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富含 AU 的元素结合蛋白在长时程突触可塑性过程中负调控 Aplysia 的 CCAAT 增强子结合蛋白 mRNA 的稳定性。

AU-rich element-binding protein negatively regulates CCAAT enhancer-binding protein mRNA stability during long-term synaptic plasticity in Aplysia.

机构信息

National Creative Research Initiative Center for Memory, Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul, Korea.

出版信息

Proc Natl Acad Sci U S A. 2012 Sep 18;109(38):15520-5. doi: 10.1073/pnas.1116224109. Epub 2012 Sep 4.

DOI:10.1073/pnas.1116224109
PMID:22949683
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3458389/
Abstract

The consolidation of long-term memory for sensitization and synaptic facilitation in Aplysia requires synthesis of new mRNA including the immediate early gene Aplysia CCAAT enhancer-binding protein (ApC/EBP). After the rapid induction of ApC/EBP expression in response to repeated treatments of 5-hydroxytryptamine (5-HT), ApC/EBP mRNA is temporarily expressed in sensory neurons of sensory-to-motor synapses. However, the molecular mechanism underlying the rapid degradation of ApC/EBP transcript is not known. Here, we cloned an AU-rich element (ARE)-binding protein, ApAUF1, which functions as a destabilizing factor for ApC/EBP mRNA. ApAUF1 was found to bind to the 3' UTR of ApC/EBP mRNA that contains AREs and subsequently reduces the expression of ApC/EBP 3' UTR-containing reporter genes. Moreover, overexpression of ApAUF1 inhibited the induction of ApC/EBP mRNA in sensory neurons and also impaired long-term facilitation of sensory-to-motor synapses by repetitive 5-HT treatments. These results provide evidence for a critical role of the posttranscriptional modification of ApC/EBP mRNA during the consolidation of synaptic plasticity.

摘要

长时程记忆的巩固对于敏感化和突触易化来说是必需的，在海兔中，这需要新的 mRNA 的合成，包括即刻早期基因 Aplysia CCAAT 增强子结合蛋白（ApC/EBP）。在对 5-羟色胺（5-HT）进行重复处理后，ApC/EBP 表达迅速诱导，ApC/EBP mRNA 暂时在感觉神经元中表达，这些感觉神经元与感觉-运动突触有关。然而，ApC/EBP 转录本快速降解的分子机制尚不清楚。在这里，我们克隆了一个富含 AU 的元件（ARE）结合蛋白 ApAUF1，它作为 ApC/EBP mRNA 的不稳定因子发挥作用。发现 ApAUF1 与含有 ARE 的 ApC/EBP mRNA 的 3'UTR 结合，随后降低含有 ApC/EBP 3'UTR 的报告基因的表达。此外，ApAUF1 的过表达抑制了感觉神经元中 ApC/EBP mRNA 的诱导，也损害了重复 5-HT 处理引起的感觉-运动突触的长时程易化。这些结果为突触可塑性巩固过程中 ApC/EBP mRNA 的转录后修饰提供了证据。

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