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Transcriptomic analyses of gastrulation-stage C57BL/6J and C57BL/6NHsd mouse embryos with differential susceptibility to alcohol

ABSTRACT: Transcriptomic analyses of gastrulation-stage C57BL/6J and C57BL/6NHsd mouse embryos with differential susceptibility to alcohol

PROVIDER: PRJNA687548 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13298100_1.fastq.gz	Fastqsanger.gz
	SRR13298100_2.fastq.gz	Fastqsanger.gz
	SRR13298101_1.fastq.gz	Fastqsanger.gz
	SRR13298101_2.fastq.gz	Fastqsanger.gz
	SRR13298102_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analyses of gastrulation-stage C57BL/6J and C57BL/6NHsd mouse embryos with differential susceptibility to alcohol

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: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.

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