Mus musculus breed:C57BL/6J
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA415493 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6208990.fastq.gz | Fastqsanger.gz | |||
| SRR6209000.fastq.gz | Fastqsanger.gz | |||
| SRR6209010.fastq.gz | Fastqsanger.gz | |||
| SRR6209020.fastq.gz | Fastqsanger.gz | |||
| SRR6209030.fastq.gz | Fastqsanger.gz |
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Project description:Prenatal alcohol exposure during mouse gastrulation (embryonic day [E] 7 in mice, corresponding to ~3rd week of human pregnancy) impairs eye, facial, and cortical development, recapitulating birth defects characteristic of Fetal Alcohol Syndrome (FAS). However, the impact of sex on the prevalence or severity of craniofacial features associated with FAS is currently unknown. The current study administered either alcohol (2.9g/kg, two i.p. doses, four hours apart) or vehicle control to pregnant C57BL/6J females on E7 and assessed fetal morphology at E17. Whereas sex did not affect fetal size in vehicle-treated litters, alcohol-exposed females were smaller than both control females and alcohol-treated males. Alcohol exposure increased the incidence of eye defects to a similar degree in males and females. Together, this suggests that females might be more sensitive to the general developmental effects of alcohol, but not to the effects of alcohol specifically on the craniofacies. We also established a developmental transcriptional baseline via whole transcriptomic analysis of untreated E7 embryos, and found 214 differentially expressed genes in females vs. males, including those in pathways related to cilia and mitochondria structure and function, histone demethylase activity, and pluripotency.
2024-03-19 | GSE239355 | 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/.
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Project description:Epigenetic Effects of Prenatal Ethanol Exposure: High Resolution Genome-Wide DNA Methylation Profiling in a Mouse Model for Fetal Alcohol Syndrome
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Project description:Cerebral organoids â three-dimensional cultures of human cerebral tissue derived from pluripotent stem cells â have emerged as models of human cortical development. However, the extent to which in vitro organoid systems recapitulate neural progenitor cell proliferation and neuronal differentiation programs observed in vivo remains unclear. Here we use single-cell RNA sequencing (scRNA-seq) to dissect and compare cell composition and progenitor-to-neuron lineage relationships in human cerebral organoids and fetal neocortex. Covariation network analysis using the fetal neocortex data reveals known and novel interactions among genes central to neural progenitor proliferation and neuronal differentiation. In the organoid, we detect diverse progenitors and differentiated cell types of neuronal and mesenchymal lineages, and identify cells that derived from regions resembling the fetal neocortex. We find that these organoid cortical cells use gene expression programs remarkably similar to those of the fetal tissue in order to organize into cerebral cortex-like regions. Our comparison of in vivo and in vitro cortical single cell transcriptomes illuminates the genetic features underlying human cortical development that can be studied in organoid cultures. 734 single-cell transcriptomes from human fetal neocortex or human cerebral organoids from multiple time points were analyzed in this study. All single cell samples were processed on the microfluidic Fluidigm C1 platform and contain 92 external RNA spike-ins. Fetal neocortex data were generated at 12 weeks post conception (chip 1: 81 cells; chip 2: 83 cells) and 13 weeks post conception (62 cells). Cerebral organoid data were generated from dissociated whole organoids derived from induced pluripotent stem cell line 409B2 (iPSC 409B2) at 33 days (40 cells), 35 days (68 cells), 37 days (71 cells), 41 days (74 cells), and 65 days (80 cells) after the start of embryoid body culture. Cerebral organoid data were also generated from microdissected cortical-like regions from H9 embryonic stem cell derived organoids at 53 days (region 1, 48 cells; region 2, 48 cells) or from iPSC 409B2 organoids at 58 days (region 3, 43 cells; region 4, 36 cells).
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Project description:This SuperSeries is composed of the following subset Series: GSE23105: Postnatal Growth Restriction and Gene Expression Changes in a Mouse Model of Fetal Alcohol Syndrome (Kidney) GSE23106: Postnatal Growth Restriction and Gene Expression Changes in a Mouse Model of Fetal Alcohol Syndrome (Liver) Refer to individual Series
2010-09-30 | E-GEOD-23115 | biostudies-arrayexpress
Project description:Cerebral organoids – three-dimensional cultures of human cerebral tissue derived from pluripotent stem cells – have emerged as models of human cortical development. However, the extent to which in vitro organoid systems recapitulate neural progenitor cell proliferation and neuronal differentiation programs observed in vivo remains unclear. Here we use single-cell RNA sequencing (scRNA-seq) to dissect and compare cell composition and progenitor-to-neuron lineage relationships in human cerebral organoids and fetal neocortex. Covariation network analysis using the fetal neocortex data reveals known and novel interactions among genes central to neural progenitor proliferation and neuronal differentiation. In the organoid, we detect diverse progenitors and differentiated cell types of neuronal and mesenchymal lineages, and identify cells that derived from regions resembling the fetal neocortex. We find that these organoid cortical cells use gene expression programs remarkably similar to those of the fetal tissue in order to organize into cerebral cortex-like regions. Our comparison of in vivo and in vitro cortical single cell transcriptomes illuminates the genetic features underlying human cortical development that can be studied in organoid cultures.
2015-12-07 | GSE75140 | GEO
Project description:Cerebral cortical-derived neurosphere cultures were exposed to ethanol to model heavy alcohol exposure during the period of cortical neurogenesis Keywords: Compared differentiated neurospheres pre-exposed to ethanol to untreated differentiated neurospheres
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Project description:Mouse model for Fetal Alcohol Syndrome. Embryos exposed to alcohol in controlled environment to assess teratogenic effects. Fetal Alcohol Syndrome (FAS) is a leading developmental disorder. To date, a holistic view of molecular gene changes is largely unexplored. Using microarray analysis of whole embryo mouse culture with strict-control over alcohol-level, we found, directly related alcohol-metabolism, a reduction of retinol binding protein 1(Rbp1), and a, de novo expression of aldehyde dehydrogenase 1B1 (ALDH1B1). Remarkably, four key hemopoiesis genes (glycophorin A, adducin 2, beta-2 microglobulin, and ceruloplasmin) became absent, and many histone variants genes were reduced. Hypothesis-driven informatics analysis and intersection analysis of two independent experiments indicated that the altered genes are involved in cell growth, hemopoiesis, histone modification, eye and heart development, and a collective reduction in expression of growth factor genes (Igf1, Efemp1, Tieg, and Edil3) and neural specification genes (neurogenin, Sox 5, bHLHb5). Down-regulated neural specification phenotypes further supported the above findings. Further more, the gene expression profile indicated distinct subgroups which overlapped with the teratogenesis of the open- and the closed-neural tubes known in FAS. In summary, our data reveal genes alteration with causal potential for dysmorpology (e.g. retinoic acid, neuronal specification, and neurotrophic factors, and epigenetics related histone genes) and those downstream responsive genes related to alcohol metabolism, and developmental teratogenesis. Experiment Overall Design: Comparison of whole embryo gene expression after exposure to ethanol for 46 hours. Note 2 independent experiments completed.
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Project description:Mouse model for Fetal Alcohol Syndrome. Embryos exposed to alcohol in controlled environment to assess teratogenic effects. Fetal Alcohol Syndrome (FAS) is a leading developmental disorder. To date, a holistic view of molecular gene changes is largely unexplored. Using microarray analysis of whole embryo mouse culture with strict-control over alcohol-level, we found, directly related alcohol-metabolism, a reduction of retinol binding protein 1(Rbp1), and a, de novo expression of aldehyde dehydrogenase 1B1 (ALDH1B1). Remarkably, four key hemopoiesis genes (glycophorin A, adducin 2, beta-2 microglobulin, and ceruloplasmin) became absent, and many histone variants genes were reduced. Hypothesis-driven informatics analysis and intersection analysis of two independent experiments indicated that the altered genes are involved in cell growth, hemopoiesis, histone modification, eye and heart development, and a collective reduction in expression of growth factor genes (Igf1, Efemp1, Tieg, and Edil3) and neural specification genes (neurogenin, Sox 5, bHLHb5). Down-regulated neural specification phenotypes further supported the above findings. Further more, the gene expression profile indicated distinct subgroups which overlapped with the teratogenesis of the open- and the closed-neural tubes known in FAS. In summary, our data reveal genes alteration with causal potential for dysmorpology (e.g. retinoic acid, neuronal specification, and neurotrophic factors, and epigenetics related histone genes) and those downstream responsive genes related to alcohol metabolism, and developmental teratogenesis. Keywords: comparison of gene expression profiles for treated vs. control
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