Vitamin E deficiency disrupts gene expression networks during zebrafish development
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA692200 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13437200.fastq.gz | Fastqsanger.gz | |||
| SRR13437201.fastq.gz | Fastqsanger.gz | |||
| SRR13437202.fastq.gz | Fastqsanger.gz | |||
| SRR13437203.fastq.gz | Fastqsanger.gz | |||
| SRR13437204.fastq.gz | Fastqsanger.gz |
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Project description:Vitamin E (VitE) is essential for vertebrate embryogenesis, but the mechanisms involved remain unknown. To study embryonic development, we fed zebrafish adults (>45 days) either VitE sufficient (E+) or deficient (E–) diets for >80 days, then the fish were spawned to generate E+ and E– embryos. To evaluate the transcriptional basis of the metabolic and phenotypic outcomes, E+ and E– embryos at 12-, 18- and 24 hours post-fertilization (hpf) were subjected to gene expression profiling by RNASeq. Hierarchical clustering, over representation analyses and gene set enrichment analyses were performed with differentially expressed genes. E– embryos experienced overall disruption to gene expression associated with gene transcription, metabolism, intracellular signaling and the formation of embryonic structures. Thus, the apparently moderate changes in lipid peroxidation and metabolic alterations due to VitE deficiency result in major genetic and transcriptional dysregulation as early as 12 hpf, leading to metabolic dysfunction and ultimately lethal outcomes.
2021-01-15 | GSE164848 | GEO
Project description:Vitamin E (VitE) is essential for vertebrate embryogenesis, but the mechanisms involved remain unknown. To study embryonic development, we fed zebrafish adults (>55 days) either VitE sufficient (E+) or deficient (E-) diets for >80 days, then the fish were spawned to generate E+ and E- embryos. To evaluate the transcriptional basis of the metabolic and phenotypic outcomes, E+ and E- embryos at 12, 18 and 24 h post-fertilization (hpf) were subjected to gene expression profiling by RNASeq. Hierarchical clustering, over-representation analyses and gene set enrichment analyses were performed with differentially expressed genes. E- embryos experienced overall disruption to gene expression associated with gene transcription, carbohydrate and energy metabolism, intracellular signaling and the formation of embryonic structures. mTOR was apparently a major controller of these changes. Thus, embryonic VitE deficiency results in genetic and transcriptional dysregulation as early as 12 hpf, leading to metabolic dysfunction and ultimately lethal outcomes.
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Project description:Vitamin D deficiency and mutations in Vitamin D Receptor (VDR) are associated with liver disease and obesity, but the functions of vitamin D signaling in metabolism are poorly understood. Though vitamin D signaling is best known for its functions in mineral homeostasis and skeleton calcification in terrestrial vertebrates, this is unlikely to be the evolutionary function of vitamin D signaling. We utilize tissue-specific genetic modulation of Vdr signaling to investigate the function of the vitamin D endocrine system in zebrafish. We find that hepatocyte Vdr regulates organismal response to nutritional cues and coordinates hepatic and organismal energy metabolism by balancing energy storage and tissue growth.
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Project description:Vitamin D, a fat-soluble vitamin, plays a critical role in calcium homeostasis, the immune system, and normal development. Many epidemiological cohort studies globally have found high prevalence rates of vitamin D deficiency and insufficiency, recognized as an important health issue that needs to be solved. In particular, reproductive age and pregnant women low in vitamin D status may confer risks of diseases like obesity on their offspring. While observational studies have suggested associations between prenatal vitamin D deficiency and metabolic phenotypes in offspring, not yet determined is whether prenatal vitamin D deficiency permanently alters the development of the liver, a major metabolic organ. We tested the histopathology and the transcriptomic profiles of livers from male C57BL/6J mice exposed to prenatal vitamin D deficiency through a maternal dietary intervention model. We found that prenatal vitamin D deficiency increases the prevalence of histopathological changes in the liver, and alters its gene expression profile. Cell subtype proportion analysis showed that the liver of prenatal vitamin D deficiency alters non-parenchymal cells of the liver, specifically macrophages, a subset of endothelial cells, and dendritic cells. Our results indicate the long-term memory of prenatal vitamin D deficiency exposure in the adult liver, a potential contributor to offspring health risks.
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Project description:Transcriptomic analysis of lungs from newborn rats born to vitamin D adequate and vitamin D deficient mothers Vitamin D deficiency during pregnancy is common and is related to several maternal and fetal morbidities. Past studies suggest that vitamin D plays a role in normal lung development and we have shown that vitamin D regulates lung alveolar and vascular growth and preserves lung structure in experimental bronchopulmonary dysplasia (BPD) through improved pro-angiogeneic signaling. In addition, maternal vitamin D deficiency causes abnormal airway, alveolar, and vascular growth, as well as impaired lung function and airway hyper-reactivity in newborn rats. However, the mechanisms responsible for these physiologic effects are unknown. To gain insight into the role that maternal vitamin D status has on fetal lung development we used an unbiased transcriptomic approach to identify pathways altered in the lungs of offspring from vitamin D deficient dams.
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Project description:We report genes and molecular pathways that respond to vitamin A deficiency.
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Project description:Animals possess control mechanisms to synchronize organ and organismal size during growth, to maintain tissue integrity through homeostatic cell proliferation, and to counter major injury with regeneration. A principal research goal is to elucidate mitogenic triggers that underlie these mechanisms. Here, from a large-scale in vivo chemical screen, we discovered that analogues of the essential nutrient vitamin D potently activate heart muscle cell division in larval zebrafish. Unexpectedly, loss- and gain-of-function methods to modulate vitamin D signaling altered metabolic and cell cycle gene expression in zebrafish larvae and dictated rates of organismal growth. Systemic vitamin D treatment sharply increased in vivo cell proliferation in a variety of adult cell types including cardiomyocytes, hepatocytes, osteoblasts, cardiac mesothelium, skin and corneal epithelium, and retina, and enhanced injury-induced heart and appendage regeneration. Our experiments identify vitamin D signaling as a broad growth- and regeneration-initiating influence throughout the life stages of a vertebrate model system.
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Project description:Maternal Vitamin C is required in vivo for proper DNA demethylation and development of fetal germ cells in a mouse model of Vitamin C deficiency. Withdrawal of Vitamin C from the maternal diet does not affect overall embryonic development but leads to defects in the fetal germline, which persist well after Vitamin C re-supply during late gestation. The transcriptome of germ cells from Vitamin C-deficient embryos is remarkably similar to that of embryos carrying a mutation in Tet1, which is responsible for DNA demethylation and activation of regulators of meiosis. In agreement with these results, Vitamin C deficiency leads to an aberrant DNA methylation profile that includes incomplete demethylation of key regulators of meiosis and transposable elements. These findings reveal that deficiency in Vitamin C during gestation recapitulates a mutation in Tet1 and disrupts germline reprogramming and development. Our work further indicate that the embryonic germline is sensitive to perturbations of the maternal diet, providing a potential intergenerational mechanism for adjusting fecundity to environmental quality.
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