Vitamin E Deficiency Disrupts Gene Expression Networks during Zebrafish Development

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....

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Bibliographic Details
Published in:Nutrients 2021-01, Vol.13 (2), p.468
Main Authors: Head, Brian, Ramsey, Stephen A, Kioussi, Chrissa, Tanguay, Robyn L, Traber, Maret G
Format: Article
Language:English
Subjects:
Analysis
Brain research
Carbohydrate metabolism
Carbohydrates
Clustering
Data processing
Diet
E+, VitE sufficient
Embryogenesis
Embryonic development
Embryonic growth stage
Embryos
Energy metabolism
E–, VitE deficient
Fertilization
Gene expression
Generalized linear models
Genes
Genetic aspects
Genetic research
Genetic transcription
Genomes
hours post-fertilization
hpf
Intracellular signalling
Laboratories
Metabolism
Nervous system
Nutrient deficiency
Ontology
Physiological aspects
Proteins
Tocopherol
TOR protein
Transcription
Transcription factors
Vertebrates
Vitamin E
VitE
Zebrafish
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Summary: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.
ISSN:2072-6643
2072-6643
DOI:10.3390/nu13020468