Fibril structures of diabetes-related amylin variants reveal a basis for surface-templated assembly.
Rodrigo U GallardoMatthew G IadanzaYong XuGeorge R HeathRichard FosterSheena E RadfordNeil A RansonPublished in: Nature structural & molecular biology (2020)
Aggregation of the peptide hormone amylin into amyloid deposits is a pathological hallmark of type-2 diabetes (T2D). While no causal link between T2D and amyloid has been established, the S20G mutation in amylin is associated with early-onset T2D. Here we report cryo-EM structures of amyloid fibrils of wild-type human amylin and its S20G variant. The wild-type fibril structure, solved to 3.6-Å resolution, contains two protofilaments, each built from S-shaped subunits. S20G fibrils, by contrast, contain two major polymorphs. Their structures, solved at 3.9-Å and 4.0-Å resolution, respectively, share a common two-protofilament core that is distinct from the wild-type structure. Remarkably, one polymorph contains a third subunit with another, distinct, cross-β conformation. The presence of two different backbone conformations within the same fibril may explain the increased aggregation propensity of S20G, and illustrates a potential structural basis for surface-templated fibril assembly.
Keyphrases
- wild type
- early onset
- structural basis
- high resolution
- late onset
- endothelial cells
- type diabetes
- single molecule
- cardiovascular disease
- magnetic resonance
- copy number
- genome wide
- single cell
- glycemic control
- metabolic syndrome
- dna methylation
- mass spectrometry
- skeletal muscle
- adipose tissue
- weight loss
- climate change
- crystal structure