van Heeringen SJ; Takebayashi-Suzuki K; Veenstra GJC; Taira M
[Ad] Endereço:Amphibian Research Center, Graduate School of Science, Hiroshima University, 1-3-1 Kagamiyama, Higashi-Hiroshima 739-8526, Japan. Electronic address: asuzuki@hiroshima-u.ac.jp.
[Ti] Título:Genomic organization and modulation of gene expression of the TGF-ß and FGF pathways in the allotetraploid frog Xenopus laevis.
[So] Source:Dev Biol;426(2):336-359, 2017 06 15.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inductive interactions mediated by the TGF-ß and FGF-MAPK pathways are essential for specification of the germ layers and embryonic body axes during early vertebrate embryogenesis. TGF-ß and FGF ligands signal through receptor Ser/Thr and Tyr kinases, respectively, and these signaling pathways cross-talk to regulate transcription and cell behavior. The allotetraploid Xenopus laevis and its ancestral diploid Xenopus tropicalis are versatile model organisms with which to study the inductive interactions and mechanisms of these signal transduction pathways. Here we have analyzed the draft genome of X. laevis with respect to the genomic organization and differential expression of genes in the TGF-ß and FGF pathways. Genomic structure and gene expression analyses of pathway components in X. laevis revealed that genetic modulations, including deletions resulting in singletons and differential expression of homeologs, have occurred frequently among extracellular regulatory factors of the TGF-ß pathway after allotetraploidization. Moreover, differential gene expression was found for factors regulating various cellular responses including co-receptors, decoy receptors, and intracellular negative regulators in both the TGF-ß and FGF-MAPK pathways. We summarize the patterns of genetic alterations in the allotetraploid frog X. laevis and discuss the importance of these changes with regard to developmental processes.
[Mh] Termos MeSH primário: Indução Embrionária/genética
Fatores de Crescimento de Fibroblastos/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Transdução de Sinais/genética
Fator de Crescimento Transformador beta/metabolismo
Proteínas de Xenopus/metabolismo
Xenopus laevis/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Padronização Corporal/genética
Diploide
Embrião não Mamífero/metabolismo
Epigênese Genética
Fatores de Crescimento de Fibroblastos/genética
Especiação Genética
Genômica
Ligantes
Sistema de Sinalização das MAP Quinases/genética
Anotação de Sequência Molecular
Receptores de Fatores de Crescimento/fisiologia
Proteínas Smad/metabolismo
Tetraploidia
Fator de Crescimento Transformador beta/genética
Xenopus/genética
Proteínas de Xenopus/genética
Xenopus laevis/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ligands); 0 (Receptors, Growth Factor); 0 (Smad Proteins); 0 (Transforming Growth Factor beta); 0 (Xenopus Proteins); 62031-54-3 (Fibroblast Growth Factors)
[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:161004
[St] Status:MEDLINE


  6 / 3412 MEDLINE  
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[PMID]:27911385
[Au] Autor:Wilde S; Logan MP
[Ad] Endereço:Randall Division of Cell and Molecular Biophysics, King's College London, Guy's Campus; susan.miller@kcl.ac.uk.
[Ti] Título:Application of Impermeable Barriers Combined with Candidate Factor Soaked Beads to Study Inductive Signals in the Chick.
[So] Source:J Vis Exp;(117), 2016 Nov 17.
[Is] ISSN:1940-087X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The chick embryo provides a superb vertebrate model that can be used to dissect developmental questions in a direct way. Its accessibility and robustness following surgical intervention are key experimental strengths. Mica plates were the first barriers used to prevent chick limb bud initiation . Protocols that use aluminum foil as an impermeable barrier to wing bud or leg bud induction and or initiation are described. We combine this technique with bead placement lateral to the barrier to exogenously supply candidate endogenous factors that have been blocked by the barrier. The results are analyzed using in situ hybridization of subsequent gene expression. Our main focus is on the role of retinoic acid signaling in the induction and later initiation of the chick embryo fore and hindlimb. We use BMS 493 (an inverse agonist of retinoic acid receptors (RAR)) soaked beads implanted in the lateral plate mesoderm (LPM) to mimic the effect of a barrier placed between the somites (a source of retinoic acid (RA)) and the LPM from which limb buds grow. Modified versions of these protocols could also be used to address other questions on the origin and timing of inductive cues. Provided the region of the chick embryo is accessible at the relevant developmental stage, a barrier could be placed between the two tissues and consequent changes in development studied. Examples may be found in the developing brain, axis extension and in organ development, such as liver or kidney induction.
[Mh] Termos MeSH primário: Indução Embrionária
Regulação da Expressão Gênica no Desenvolvimento
[Mh] Termos MeSH secundário: Animais
Embrião de Galinha
Hibridização In Situ
Mesoderma
Somitos
Tretinoína
Asas de Animais
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
5688UTC01R (Tretinoin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161203
[St] Status:MEDLINE
[do] DOI:10.3791/54618


  7 / 3412 MEDLINE  
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[PMID]:27492475
[Au] Autor:Mass E; Ballesteros I; Farlik M; Halbritter F; Günther P; Crozet L; Jacome-Galarza CE; Händler K; Klughammer J; Kobayashi Y; Gomez-Perdiguero E; Schultze JL; Beyer M; Bock C; Geissmann F
[Ad] Endereço:Immunology Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
[Ti] Título:Specification of tissue-resident macrophages during organogenesis.
[So] Source:Science;353(6304), 2016 09 09.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tissue-resident macrophages support embryonic development and tissue homeostasis and repair. The mechanisms that control their differentiation remain unclear. We report here that erythro-myeloid progenitors in mice generate premacrophages (pMacs) that simultaneously colonize the whole embryo from embryonic day 9.5 in a chemokine-receptor-dependent manner. The core macrophage program initiated in pMacs is rapidly diversified as expression of transcriptional regulators becomes tissue-specific in early macrophages. This process appears essential for macrophage specification and maintenance, as inactivation of Id3 impairs the development of liver macrophages and results in selective Kupffer cell deficiency in adults. We propose that macrophage differentiation is an integral part of organogenesis, as colonization of organ anlagen by pMacs is followed by their specification into tissue macrophages, hereby generating the macrophage diversity observed in postnatal tissues.
[Mh] Termos MeSH primário: Diferenciação Celular/genética
Embrião de Mamíferos/citologia
Regulação da Expressão Gênica no Desenvolvimento
Macrófagos/citologia
Células Progenitoras Mieloides/citologia
Organogênese
[Mh] Termos MeSH secundário: Animais
Receptor 1 de Quimiocina CX3C
Desenvolvimento Embrionário
Indução Embrionária
Células Precursoras Eritroides/citologia
Células Precursoras Eritroides/metabolismo
Feminino
Hematopoese/genética
Hematopoese/fisiologia
Proteínas Inibidoras de Diferenciação/metabolismo
Macrófagos do Fígado/citologia
Macrófagos do Fígado/metabolismo
Macrófagos/metabolismo
Camundongos
Camundongos Mutantes
Células Progenitoras Mieloides/metabolismo
Especificidade de Órgãos
Receptores de Quimiocinas/genética
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CX3C Chemokine Receptor 1); 0 (Cx3cr1 protein, mouse); 0 (Inhibitor of Differentiation Proteins); 0 (Receptors, Chemokine); 135845-89-5 (Idb3 protein, mouse)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160806
[St] Status:MEDLINE


  8 / 3412 MEDLINE  
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[PMID]:27288708
[Au] Autor:Grimbert S; Tietze K; Barkoulas M; Sternberg PW; Félix MA; Braendle C
[Ad] Endereço:Centre National de la Recherche Scientifique (CNRS) UMR7277 - Institut National de la Santé et de la Recherche Médicale (INSERM) U1091, Université Nice Sophia Antipolis, 06108 Nice cedex 02, France.
[Ti] Título:Anchor cell signaling and vulval precursor cell positioning establish a reproducible spatial context during C. elegans vulval induction.
[So] Source:Dev Biol;416(1):123-135, 2016 08 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:How cells coordinate their spatial positioning through intercellular signaling events is poorly understood. Here we address this topic using Caenorhabditis elegans vulval patterning during which hypodermal vulval precursor cells (VPCs) adopt distinct cell fates determined by their relative positions to the gonadal anchor cell (AC). LIN-3/EGF signaling by the AC induces the central VPC, P6.p, to adopt a 1° vulval fate. Exact alignment of AC and VPCs is thus critical for correct fate patterning, yet, as we show here, the initial AC-VPC positioning is both highly variable and asymmetric among individuals, with AC and P6.p only becoming aligned at the early L3 stage. Cell ablations and mutant analysis indicate that VPCs, most prominently 1° cells, move towards the AC. We identify AC-released LIN-3/EGF as a major attractive signal, which therefore plays a dual role in vulval patterning (cell alignment and fate induction). Additionally, compromising Wnt pathway components also induces AC-VPC alignment errors, with loss of posterior Wnt signaling increasing stochastic vulval centering on P5.p. Our results illustrate how intercellular signaling reduces initial spatial variability in cell positioning to generate reproducible interactions across tissues.
[Mh] Termos MeSH primário: Indução Embrionária
Transdução de Sinais
Células-Tronco
Vulva/embriologia
[Mh] Termos MeSH secundário: Animais
Padronização Corporal
Caenorhabditis elegans
Proteínas de Caenorhabditis elegans/metabolismo
Linhagem da Célula
Movimento Celular
Feminino
Vulva/citologia
Proteínas Wnt/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (Wnt Proteins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160612
[St] Status:MEDLINE


  9 / 3412 MEDLINE  
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[PMID]:27265866
[Au] Autor:Kodama H; Miyata Y; Kuwajima M; Izuchi R; Kobayashi A; Gyoja F; Onuma TA; Kumano G; Nishida H
[Ad] Endereço:Department of Biological Sciences, Graduate School of Science, Osaka University, Toyonaka, Osaka 560-0043, Japan.
[Ti] Título:Redundant mechanisms are involved in suppression of default cell fates during embryonic mesenchyme and notochord induction in ascidians.
[So] Source:Dev Biol;416(1):162-172, 2016 08 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During embryonic induction, the responding cells invoke an induced developmental program, whereas in the absence of an inducing signal, they assume a default uninduced cell fate. Suppression of the default fate during the inductive event is crucial for choice of the binary cell fate. In contrast to the mechanisms that promote an induced cell fate, those that suppress the default fate have been overlooked. Upon induction, intracellular signal transduction results in activation of genes encoding key transcription factors for induced tissue differentiation. It is elusive whether an induced key transcription factor has dual functions involving suppression of the default fates and promotion of the induced fate, or whether suppression of the default fate is independently regulated by other factors that are also downstream of the signaling cascade. We show that during ascidian embryonic induction, default fates were suppressed by multifold redundant mechanisms. The key transcription factor, Twist-related.a, which is required for mesenchyme differentiation, and another independent transcription factor, Lhx3, which is dispensable for mesenchyme differentiation, sequentially and redundantly suppress the default muscle fate in induced mesenchyme cells. Similarly in notochord induction, Brachyury, which is required for notochord differentiation, and other factors, Lhx3 and Mnx, are likely to suppress the default nerve cord fate redundantly. Lhx3 commonly suppresses the default fates in two kinds of induction. Mis-activation of the autonomously executed default program in induced cells is detrimental to choice of the binary cell fate. Multifold redundant mechanisms would be required for suppression of the default fate to be secure.
[Mh] Termos MeSH primário: Linhagem da Célula
Indução Embrionária
Mesoderma/embriologia
Notocorda/embriologia
Urocordados/embriologia
[Mh] Termos MeSH secundário: Animais
Indução Embrionária/genética
Regulação da Expressão Gênica no Desenvolvimento
Mesoderma/citologia
Músculos/embriologia
Notocorda/citologia
Fatores de Transcrição/metabolismo
Urocordados/citologia
Urocordados/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Transcription Factors)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160607
[St] Status:MEDLINE


  10 / 3412 MEDLINE  
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[PMID]:27265864
[Au] Autor:Talbot JC; Nichols JT; Yan YL; Leonard IF; BreMiller RA; Amacher SL; Postlethwait JH; Kimmel CB
[Ad] Endereço:Institute of Neuroscience, 1254 University of Oregon, Eugene, OR 97403, USA; Departments of Molecular Genetics and Biological Chemistry and Pharmacology, The Ohio State University, Columbus, OH 43210, USA. Electronic address: talbot.39@osu.edu.
[Ti] Título:Pharyngeal morphogenesis requires fras1-itga8-dependent epithelial-mesenchymal interaction.
[So] Source:Dev Biol;416(1):136-148, 2016 08 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Both Fras1 and Itga8 connect mesenchymal cells to epithelia by way of an extracellular 'Fraser protein complex' that functions in signaling and adhesion; these proteins are vital to the development of several vertebrate organs. We previously found that zebrafish fras1 mutants have craniofacial defects, specifically, shortened symplectic cartilages and cartilage fusions that spare joint elements. During a forward mutagenesis screen, we identified a new zebrafish mutation, b1161, that we show here disrupts itga8, as confirmed using CRISPR-generated itga8 alleles. fras1 and itga8 single mutants and double mutants have similar craniofacial phenotypes, a result expected if loss of either gene disrupts function of the Fraser protein complex. Unlike fras1 mutants or other Fraser-related mutants, itga8 mutants do not show blistered tail fins. Thus, the function of the Fraser complex differs in the craniofacial skeleton and the tail fin. Focusing on the face, we find that itga8 mutants consistently show defective outpocketing of a late-forming portion of the first pharyngeal pouch, and variably express skeletal defects, matching previously characterized fras1 mutant phenotypes. In itga8 and fras1 mutants, skeletal severity varies markedly between sides, indicating that both mutants have increased developmental instability. Whereas fras1 is expressed in epithelia, we show that itga8 is expressed complementarily in facial mesenchyme. Paired with the observed phenotypic similarity, this expression indicates that the genes function in epithelial-mesenchymal interactions. Similar interactions between Fras1 and Itga8 have previously been found in mouse kidney, where these genes both regulate Nephronectin (Npnt) protein abundance. We find that zebrafish facial tissues express both npnt and the Fraser gene fibrillin2b (fbn2b), but their transcript levels do not depend on fras1 or itga8 function. Using a revertible fras1 allele, we find that the critical window for fras1 function in the craniofacial skeleton is between 1.5 and 3 days post fertilization, which coincides with the onset of fras1-dependent and itga8-dependent morphogenesis. We propose a model wherein Fras1 and Itga8 interact during late pharyngeal pouch morphogenesis to sculpt pharyngeal arches through epithelial-mesenchymal interactions, thereby stabilizing the developing craniofacial skeleton.
[Mh] Termos MeSH primário: Região Branquial/embriologia
Epitélio/embriologia
Proteínas da Matriz Extracelular/fisiologia
Integrinas/fisiologia
Mesoderma/embriologia
Proteínas de Peixe-Zebra/fisiologia
[Mh] Termos MeSH secundário: Animais
Repetições Palindrômicas Curtas Agrupadas e Regularmente Espaçadas
Indução Embrionária
Epitélio/metabolismo
Proteínas da Matriz Extracelular/genética
Proteínas da Matriz Extracelular/metabolismo
Ossos Faciais/embriologia
Fibrilina-2/metabolismo
Integrinas/genética
Mesoderma/metabolismo
Morfogênese
Mutação
RNA Mensageiro
Peixe-Zebra
Proteínas de Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Extracellular Matrix Proteins); 0 (Fibrillin-2); 0 (Fras1 protein, zebrafish); 0 (Integrins); 0 (RNA, Messenger); 0 (Zebrafish Proteins); 0 (itga8 protein, zebrafish); 0 (nephronectin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160607
[St] Status:MEDLINE



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