Vitamin E deficiency disrupts gene expression networks during zebrafish development. 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 (>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. Overall design: RNA extracted from whole zebrafish embryos with (E+) and without (E–) Vitamin E at 12, 18 and 24 hours post-fertilization