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首页> 外文期刊>Molecular and Cellular Biology >Serotonin Increases Phosphorylation of Synaptic 4EBP through TOR, but Eukaryotic Initiation Factor 4E Levels Do Not Limit Somatic Cap-Dependent Translation in Aplysia Neurons
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Serotonin Increases Phosphorylation of Synaptic 4EBP through TOR, but Eukaryotic Initiation Factor 4E Levels Do Not Limit Somatic Cap-Dependent Translation in Aplysia Neurons

机译：5-羟色胺通过TOR增强突触4EBP的磷酸化，但真核起始因子4E水平不限制海浪神经元中体细胞帽依赖性翻译。

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The target of rapamycin (TOR) plays an important role in memory formation in Aplysia californica. Here, we characterize one of the downstream targets of TOR, the eukaryotic initiation factor 4E (eIF4E) binding protein (4EBP) from Aplysia. Aplysia 4EBP contains the four critical phosphorylation sites regulated by TOR as well as an N-terminal RAIP motif and a C-terminal TOS site. Aplysia 4EBP was hypophosphorylated in synaptosomes, and serotonin addition caused a rapamycin-sensitive increase in 4EBP phosphorylation both in synaptosomes and in isolated neurites. Aplysia 4EBP was regulated in a fashion similar to that of mammalian 4EBPs, binding to eIF4E when dephosphorylated and releasing eIF4E after phosphorylation. Overexpression of 4EBP in the soma of Aplysia neurons caused a specific decrease in cap-dependent translation that was rescued by concomitant overexpression of eIF4E. However, eIF4E overexpression by itself did not increase cap-dependent translation, suggesting that increasing levels of free eIF4E by phosphorylating 4EBP is not important in regulating cap-dependent translation in the cell soma. Total levels of eIF4E were also regulated by 4EBP, suggesting that 4EBP can also act as an eIF4E chaperone. These studies demonstrate the conserved nature of 4EBP regulation and its role in cap-dependent translation and suggest differential roles of 4EBP phosphorylation in the soma and synapse.
机译：雷帕霉素（TOR）的靶标在的记忆形成中起重要作用。在这里，我们表征了TOR的下游靶标之一，即 Aplysia的真核起始因子4E（eIF4E）结合蛋白（4EBP）。 Aplysia 4EBP包含受TOR调控的四个关键磷酸化位点，以及一个N端RAIP基序和一个C端TOS位。 Aplysia 4EBP在突触小体中被低磷酸化，5-羟色胺的添加引起雷帕霉素敏感的突触小体和分离的神经突中4EBP磷酸化的增加。 Aplysia 4EBP的调控方式与哺乳动物4EBP相似，去磷酸化时与eIF4E结合，并在磷酸化后释放eIF4E。在 Aplysia 神经元的体细胞中4EBP的过表达导致帽依赖性翻译的特定减少，而eIF4E的过表达可以缓解这种依赖性。但是，eIF4E自身的过表达并没有增加帽依赖性翻译，这表明通过磷酸化4EBP来增加游离eIF4E的水平在调节细胞体中的帽依赖性翻译中并不重要。 eIF4E的总水平也受到4EBP的调节，这表明4EBP也可以充当eIF4E分子伴侣。这些研究证明了4EBP调节的保守性质及其在帽依赖性翻译中的作用，并暗示了4EBP磷酸化在体细胞和突触中的不同作用。

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