scholarly journals Greb1 is required for axial elongation and segmentation in vertebrate embryos

2019 ◽  
Author(s):  
Ravindra Singh Prajapati ◽  
Richard Mitter ◽  
Annalisa Vezzaro ◽  
David Ish-Horowicz
Keyword(s):  
Estrogen Receptor ◽  
Embryonic Development ◽  
Clock Gene ◽  
Zebrafish Embryos ◽  
Presomitic Mesoderm ◽  
Axial Elongation ◽  
No Tail ◽  
Vertebrate Embryos ◽  
Progenitor Maintenance ◽  
Segmentation Clock Gene

ABSTRACTDuring vertebrate embryonic development, the formation of axial structures is driven by a population of stem-like cells that reside in a region of the tailbud called the chordoneural hinge (CNH). We have compared the CNH transcriptome with those of surrounding tissues and shown that the CNH and tailbud mesoderm are transcriptionally similar, and distinct from the presomitic mesoderm. Amongst CNH-enriched genes are several that are required for axial elongation, including Wnt3a, Cdx2, Brachyury/T and Fgf8, and androgen/estrogen receptor nuclear signalling components such as Greb1. We show that the pattern and duration of tailbud Greb1 expression is conserved in mouse, zebrafish, and chicken embryos, and that Greb1 is required for axial elongation and somitogenesis in zebrafish embryos. The axial truncation phenotype of Greb1 morphant embryos is explained by much reduced expression of No tail (Ntl/Brachyury) which is required for axial progenitor maintenance. Posterior segmentation defects in the morphants (including misexpression of genes such as mespb, myoD and papC) appear to result, in part, from lost expression of the segmentation clock gene, her7.

scholarly journals Greb1 is required for axial elongation and segmentation in vertebrate embryos

Biology Open ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. bio047290
Author(s):  
Ravindra Singh Prajapati ◽  
Richard Mitter ◽  
Annalisa Vezzaro ◽  
David Ish-Horowicz
Keyword(s):  
Axial Elongation ◽  
Vertebrate Embryos

Effects of Quillaja Saponin (Quillaja saponaria) on Early Embryonic Zebrafish (Danio rerio) Development

2008 ◽  
Vol 27 (3) ◽  
pp. 273-278 ◽  
Author(s):  
Sherif M. Hassan ◽  
Eid. A. Moussa ◽  
Louise C. Abbott
Keyword(s):  
Embryonic Development ◽  
Organic Compounds ◽  
Negative Control ◽  
Zebrafish Embryos ◽  
Growth Promoter ◽  
Foaming Agent ◽  
Quillaja Saponaria ◽  
Hatching Time ◽  
Morphological Deformities ◽  
Quillaja Saponin

Although much attention has focused on environmental contamination by heavy metals, pesticides, and polychlorinated biphenyls, potential deleterious effects of naturally occurring organic compounds have received much less consideration. Saponins, which are glycosides found in many plants, are important, environmentally ubiquitous organic compounds. Saponins have both beneficial and deleterious effects in adults, but little is known about how saponins effect early vertebrate embryonic development. The authors tested the toxicity of quillaja saponin using a zebrafish embryo assay. Quillaja saponin, extracted from bark of the tree, Quillaja saponaria, is a common foaming agent used in foods and beverages. At 6 h post fertilization, zebrafish embryos were exposed to five concentrations (0 [negative control], 1, 5, 10 or 20 μg) of quillaja saponin per milliliter of medium. Zebrafish embryos exposed to 2% ethanol were positive controls (100% embryonic death). Embryos were assessed at 30, 54, and 72 h post fertilization for changes in embryonic development, mortality, time of hatching, and morphological deformities. Embryos exposed to 1 and 5 μg saponin were healthy, showed no obvious deformities, but exhibited shrinkage of the chorion. Hatching time for zebrafish embryos exposed to 1 and 5 μg/ml saponin decreased by 18 h compared to unexposed embryos. Zebrafish embryos treated with 5 μg/ml saponin responded less to touch than embryos treated with 1 μg/ml saponin or controls. Zebrafish embryos exposed to more than 5 μg/ml saponin exhibited 100% embryonic mortality. These results indicate that exposure to 5 μg/ml or less of quillaja saponin acts as a growth promoter, whereas concentrations of 10 μg/ml or greater are lethal.

The zebrafish T-box genesno tailandspadetailare required for development of trunk and tail mesoderm and medial floor plate

Development ◽  
2002 ◽  
Vol 129 (14) ◽  
pp. 3311-3323 ◽  
Author(s):  
Sharon L. Amacher ◽  
Bruce W. Draper ◽  
Brian R. Summers ◽  
Charles B. Kimmel
Keyword(s):  
Embryonic Development ◽  
Neural Tube ◽  
Transcriptional Regulators ◽  
Floor Plate ◽  
Wild Type ◽  
T Box ◽  
No Tail ◽  
Ventral Neural Tube ◽  
Plate Formation ◽  
In Cells

T-box genes encode transcriptional regulators that control many aspects of embryonic development. Here, we demonstrate that the mesodermally expressed zebrafish spadetail (spt)/VegT and no tail (ntl)/Brachyury T-box genes are semi-redundantly and cell-autonomously required for formation of all trunk and tail mesoderm. Despite the lack of posterior mesoderm in spt–;ntl– embryos, dorsal-ventral neural tube patterning is relatively normal, with the notable exception that posterior medial floor plate is completely absent. This contrasts sharply with observations in single mutants, as mutations singly in ntl or spt enhance posterior medial floor plate development. We find that ntl function is required to repress medial floor plate and promote notochord fate in cells of the wild-type notochord domain and that spt and ntl together are required non cell-autonomously for medial floor plate formation, suggesting that an inducing signal present in wild-type mesoderm is lacking in spt–;ntl– embryos.

scholarly journals Activator-to-Repressor Conversion of T-Box Transcription Factors by the Ripply Family of Groucho/TLE-Associated Mediators

2008 ◽  
Vol 28 (10) ◽  
pp. 3236-3244 ◽  
Author(s):  
Akinori Kawamura ◽  
Sumito Koshida ◽  
Shinji Takada
Keyword(s):  
Transcription Factors ◽  
Transcriptional Activation ◽  
Cultured Cells ◽  
Biological Significance ◽  
Zebrafish Embryos ◽  
Mutant Form ◽  
Dna Binding Domain ◽  
T Box ◽  
No Tail ◽  
Posterior Trunk

ABSTRACT The T-box family of transcription factors, defined by a conserved DNA binding domain called the T-box, regulate various aspects of embryogenesis by activating and/or repressing downstream genes. In spite of the biological significance of the T-box proteins, how they regulate transcription remains to be elucidated. Here we show that the Groucho/TLE-associated protein Ripply converts T-box proteins from activators to repressors. In cultured cells, zebrafish Ripply1, an essential component in somite segmentation, and its structural relatives, Ripply2 and -3, suppress the transcriptional activation mediated by the T-box protein Tbx24, which is coexpressed with ripply1 during segmentation. Ripply1 associates with Tbx24 and converts it to a repressor. Ripply1 also antagonizes the transcriptional activation of another T-box protein, No tail (Ntl), the zebrafish ortholog of Brachyury. Furthermore, injection of a high dosage of ripply1 mRNA into zebrafish eggs causes defective development of the posterior trunk, similar to the phenotype observed in homozygous mutants of ntl. A mutant form of Ripply1 defective in association with Tbx24 also lacks activity in zebrafish embryos. These results indicate that the intrinsic transcriptional property of T-box proteins is controlled by Ripply family proteins, which act as specific adaptors that recruit the global corepressor Groucho/TLE to T-box proteins.

Transcriptional Activities of the Orphan Nuclear Receptor ERRα (Estrogen Receptor-Related Receptor-α)

1999 ◽  
Vol 13 (5) ◽  
pp. 764-773 ◽  
Author(s):  
Jean-Marc Vanacker ◽  
Edith Bonnelye ◽  
Sandrine Chopin-Delannoy ◽  
Cateline Delmarre ◽  
Vincent Cavaillès ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Embryonic Development ◽  
Nuclear Receptor ◽  
Target Sequence ◽  
Orphan Nuclear Receptor ◽  
Response Element ◽  
Specific Target ◽  
Adult Tissues ◽  
Target Sequences

Abstract Estrogen receptor-related receptor α (ERRα) is an orphan nuclear receptor closely related to the estrogen receptor (ER), whose expression covers various stages of embryonic development and persists in certain adult tissues. We show that ERRα binds as a homodimer on a specific target sequence, the SFRE (SF-1 response element), already known to respond to the orphan nuclear receptor SF-1. Target sequences that are related to the SFRE and that discriminate between ERRα and SF-1 were identified. We have also analyzed the transcriptional properties of the ERRα originating from various species. All ERRα orthologs act as potent transactivators through the consensus SFRE. ERRα activity depends on the putative AF2AD domain, as well as on a serum compound that is withdrawn by charcoal treatment, suggesting the existence of a critical regulating factor brought by serum.

scholarly journals G protein-coupled estrogen receptor regulates heart rate by modulating thyroid hormone levels in zebrafish embryos

2016 ◽  
Author(s):  
Shannon N Romano ◽  
Hailey E Edwards ◽  
Xiangqin Cui ◽  
Daniel A Gorelick
Keyword(s):  
Heart Rate ◽  
Estrogen Receptor ◽  
Thyroid Hormone ◽  
G Protein ◽  
Sex Differentiation ◽  
Zebrafish Embryos ◽  
Basal Heart Rate ◽  
Normal Heart Rate ◽  
G Protein Coupled

AbstractEstrogens act by binding to estrogen receptors alpha and beta (ERα, ERβ), ligand-dependent transcription factors that play crucial roles in sex differentiation, tumor growth and cardiovascular physiology. Estrogens also activate the G protein-coupled estrogen receptor (GPER), however the function of GPER in vivo is less well understood. Here we find that GPER is required for normal heart rate in zebrafish embryos. Acute exposure to estrogens increased heart rate in wildtype and in ERα and ERβ mutant embryos but not in GPER mutants. GPER mutant embryos exhibited reduced basal heart rate, while heart rate was normal in ERα and ERβ mutants. We detected gper transcript in discrete regions of the brain and pituitary but not in the heart, suggesting that GPER acts centrally to regulate heart rate. In the pituitary, we observed gper expression in cells that regulate levels of thyroid hormone triiodothyronine (T3), a hormone known to increase heart rate. GPER mutant embryos showed a mean 50% reduction in T3 levels compared to wildtype, while exposure to exogenous T3 rescued the reduced heart rate phenotype in GPER mutants. Our results demonstrate that estradiol plays a previously unappreciated role in the acute modulation of heart rate during zebrafish embryonic development and suggest that GPER regulates basal heart rate by altering total T3 levels.

scholarly journals Wnt Signaling in Neural Crest Ontogenesis and Oncogenesis

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1173 ◽  
Author(s):  
Yu Ji ◽  
Hongyan Hao ◽  
Kurt Reynolds ◽  
Moira McMahon ◽  
Chengji J. Zhou
Keyword(s):  
Embryonic Development ◽  
Wnt Signaling ◽  
Neural Crest ◽  
Cell Types ◽  
Multipotent Stem Cells ◽  
Peripheral Neurons ◽  
Dorsal Edge ◽  
Cell Induction ◽  
Vertebrate Embryos ◽  
Anterior Posterior

Neural crest (NC) cells are a temporary population of multipotent stem cells that generate a diverse array of cell types, including craniofacial bone and cartilage, smooth muscle cells, melanocytes, and peripheral neurons and glia during embryonic development. Defective neural crest development can cause severe and common structural birth defects, such as craniofacial anomalies and congenital heart disease. In the early vertebrate embryos, NC cells emerge from the dorsal edge of the neural tube during neurulation and then migrate extensively throughout the anterior-posterior body axis to generate numerous derivatives. Wnt signaling plays essential roles in embryonic development and cancer. This review summarizes current understanding of Wnt signaling in NC cell induction, delamination, migration, multipotency, and fate determination, as well as in NC-derived cancers.

Correlated downregulation of estrogen receptor beta and the circadian clock gene Per1 in human colorectal cancer

2009 ◽  
Vol 48 (7) ◽  
pp. 642-647 ◽  
Author(s):  
Nazanin Mostafaie ◽  
Enikö Kállay ◽  
Elisabeth Sauerzapf ◽  
Elisabeth Bonner ◽  
Stefan Kriwanek ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Estrogen Receptor ◽  
Circadian Clock ◽  
Clock Gene ◽  
Estrogen Receptor Beta ◽  
Human Colorectal Cancer ◽  
Circadian Clock Gene ◽  
Receptor Beta
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