Identification of BMP-regulated genes in early gastrulation stage zebrafish embryos
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ABSTRACT:
PROVIDER: PRJNA557436 | ENA |
REPOSITORIES: ENA
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Project description:We report the systematic identification of BMP (bone morphogenetic protein) target genes in zebrafish during dorsal-ventral patterning using RNA-sequencing.
2020-07-30 | GSE135100 | GEO
Project description:The aim of this study was to identify genes that are regulated by Bmp signaling with the zebrafish heart at the heart cone stage around 21-23 hours post fertilization. In total, 4 samples based on cDNA from extracted cardiac tissue were analyzed: 2 samples of Tg(hsp70l:bmp2b)fr13 transgenic embryos heatshocked at 18 hpf and 2 WT control samples.
2013-03-25 | E-GEOD-43888 | biostudies-arrayexpress
Project description:Gastrulation is a milestone event of embryonic development, during which germ layers are specified and reassigned into the body plan. Due to the inaccessibility in vivo at this stage and the ethical limitations, gastrulation currently remains a mystery in primates. Here, we report the establishment of an in vitro system to culture cynomolgus monkey embryos after up to 20 days to develop beyond the initiation of gastrulation. The histology, immunostaining and single cell sequencing results showed that the in vitro cultured embryos largely recapitulated the key events of early post-implantation development, and initiated gastrulation in primates. Considering the high similarities between monkeys and humans, this system will provide a unique platform for the investigations of human early post-implantation development at physiological, pathological and environmental conditions.
2019-11-01 | GSE130114 | GEO
Project description:The aim of this study was to identify genes that are regulated by Bmp signaling with the zebrafish heart at the heart cone stage around 21-23 hours post fertilization.
2013-03-25 | GSE43888 | GEO
Project description:Investigation of whole genome gene expression level changes in nanog-like knockdown embryos , compared to the control-MO injected embryos. Knockdown of nanog-like impaired early gastrulation. To globally analyze which target genes Nanog-like regulates during early embryogenesis, we performed a genome-wide transcription analysis using sphere stage (4 hpf) nanog-like morphants.
2011-12-28 | GSE34682 | GEO
Project description:Investigation of whole genome gene expression level changes in nanog-like knockdown embryos , compared to the control-MO injected embryos. Knockdown of nanog-like impaired early gastrulation. To globally analyze which target genes Nanog-like regulates during early embryogenesis, we performed a genome-wide transcription analysis using sphere stage (4 hpf) nanog-like morphants. A six chip study using total RNA recovered from three separate control-MO injected embryos and three separate nanog-like-MO1 injected embryos at the sphere stage
2011-12-28 | E-GEOD-34682 | biostudies-arrayexpress
Project description:Current knowledge of the mechanisms of cell migration is based on differentiated cells in culture where it is known that the actomyosin machinery drives migration via dynamic interactions with the extracellular matrix and adhesion complexes. However, unlike differentiated cells, cells in early metazoan embryos also dynamically change cell sizes as they migrate. The relevance of cell size to cell migration and embryonic development is not known. Here we investigate these phenomena in zebrafish embryos, a model system in which reductive cell divisions causes cell sizes to decrease naturally over time as cells migrate collectively to sculpt the embryonic body plan. Because mutations that can perturb cell sizes so early in development do not exist, we generate haploid and tetraploid zebrafish embryos and show that cell sizes in such embryos are smaller and larger than the diploid norm, respectively. Cells in embryos made of smaller or larger than normal cells migrate sub-optimally, leading to gastrulation defects. Multiple lines of evidence suggest that the observed defects originate from altered cell size, and not from pleotropic effects of altered ploidy. This interpretation is strengthened by finding that gastrulation defects are rescued by increasing cell sizes in embryos wherein cell sizes are smaller than normal. We show that the migration defects are cell-autonomous by live imaging migrating haploid and tetraploid cells during gastrulation in chimeric diploid embryos. Analysis of membrane protrusion dynamics in single cells shows that cells normally extend protrusions non-uniformly during migration, a phenomenon which is perturbed when cell sizes deviate from the norm. Thus, an optimal range of developmental stage-specific cell sizes appears necessary for collective cell migration to correctly position cells in space and time to shape an amorphous ball of blastoderm into an embryo.
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Project description:In animal models, Nipbl-deficiency phenocopies gene expression changes and birth defects seen in Cornelia de Lange Syndrome (CdLS), the most common cause of which is Nipbl-haploinsufficiency. Previous studies in Nipbl+/- mice identified aberrant gene expression and heart defects as early as cardiac crescent (CC) stage. Here, we performed single-cell RNA-sequencing on wildtype (WT) and Nipbl+/- mouse embryos at CC- and earlier (gastrulation) stages. Nipbl+/- embryos had fewer mesoderm cells than WT and altered proportions of mesodermal cell subpopulations. These findings were associated with an underexpression of genes implicated in driving specific mesodermal lineages. Nipbl+/- embryos also misexpressed developmentally-critical genes, including the transcription factor, Nanog, and genes governing left-right and anterior-posterior patterning. These events of cell misallocation and transcriptional dysregulation foreshadowed defects in tissue composition and patterning that arise later in Nipbl+/- mice, offering insights into early developmental contributions to birth defects in CdLS.
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Project description:Transcriptional profiling of Mtx2 morphants at 30% epiboly stage, shield stage and tailbud stage of embryonic development: Coordinated cell movements of gastrulation reshape the uniform blastula into a structured gastrula with three fundamental axes and an internal germ layer of mesoderm. Genetic regulation of the forces which drive gastrulation is incompletely understood. We employed a microarray screen in zebrafish for genes which participate in epibloy, and identified many with biochemical roles in endocytosis, microtubule remodeling, cell adhesion and transcription.
2016-12-31 | GSE73812 | GEO
Project description:Craniofacial and CNS malformations characteristic of Fetal Alcohol Syndrome are caused by alcohol exposure during gastrulation (embryonic day [E]7 in mice; 2nd – 3rd week of human pregnancy). Genetics are a known contributor to differences in alcohol sensitivity in humans, and between different animal model strains such as C57BL/6J and C57BL/6NHsd mice. To investigate how these two genetically similar mouse strains differ in alcohol sensitivity, we profiled gene expression at baseline (E7.0) and 6 or 12 hours after alcohol exposure (E7.25–E7.5) in gastrulation-stage embryos. Many of the baseline transcriptional differences across strains were associated with immune signaling, indicative of their molecular divergence. Alcohol exposure was associated with a more pronounced transcriptional effect in 6J than in 6N, matching the 6J’s increased sensitivity. Alcohol exposure upregulated pathways related to cell death, stress, and hypoxia, and downregulated proliferation and morphogenic pathways. Dysregulated genes were also associated with craniofacial and CNS defects, but only in the 6J embryos. These data demonstrate the genetic variation that can contribute to the effects of prenatal alcohol and identify impacted molecular pathways, including higher baseline expression of inflammatory signaling genes in 6J embryos that likely increases sensitivity to teratogens such as alcohol. Collectively, our data provide a valuable resource that not only enables the discovery of biomarkers pertinent to prenatal alcohol exposure, but also facilitates the transcriptional comparison of two genetically similar mouse strains at three finely resolved developmental timepoints. To this end, we developed a web-based interactive tool to aid in data exploration available at http://parnell-lab.med.unc.edu/Embryo-Transcriptomics/.
2021-06-01 | GSE163796 | GEO