Cryo-EM structure of hnRNPDL-2 fibrils, a functional amyloid associated with limb-girdle muscular dystrophy D3

hnRNPDL is a ribonucleoprotein (RNP) involved in transcription and RNA-processing that hosts missense mutations causing limb-girdle muscular dystrophy D3 (LGMD D3). Mammalian-specific alternative splicing (AS) renders three natural isoforms, hnRNPDL-2 being predominant in humans. We present the cryo...

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Detalles Bibliográficos
Autores: Garcia-Pardo, Javier|||0000-0001-9179-6371, Bartolomé-Nafría, Andrea|||0000-0003-3114-1415, Chaves-Sanjuan, Antonio|||0000-0003-3287-9024, Gil-Garcia, Marcos|||0000-0002-7457-7860, Visentin, Cristina|||0000-0003-2705-1417, Bolognesi, Martino|||0000-0002-9253-5170, Ricagno, Stefano|||0000-0001-6678-5873, Ventura, Salvador|||0000-0002-9652-6351
Tipo de recurso: artículo
Fecha de publicación:2023
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:270882
Acceso en línea:https://ddd.uab.cat/record/270882
https://dx.doi.org/urn:doi:10.1038/s41467-023-35854-0
Access Level:acceso abierto
Palabra clave:Cryoelectron microscopy
Alternative splicing
Protein aggregation
Descripción
Sumario:hnRNPDL is a ribonucleoprotein (RNP) involved in transcription and RNA-processing that hosts missense mutations causing limb-girdle muscular dystrophy D3 (LGMD D3). Mammalian-specific alternative splicing (AS) renders three natural isoforms, hnRNPDL-2 being predominant in humans. We present the cryo-electron microscopy structure of full-length hnRNPDL-2 amyloid fibrils, which are stable, non-toxic, and bind nucleic acids. The high-resolution amyloid core consists of a single Gly/Tyr-rich and highly hydrophilic filament containing internal water channels. The RNA binding domains are located as a solenoidal coat around the core. The architecture and activity of hnRNPDL-2 fibrils are reminiscent of functional amyloids, our results suggesting that LGMD D3 might be a loss-of-function disease associated with impaired fibrillation. Strikingly, the fibril core matches exon 6, absent in the soluble hnRNPDL-3 isoform. This provides structural evidence for AS controlling hnRNPDL assembly by precisely including/skipping an amyloid exon, a mechanism that holds the potential to generate functional diversity in RNPs. The authors report the Cryo-EM of hnRNPDL-2 fibrils. The structure highlights features of a functional amyloid associated with limb-girdle muscular dystrophy-3 and explains how alternative splicing controls the assembly of this ribonucleoprotein.