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Cryo-EM structure of ex vivo fibrils associated with extreme AA amyloidosis prevalence in a cat shelter.

Tim SchulteAntonio Chaves-SanjuanGiulia MazziniValentina SperanziniFrancesca LavatelliFilippo FerriCarlo PalizzottoMaria MazzaPaolo MilaniMario NuvoloneAnne-Cathrine VogtMonique VogelGiovanni PalladiniGiampaolo MerliniMartino BolognesiSilvia FerroEric ZiniStefano Ricagno
Published in: Nature communications (2022)
AA amyloidosis is a systemic disease characterized by deposition of misfolded serum amyloid A protein (SAA) into cross-β amyloid in multiple organs in humans and animals. AA amyloidosis occurs at high SAA serum levels during chronic inflammation. Prion-like transmission was reported as possible cause of extreme AA amyloidosis prevalence in captive animals, e.g. 70% in cheetah and 57-73% in domestic short hair (DSH) cats kept in zoos and shelters, respectively. Herein, we present the 3.3 Å cryo-EM structure of AA amyloid extracted post-mortem from the kidney of a DSH cat with renal failure, deceased in a shelter with extreme disease prevalence. The structure reveals a cross-β architecture assembled from two 76-residue long proto-filaments. Despite >70% sequence homology to mouse and human SAA, the cat SAA variant adopts a distinct amyloid fold. Inclusion of an eight-residue insert unique to feline SAA contributes to increased amyloid stability. The presented feline AA amyloid structure is fully compatible with the 99% identical amino acid sequence of amyloid fragments of captive cheetah.
Keyphrases
  • amino acid
  • risk factors
  • climate change
  • multiple myeloma
  • endothelial cells
  • small molecule
  • binding protein
  • protein protein
  • kidney transplantation