Preimplantation mouse embryos interact minimally with their environment, and development is largely driven by metabolic processes. During the earliest cleavage stages, metabolism is rigid, with maternal deposits enforcing a redox state that facilitates zygotic genome activation. As maternal control falls, metabolic shuttles are activated, increasing glycolysis and equilibrating the TCA cycle. The resulting flexibility of nutrient utilization and metabolic plasticity facilitates unidirectional developmental progression such that later stage embryos proceed to form blastocysts without any exogenously added nutrients. We explore the mechanisms that govern this choreographed sequence that balances the deposition, degradation, synthesis and function of metabolic enzymes with redox control, bioenergetics and biosynthesis. Cancer cells follow a distinct metabolic strategy from that of the preimplantation embryo. However, important shared features emerge under reductive stress. We conclude that metabolic plasticity drives normal development while stress conditions mimic hallmark events in Cancer Metabolism.

中文翻译：

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代谢可塑性驱动哺乳动物胚胎发生过程中的发育。

植入前的小鼠胚胎与其周围环境的相互作用极小，并且发育很大程度上受代谢过程驱动。在最早的切割阶段，新陈代谢是刚性的，母体沉积物会增强氧化还原状态，从而促进合子基因组的激活。随着母体控制的下降，新陈代谢梭被激活，增加了糖酵解并平衡了TCA循环。养分利用的灵活性和新陈代谢的可塑性促进了单向发育的进程，因此后期的胚胎开始形成胚泡而没有任何外源添加的养分。我们探索控制这种编排序列的机制，该序列平衡了氧化还原控制，生物能和生物合成的代谢酶的沉积，降解，合成和功能。癌细胞遵循与植入前胚胎不同的代谢策略。但是，重要的共同特征在缓解压力下出现。我们得出的结论是，代谢可塑性驱动正常发育，而压力条件则模仿癌症代谢中的标志性事件。