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Zebrafish embryos treated with Retinoic Acid or Retinoic acid antagonist during gastrulation and early somitogenesis.

ABSTRACT: Retinoic acid (RA) is an important developmental signaling molecule responsible for the patterning of multiple vertebrate tissues. RA is also a potent teratogen, causing multi-organ birth defects in humans. Endogenous RA levels must therefore be tightly controlled in the developing embryo. In order to understand the RA function and regulation at the genomic level, we used a microarray approach to identify genes that function as negative feedback regulators of retinoic acid signaling. To that end, we treated embryos with different chemicals: DMSO as control, AGN193019 as RA antagonist at high concentration 10uM and low concentration 1uM, as well as 0.33uM RA. Each treatment has four biological replicates. We screened for genes expressed in early somite-stage embryos that respond oppositely to treatment with RA versus RA antagonists, and validated them by whole-mount RNA in situ hybridization.

ORGANISM(S): Danio rerio

PROVIDER: GSE16264 | GEO | 2009/05/29

SECONDARY ACCESSION(S): PRJNA115103

REPOSITORIES: GEO

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Transcription profiling of Zebrafish embryos treated with Retinoic Acid or Retinoic acid antagonist during gastrulation and early somitogenesis

Project description:Retinoic acid (RA) is an important developmental signaling molecule responsible for the patterning of multiple vertebrate tissues. RA is also a potent teratogen, causing multi-organ birth defects in humans. Endogenous RA levels must therefore be tightly controlled in the developing embryo. In order to understand the RA function and regulation at the genomic level, we used a microarray approach to identify genes that function as negative feedback regulators of retinoic acid signaling. To that end, we treated embryos with different chemicals: DMSO as control, AGN193019 as RA antagonist at high concentration 10uM and low concentration 1uM, as well as 0.33uM RA. Each treatment has four biological replicates. We screened for genes expressed in early somite-stage embryos that respond oppositely to treatment with RA versus RA antagonists, and validated them by whole-mount RNA in situ hybridization. Experiment Overall Design: Each treatment was performed four times, for a total of 16 independent samples (4 x 0.33 ÂµM RA, 4 x 10 ÂµM AGN193109, 4 x 1 ÂµM AGN193109 and 4 x DMSO control).

2009-06-08 | E-GEOD-16264 | biostudies-arrayexpress

Global identification of retinoic acid regulated genes

Project description:Retinoic acid (RA) signaling plays a major role in controlling several developmental processes in vertebrate embryos. RA repression of caudal Fgf8 has emerged as a crucial mechanism through which RA controls body axis extension, somitogenesis, and spinal cord neurogenesis. The role of RA in Fgf8 repression is supported by mechanistic studies demonstrating direct RA repression through a nearby RA response element that recruits NCOR in an RA-dependent manner. RA is also required for balanced neuromesodermal progenitor differentiation needed for coordinated generation of mesodermal progenitors for somites and neural progenitors for spinal cord. As many pathways are controlled by RA, we performed RNA-seq analysis comparing wild-type embryos with Aldh1a2 mutants that lack the ability to produce RA. This analysis identified a few hundred genes whose expression is significantly altered when RA is absent, thus providing candidate genes for further analysis to discover RA-regulated genes essential for development.

2019-05-22 | GSE131584 | GEO

Transcriptome analysis of Xenopus orofacial tissues deficient in retinoic acid receptor function

Project description:Xenopus laevis embryos were treated with a retinoic acid inhibitior during early orofacial development. The facial tissues were dissected, removing eye and brain tissue from the analysis. RA regulates midface development, we sought to determine global changes in gene expression when RA function is pharmacologically disrupted

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Expression data from retinoic acid-sufficient and retinoic acid-deficient human airway smooth muscle [human primary ASMs]

Project description:Observational studies in human suggest involvement of vitamin A/retinoic acid (RA) signaling in the regulation of airway smooth muscle (ASM) function, but the precise mechanisms by which RA impacts ASM phenotype is not clear. Here, we generated trascriptional profiles from primary human ASM from 3 unrelated donoros cultured in control medium or medium containing BMS493 (an retinoic acid receptor antagonist)

2018-12-25 | GSE116845 | GEO

Genome wide sequencing analysis of primary cardiomyocytes treated with all-trans retinoic acid

Project description:The retinoic acid (RA) signaling pathway is essential for cardiac development; however, cardiomyocytes, the main cell type of the heart, are considered to be unresposive to RA signaling. The goal of this study was to examine the effects of all-trans RA (atRA) treatment on cardiomyocytes isolated from E18.5 mouse embryos. We found that cardiomyocytes, contrary to previous findings, are indeed repsonsive to RA signaling and that many genes involved in cardiac developmental and repair processes were significantly deregulated upon atRA trearment. These findings have important implications for the heart development and regeneration fields.

2021-04-01 | GSE161429 | GEO

H9c2 cell response after retinoic acid stimuli

Project description:During culture, H9c2 cells acquire a myotubule phenotype where a critical component is the inclusion of retinoic acid (RA). The results from some authors on H9c2 suggested that thousands of genes respond to RA stimuli, while other authors report hundreds of genes responding to RA over different cell types. We investigated the response to RA in H9c2 cells controlling for culture time.

2022-12-22 | GSE221596 | GEO

Nervous system development related gene expression regulation in the zebrafish embryo after exposure to valproic acid and retinoic acid: a genome wide approach

Project description:In our search for biomarkers of maldevelopment, we focused on chemically-induced perturbation of the retinoic acid signaling pathway (RA-SP), a major pathway implicated in a plethora of developmental processes. A genome-wide expression screening was was performed on zebrafish embryos treated with two teratogens, all-trans retinoic acid (ATRA) and valproic acid (VPA), and a negative control, folic acid (FA).

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RNA-seq analysis of retinoic acid treated mouse neuromesodermal progenitors

Project description:Bipotent neuromesodermal progenitors (NMPs) residing in the caudal epiblast drive coordinated body axis extension by generating both posterior neuroectoderm and presomitic mesoderm. Retinoic acid (RA) is required for body axis extension, however the early molecular response to RA signaling is poorly defined, as is its relationship to NMP biology. As endogenous RA is first seen near the time when NMPs appear, we used WNT/FGF agonists to differentiate embryonic stem cells to NMPs which were then treated with a short 2-h pulse of 25 nM RA or 1 µM RA followed by RNA-seq transcriptome analysis. Differential expression analysis of this dataset indicated that treatment with 25 nM RA, but not 1 µM RA, provided physiologically relevant findings. The 25 nM RA dataset yielded a cohort of previously known caudal RA target genes including Fgf8 (repressed) and Sox2 (activated), plus novel early RA signaling targets with nearby conserved RA response elements. Importantly, validation of top-ranked genes in vivo using RA-deficient Raldh2-/- embryos identified novel examples of RA activation (Nkx1-2, Zfp503, Zfp703, Gbx2, Fgf15, Nt5e) or RA repression (Id1) of genes expressed in the NMP niche or progeny. These findings provide evidence for early instructive and permissive roles of RA in controlling differentiation of NMPs to neural and mesodermal lineages.

2016-12-22 | GSE83251 | GEO

Human epidermal keratinocytes treated with retinoic acid or thyroid hormone

Project description:Targets of Retinoic Acid (RA) were identified in primary human epidermal keratinocytes grown in the presence or absence of all-trans retinoic acid for 1, 4, 24, 48 and 72 hours. Targets of Thyroid Hormone (T3) were identified in primary human epidermal keratinocytes grown in the presence or absence of the hormone; same controls as for RA.

2010-06-11 | GSE22298 | GEO

Global identification of retinoic acid regulated enhancers and silencers

Project description:Retinoic acid (RA) is known to regulate many genes during development by acting as a ligand for nuclear RA receptors that bind RA response elements (RAREs). However, identification of RAREs required to activate or repress specific genes during development has been quite difficult. Here, we focused on identification of RAREs in the developing trunk of vertebrate embryos during the early stages of body axis extension when RA controls neuromesodermal progenitor differentiation, spinal cord neurogenesis, somitogenesis, and forelimb bud initiation. Trunks from wild-type and Aldh1a2-/- mutants lacking RA synthesis were compared using ChIP-seq analysis for H3K27ac (a marker of gene activation) and H3K27me3 (a marker of gene repression) as well as RNA-seq analysis. We identified numerous RAREs, defined as elements displaying differential deposition of H3K27ac and/or H3K27me3 marks in Aldh1a2-/- vs wild-type that contain a canonical RARE sequence and are near genes that have altered expression when RA is missing. Our findings were able to differentiate genes likely to be directly regulated by RA via a RARE versus genes regulated by another factor further downstream. We identified several RA-regulated genes associated with changes in both H3K27ac and H3K27me3 near a RARE, providing new insight into how RAREs function in vivo.

2019-05-23 | GSE131624 | GEO

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