Cited by 251Genetics and Neurodevelopmental DisordersNeuroscience and Neuropharmacology ResearchAutism Spectrum Disorder Research

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Disrupted Homer scaffolds mediate abnormal mGluR5 function in a mouse model of fragile X syndrome

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Ronesi, Jennifer A, Collins, Katie A, Hays, Seth A, Tsai, Nien-Pei, Guo, Weirui, Birnbaum, Shari G, Hu, Jia-Hua, Worley, Paul F, Gibson, Jay R, Huber, Kimberly M·2012·Nature Neuroscience

DOI 10.1038/nn.3033PMC PMC3288402

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Abstract

Enhanced metabotropic glutamate receptor subunit 5 (mGluR5) function is causally associated with the pathophysiology of fragile X syndrome, a leading inherited cause of intellectual disability and autism. Here we provide evidence that altered mGluR5-Homer scaffolds contribute to mGluR5 dysfunction and phenotypes in the fragile X syndrome mouse model, Fmr1 knockout (Fmr1(-/y)). In Fmr1(-/y) mice, mGluR5 was less associated with long Homer isoforms but more associated with the short Homer1a. Genetic deletion of Homer1a restored mGluR5-long Homer scaffolds and corrected several phenotypes in Fmr1(-/y) mice, including altered mGluR5 signaling, neocortical circuit dysfunction and behavior. Acute, peptide-mediated disruption of mGluR5-Homer scaffolds in wild-type mice mimicked many Fmr1(-/y) phenotypes. In contrast, Homer1a deletion did not rescue altered mGluR-dependent long-term synaptic depression or translational control of target mRNAs of fragile X mental retardation protein, the gene product of Fmr1. Our findings reveal new functions for mGluR5-Homer interactions in the brain and delineate distinct mechanisms of mGluR5 dysfunction in a mouse model of cognitive dysfunction and autism.

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1 retracted

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Authors: Ronesi, J. A., Collins, K. A., Hays, S. A., Tsai, N.-P., Guo, W., Birnbaum, S. G., Hu, J.-H., Worley, P. F., Gibson, J. R., & Huber, K. M.
Affiliations: The University of Texas Southwestern Medical Center (US)
Johns Hopkins University (US)
Corresponding author: Huber, Kimberly M
ORCID: Collins, Katie A
Hays, Seth A
Tsai, Nien-Pei
Birnbaum, Shari G
Worley, Paul F
Gibson, Jay R
Huber, Kimberly M
Venue: Nature Neuroscience
Publisher: Springer Science and Business Media LLC
Published: 2012-01-22
Volume: 15
Issue: 3
Pages: 431-440
ISSN: 1097-6256 (ISSN-L)
1546-1726
DOI: 10.1038/nn.3033
PMC: PMC3288402
OpenAlex: W2134906491
Cited by: 251
References: 50
Citations by year: 2026: 4 · 2025: 6 · 2024: 9 · 2023: 11 · 2022: 13 · 2021: 16 · 2020: 20 · 2019: 18 · 2018: 17 · 2017: 23 · 2016: 27 · 2015: 21 · 2014: 24 · 2013: 25 · 2012: 16
FWCI: 16.52
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature Neuroscience (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: Autism Speaks (AS2086)
National Institute of General Medical Sciences (GM008203, T32GM008203)
National Institute of Neurological Disorders and Stroke (R01NS045711, NS045711)
Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD052731, HD-052731, HD056370, R01HD056370)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
Keywords: fragile X syndrome, mGluR5, Homer1a, Fmr1 knockout mice, intellectual disability, autism spectrum disorder, synaptic depression, translational regulation, FMRP, cognitive impairment
MeSH terms: Homer Scaffolding Proteins, Analysis of Variance, Animals, Carrier Proteins, Cycloheximide, Disease Models, Animal, Electric Stimulation, Exploratory Behavior, Fragile X Syndrome, Gene Expression Regulation, Hippocampus, Methoxyhydroxyphenylglycol, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Nerve Net, Peptides, Physics, Protein Synthesis Inhibitors, Serine, Signal Transduction, Long-Term Potentiation, Receptors, Metabotropic Glutamate, Patch-Clamp Techniques, Rats, Long-Evans, Immunoprecipitation, Mice, Rats, Fragile X Messenger Ribonucleoprotein 1, TOR Serine-Threonine Kinases, Receptor, Metabotropic Glutamate 5, In Vitro Techniques

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Disrupted Homer scaffolds mediate abnormal mGluR5 function in a mouse model of fragile X syndrome

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