Abstract：
Trehalose 6-phosphate (Tre6P) is an essential signal metabolite that regulates the level of sucrose, linking growth and development to the metabolic status. We hypothesized that Tre6P plays a role in mediating the regulation of gene expression by sucrose. To test this, we performed transcriptomic profiling on Arabidopsis (Arabidopsis thaliana) plants that expressed a bacterial TREHALOSE 6-PHOSPHATE SYNTHASE (TPS) under the control of an ethanol-inducible promoter. Induction led to a 4-fold rise in Tre6P levels, a concomitant decrease in sucrose, significant changes (FDR ≤ 0.05) of over 13,000 transcripts, and two-fold or larger changes of over 5000 transcripts. Comparison with nine published responses to sugar availability allowed some of these changes to be linked to the rise in Tre6P, while others were probably due to lower sucrose or other indirect effects. Changes linked to Tre6P included repression of photosynthesis-related gene expression and induction of many growth-related processes including ribosome biogenesis. About 500 starvation-related genes are known to be induced by SUCROSE-NON-FERMENTING-1-RELATED KINASE 1 (SnRK1). They were largely repressed by Tre6P in a manner consistent with SnRK1 inhibition by Tre6P. SnRK1 also represses many genes that are involved in biosynthesis and growth. These responded to Tre6P in a more complex manner, pointing toward Tre6P interacting with other C-signaling pathways. Additionally, elevated Tre6P modified the expression of genes encoding regulatory subunits of the SnRK1 complex and TPS class II and FCS-LIKE ZINC FINGER proteins that are thought to modulate SnRK1 function and genes involved in circadian, TARGET OF RAPAMYCIN-, light, abscisic acid, and other hormone signaling.
摘要：
海藻糖6-磷酸（Tre6P）是调节蔗糖水平的必需信号代谢产物，将生长和发育与代谢状态联系起来。我们假设Tre6P在介导蔗糖对基因表达的调控中起作用。为了测试这个，我们对拟南芥（拟南芥）植物进行了转录组学分析，这些植物在乙醇诱导型启动子的控制下表达了细菌海藻糖6-磷酸盐合成酶（TPS）。诱导导致Tre6P水平上升4倍，伴随着蔗糖的减少，超过13,000个转录本的显著变化(FDR≤0.05)，以及超过5000个转录本的两倍或更大的变化。与9个已发表的对糖可用性的响应进行比较，这些变化中的一些与Tre6P的上升有关，而其他人可能是由于较低的蔗糖或其他间接影响。与Tre6P相关的变化包括抑制与光合作用相关的基因表达和诱导许多与生长相关的过程，包括核糖体生物发生。已知约500个饥饿相关基因被蔗糖非发酵-1相关激酶1(SnRK1)诱导。它们在很大程度上被Tre6P抑制,其方式与Tre6P抑制SnRK1一致。SnRK1还抑制许多参与生物合成和生长的基因。这些以更复杂的方式回应了Tre6P，指向与其他C信号通路相互作用的Tre6P。此外,升高的Tre6P修饰了编码SnRK1复合物和TPSII类调节亚基的基因的表达和FCS样ZINCFINGER蛋白，这些蛋白被认为调节SnRK1功能和与昼夜节律有关的基因，雷帕霉素的目标-，光,脱落酸，和其他激素信号。
