PUBLICATION

Vitamin E Deficiency Disrupts Gene Expression Networks during Zebrafish Development

Authors
Head, B., Ramsey, S.A., Kioussi, C., Tanguay, R.L., Traber, M.G.
ID
ZDB-PUB-210213-10
Date
2021
Source
Nutrients   13(2): (Journal)
Registered Authors
Tanguay, Robyn L.
Keywords
E+, VitE sufficient, E–, VitE deficient, VitE, hours post-fertilization, hpf, vitamin E, α-TTP, α-tocopherol transfer protein.
Datasets
GEO:GSE164848
MeSH Terms
  • Animals
  • Blotting, Western
  • Gene Expression Regulation, Developmental*
  • Vitamin E Deficiency/embryology
  • Vitamin E Deficiency/veterinary*
  • Zebrafish/embryology
  • Zebrafish/growth & development
PubMed
33573233 Full text @ Nutrients
Abstract
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.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping