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光控CLIP技术揭示了CA1神经元激活后FMRP对mRNA的动态调控。

Opto-CLIP reveals dynamic FMRP regulation of mRNAs upon CA1 neuronal activation.

作者信息

Singer Ruth A, Rajchin Veronika, Park Kwanghoon, Heintz Nathaniel, Darnell Robert B

机构信息

Laboratory of Molecular Neuro-oncology, The Rockefeller University, New York, NY, USA.

Laboratory of Molecular Biology, The Rockefeller University, New York, NY, USA.

出版信息

bioRxiv. 2025 Jan 15:2024.08.13.607210. doi: 10.1101/2024.08.13.607210.

Abstract

Neuronal diversity and function are intricately linked to the dynamic regulation of RNA metabolism. Electrophysiologic studies of synaptic plasticity, models for learning and memory, are disrupted in Fragile X Syndrome (FXS). FXS is characterized by the loss of FMRP, an RNA-binding protein (RBP) known to suppress translation of specific neuronal RNAs. Synaptic plasticity in CA1 excitatory hippocampal neurons is protein-synthesis dependent, suggesting a role for FMRP in FXS-related synaptic deficits. To explore this model, we developed Opto-CLIP, integrating optogenetics with cell-type specific FMRP-CLIP and RiboTag in CA1 neurons, allowing investigation of activity-induced FMRP regulation. We tracked changes in FMRP binding and ribosome-associated RNA profiles 30 minutes after neuronal activation. Our findings reveal distinct temporal dynamics for FMRP transcript regulation in the cell body versus the synapse. In the cell body, FMRP binding to transcripts encoding nuclear functions is relieved, potentially allowing rapid transcriptional responses to neuronal activation. At the synapse, FMRP binding to transcripts encoding synaptic targets was relatively stable, with variability in translational control across target categories. These results offer fresh insights into the dynamic regulation of RNA by FMRP in response to neuronal activation and provide a foundation for future research into the mechanisms of RBP-mediated synaptic plasticity.

摘要

神经元的多样性和功能与RNA代谢的动态调控密切相关。脆性X综合征(FXS)会破坏突触可塑性的电生理研究,而突触可塑性是学习和记忆的模型。FXS的特征是FMRP的缺失,FMRP是一种已知可抑制特定神经元RNA翻译的RNA结合蛋白(RBP)。CA1兴奋性海马神经元的突触可塑性依赖于蛋白质合成,这表明FMRP在与FXS相关的突触缺陷中发挥作用。为了探索这一模型,我们开发了Opto-CLIP,将光遗传学与CA1神经元中的细胞类型特异性FMRP-CLIP和RiboTag相结合,从而能够研究活性诱导的FMRP调控。我们追踪了神经元激活30分钟后FMRP结合和核糖体相关RNA谱的变化。我们的研究结果揭示了细胞体与突触中FMRP转录调控的不同时间动态。在细胞体中,FMRP与编码核功能的转录本的结合被解除,这可能允许对神经元激活进行快速转录反应。在突触处,FMRP与编码突触靶点的转录本的结合相对稳定,不同靶点类别的翻译控制存在差异。这些结果为FMRP响应神经元激活对RNA的动态调控提供了新的见解,并为未来研究RBP介导的突触可塑性机制奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b605/11781424/7807273f06f6/nihpp-2024.08.13.607210v2-f0001.jpg

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