ArticleNutrients2021
Vitamin E Deficiency Disrupts Gene Expression Networks during Zebrafish Development.
Article in Nutrients, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Deciphering the enigma of the function of alpha-tocopherol as a vitamin.Free radical biology & medicine · 2024Article
- Zebrafish ApoB-Containing Lipoprotein Metabolism: A Closer Look.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Gene Expression of CRAL_TRIO Family Proteins modulated by Vitamin E Deficiency in Zebrafish (Danio Rerio).The Journal of nutritional biochemistry · 2021Article
- Vitamin E Can Ameliorate Oxidative Damage of Ovine HepatocytesMolecules (Basel, Switzerland) · 2021Article
- RedEfish: Generation of the Polycistronic mScarlet: GSG-T2A: Ttpa Zebrafish Line.Antioxidants (Basel, Switzerland) · 2021Article
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Authors and funding
5 authors.
Funding
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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.
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