Queensland Brain Institute, The University of Queensland, Brisbane, Queensland 4072, Australia.
Universidade Federal de Alfenas, Alfenas, Minas Gerais 37130-000, Brazil.
Nat Commun. 2014 Nov 20;5:5529. doi: 10.1038/ncomms6529.
Increasing evidence suggests small non-coding RNAs (ncRNAs) such as microRNAs (miRNAs) control levels of mRNA expression during experience-related remodelling of the brain. Here we use an associative olfactory learning paradigm in the honeybee Apis mellifera to examine gene expression changes in the brain during memory formation. Brain transcriptome analysis reveals a general downregulation of protein-coding genes, including asparagine synthetase and actin, and upregulation of ncRNAs. miRNA-mRNA network predictions together with PCR validation suggest miRNAs including miR-210 and miR-932 target the downregulated protein-coding genes. Feeding cholesterol-conjugated antisense RNA to bees results in the inhibition of miR-210 and of miR-932. Loss of miR-932 impairs long-term memory formation, but not memory acquisition. Functional analyses show that miR-932 interacts with Act5C, providing evidence for direct regulation of actin expression by an miRNA. An activity-dependent increase in miR-932 expression may therefore control actin-related plasticity mechanisms and affect memory formation in the brain.
越来越多的证据表明，小非编码 RNA（ncRNAs），如 microRNAs（miRNAs），在与经验相关的大脑重塑过程中控制 mRNA 表达水平。在这里，我们使用蜜蜂 Apis mellifera 的联想嗅觉学习范式，研究在记忆形成过程中大脑中的基因表达变化。大脑转录组分析显示，包括天冬酰胺合成酶和肌动蛋白在内的蛋白质编码基因普遍下调，ncRNAs 上调。miRNA-mRNA 网络预测和 PCR 验证表明，包括 miR-210 和 miR-932 在内的 miRNA 靶向下调的蛋白质编码基因。向蜜蜂喂食胆固醇缀合的反义 RNA 会抑制 miR-210 和 miR-932。缺失 miR-932 会损害长期记忆的形成，但不影响记忆的获取。功能分析表明，miR-932 与 Act5C 相互作用，为 miRNA 对肌动蛋白表达的直接调控提供了证据。miR-932 表达的活性依赖性增加可能因此控制肌动蛋白相关的可塑性机制，并影响大脑中的记忆形成。
