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CORRECTION OF EIF4E OVERACTIVATION RESCUES TRANSLATOME IMBALANCE AND CORE ASD-LIKE BEHAVIORS IN VALPROIC ACID-INDUCED OFFSPRING MICE
Miaoqi Huangand 5 co-authors
Jinan University
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-292
Presentation
Date TBA
Board: PS02-07PM-292
Event Information
Poster Board
PS02-07PM-292
Poster
View posterAbstract
Perturbed protein synthesis is increasingly implicated in the pathogenesis of autism spectrum disorder (ASD), yet alterations in translational patterns and their underlying mechanisms remain unclear. In a mouse model of ASD based on prenatal valproic acid (VPA) exposure, we observed exaggerated global protein synthesis in the offspring cerebral cortex. Integrated polyribosome-based translatome and proteome analyses revealed marked upregulation of ribosomal and mitochondrial proteins without corresponding transcriptional changes, indicating translational dysregulation. We further identified hyperactivation of the eukaryotic translation initiation factor 4E (eIF4E) as the key driver of this aberrant translatome and the associated mitochondrial dysfunction. Notably, pharmacological inhibition of eIF4E phosphorylation during the juvenile period persistently alleviated ASD-like social deficits and stereotyped behaviors into adulthood. These findings establish that eIF4E overactivation disrupts proteostasis by preferentially enhancing the translation of mRNAs encoding ribosomal and mitochondrial proteins, thereby contributing to the core behavioral phenotypes of ASD.
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