ArticleiScience2025
FMRP-dependent translational control negatively regulates adapter protein complex 2-mediated endocytosis.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Protocol for identifying surface membrane proteins and their associated proteome from mouse cortical neuron cultures by in situ biotinylation.STAR protocols · 2026Article
- Sex-dependent epigenetic disruption of YY1 binding by prenatal BPA exposure downregulates Matr3 and alters Agap1 splicing in the offspring hippocampus.Biology of sex differences · 2025Article
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Authors and funding
9 authors.
Funding
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Abstract
Fragile X syndrome (FXS), the most common inherited intellectual disability and monogenic cause of autism, results from loss of the protein fragile X messenger ribonucleoprotein (FMRP), which regulates mRNA translation essential for brain development and synaptic plasticity. FMRP has been implicated in the synaptic localization and surface expression of various membrane proteins, yet underlying mechanisms remain unclear. Here, we identified a broad dysregulation of membrane surface and associated proteins in FMRP-deficient neurons by quantitative mass spectrometry. Among them, we found increased steady-state levels of several subunits of the clathrin-adapter protein complex 2 (AP-2), including AP2A1 and AP2B1. We demonstrate that FMRP associates and represses translation of cognate mRNAs. Increased AP-2 in FXS models resulted in enhanced endocytosis of AP-2 cargoes, including dendritic AMPA receptors. These phenotypes were rescued by shRNA downregulation of AP2B1 to wild-type levels in FMRP-deficient neurons. These results reveal a novel translational mechanism controlling adapter dependent protein sorting in neuronal cells.
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Registered trials
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