Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA.
Molecular and Cellular Biology Program, Oregon State University, Corvallis, OR 97331, USA.
Nutrients. 2021 Jan 30;13(2):468. doi: 10.3390/nu13020468.
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.
维生素 E（VitE）对脊椎动物胚胎发生至关重要，但相关机制仍不清楚。为了研究胚胎发育，我们用含有足够（E+）或缺乏（E-）维生素 E 的饮食喂养成年斑马鱼 (>55 天) 超过 80 天，然后让这些鱼产卵以产生 E+ 和 E- 胚胎。为了评估代谢和表型结果的转录基础，我们对受精后 12、18 和 24 小时的 E+和 E-胚胎进行了 RNA-Seq 基因表达谱分析。通过差异表达基因进行层次聚类、过度表达分析和基因集富集分析。E-胚胎经历了与基因转录、碳水化合物和能量代谢、细胞内信号转导以及胚胎结构形成相关的整体基因表达中断。mTOR 显然是这些变化的主要控制器。因此，胚胎 VitE 缺乏早在 12 hpf 就会导致遗传和转录失调，导致代谢功能障碍，最终导致致命后果。
