ArticleFrontiers in neural circuits2009
Temporal requirements of the fragile x mental retardation protein in modulating circadian clock circuit synaptic architecture.
Article in Frontiers in neural circuits, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 50 citations in OpenAlex.
- A rapid and dynamic role for FMRP in the plasticity of adult neurons.Nature communications · 2025Article
- Targeting the circadian modulation: novel therapeutic approaches in the management of ASD.Frontiers in psychiatry · 2024Review
- Axonal and presynaptic FMRP: Localization, signal, and functional implications.Hearing research · 2023Review
- Review
- Axonal mRNA localization and translation: local events with broad roles.Cellular and molecular life sciences : CMLS · 2021Review
- Dysregulated CRMP Mediates Circadian Deficits in a Drosophila Model of Fragile X Syndrome.Neuroscience bulletin · 2021Article
- Developmental studies in fragile X syndrome.Journal of neurodevelopmental disorders · 2020Review
- Expression of mutant CHMP2B linked to neurodegeneration in humans disrupts circadian rhythms inFASEB bioAdvances · 2019Article
- Fragile X Mental Retardation Protein positively regulates PKA anchor Rugose and PKA activity to control actin assembly in learning/memory circuitry.Neurobiology of disease · 2019Article
- Iron Deficiency Reduces Synapse Formation in the Drosophila Clock Circuit.Biological trace element research · 2019Article
- Dissecting the Genetics of Autism Spectrum Disorders: AFrontiers in physiology · 2019Review
- Modeling Fragile X Syndrome inFrontiers in molecular neuroscience · 2018Review
- ESCRT-III Membrane Trafficking Misregulation Contributes To Fragile X Syndrome Synaptic Defects.Scientific reports · 2017Article
- Infantile Amnesia: A Critical Period of Learning to Learn and Remember.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Review
- Fragile X Mental Retardation Protein Regulates Activity-Dependent Membrane Trafficking andFrontiers in molecular neuroscience · 2017Review
- The Presynaptic Microtubule Cytoskeleton in Physiological and Pathological Conditions: Lessons from Drosophila Fragile X Syndrome and Hereditary Spastic Paraplegias.Frontiers in molecular neuroscience · 2016Review
- Activity-dependent FMRP requirements in development of the neural circuitry of learning and memory.Development (Cambridge, England) · 2015Article
- Learning and behavioral deficits associated with the absence of the fragile X mental retardation protein: what a fly and mouse model can teach us.Learning & memory (Cold Spring Harbor, N.Y.) · 2014Review
- Oxytocin and vasopressin systems in genetic syndromes and neurodevelopmental disorders.Brain research · 2014Review
- New X-chromosomal interactors of dFMRP regulate axonal and synaptic morphology of brain neurons inBiotechnology, biotechnological equipment · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Loss of fragile X mental retardation 1 (FMR1) gene function is the most common cause of inherited mental retardation and autism spectrum disorders, characterized by attention disorder, hyperactivity and disruption of circadian activity cycles. Pursuit of effective intervention strategies requires determining when the FMR1 product (FMRP) is required in the regulation of neuronal circuitry controlling these behaviors. In the well-characterized Drosophila disease model, loss of the highly conserved dFMRP causes circadian arrhythmicity and conspicuous abnormalities in the circadian clock circuitry. Here, a novel Sholl Analysis was used to quantify over-elaborated synaptic architecture in dfmr1-null small ventrolateral neurons (sLN(v)s), a key subset of clock neurons. The transgenic Gene-Switch system was employed to drive conditional neuronal dFMRP expression in the dfmr1-null mutant background in order to dissect temporal requirements within the clock circuit. Introduction of dFMRP during early brain development, including the stages of neurogenesis, neuronal fate specification and early pathfinding, provided no rescue of dfmr1 mutant phenotypes. Similarly, restoring normal dFMRP expression in the adult failed to restore circadian circuit architecture. In sharp contrast, supplying dFMRP during a transient window of very late brain development, wherein synaptogenesis and substantial subsequent synaptic reorganization (e.g. use-dependent pruning) occur, provided strong morphological rescue to reestablish normal sLN(v)s synaptic arbors. We conclude that dFMRP plays a developmentally restricted role in sculpting synaptic architecture in these neurons that cannot be compensated for by later reintroduction of the protein at maturity.
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Registered trials
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 OpenQuestion graph.