ArticleNature communications2025
A rapid and dynamic role for FMRP in the plasticity of adult neurons.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Lasting effects of early-life oxytocin treatment on LTP and episodic memory in a mouse model of Fragile X syndrome.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- RNA-Based Therapeutics in Genetic Neurodevelopmental Disorders: Bridging Molecular Genetics and Precision Medicine.International journal of molecular sciences · 2026Review
- Synaptic targets of circadian clock neurons influence core clock parameters.Science advances · 2025Article
- Synaptic Targets of Circadian Clock Neurons Influence Core Clock Parameters.bioRxiv : the preprint server for biology · 2025Article
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4 authors.
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Abstract
Fragile X syndrome is a neurodevelopmental disorder caused by silencing Fragile X messenger ribonucleoprotein 1 (Fmr1), which encodes the FMRP RNA-binding protein. Although Fmr1 is expressed in adult neurons, it has been challenging to separate acute from chronic effects of loss of Fmr1. Here we use the precision of Drosophila genetics to show that FMRP acutely regulates neuronal plasticity in adult small ventral lateral circadian pacemaker neurons (s-LNvs), which show daily rhythms in their structure. We find that Fmr1 is required for structural plasticity in s-LNvs, and that reducing Fmr1 expression for only 4 hours prevented s-LNv projections from retracting. Conversely, briefly overexpressing Fmr1 blocks the activity-dependent expansion of s-LNv projections without major changes to the circadian clock or to activity-regulated gene expression. One FMRP target we identify in s-LNvs is sif, which encodes a Rac1 Guanine nucleotide exchange factor. Our data suggest that FMRP normally reduces sif mRNA translation at dusk to reduce Rac1 activity and regulate adult neuronal plasticity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.