Journal
NUTRIENTS
Volume 13, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/nu13020468
Keywords
VitE; vitamin E; E plus , VitE sufficient; E-, VitE deficient; hpf; hours post-fertilization; alpha-TTP; alpha-tocopherol transfer protein
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Funding
- National Institute of Environmental Health Sciences of the National Institutes of Health [P30ES030287]
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The study found that Vitamin E deficiency in zebrafish embryos resulted in disruption in gene expression, metabolic dysfunction, and embryonic structure formation, with mTOR playing a major role in these changes, ultimately leading to lethal outcomes as early as 12 hpf.
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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