Sequence-based identification of amyloidogenic β-hairpins reveals a prostatic acid phosphatase fragment promoting

Laetitia F Heid1, Emil Dandanell Agerschou1, Asuka A Orr2

  • 1Institut für Physikalische Biologie, Heinrich Heine University Düsseldorf, 40204 Düsseldorf, Germany.

Insights

Researchers identified potential amyloid-forming β-hairpin segments in human proteins. These segments, found in proteins linked to diseases like Alzheimer's, promote amyloid formation and could play roles in disease and functional amyloids.

Area of Science:

  • Biochemistry
  • Structural Biology
  • Proteomics

Background:

  • Amyloid fibrils, rich in β-structure, are implicated in neurodegenerative diseases (Alzheimer's, Parkinson's) and type 2 diabetes.
  • While typically parallel β-sheets, anti-parallel β-hairpins are alternative structural motifs in amyloidogenic proteins.

Purpose of the Study:

  • To investigate the role of β-hairpins in amyloid formation.
  • To identify potential β-hairpin-forming amyloidogenic segments within the human proteome.

Main Methods:

  • Bioinformatic prediction of β-hairpin-forming segments based on sequence similarity to known amyloidogenic β-hairpins (Aβ, α-synuclein, IAPP).
  • Utilized criteria including hydrophobic/aromatic amino acid proximity and TANGO aggregation scores.
  • Experimental validation using Thioflavin T assay and Nuclear Magnetic Resonance (NMR) spectroscopy with engineered protein β-wrapin AS10.

Main Results:

  • Identified 2505 potential β-hairpin-forming amyloidogenic segments in 2098 human proteins.
  • Experimental validation confirmed β-hairpin formation in 4 out of 8 tested segments and aggregation into Thioflavin T-positive structures in 7 out of 8.
  • A prostatic acid phosphatase (PAP) segment (185-208) was found to promote nucleation of semen amyloids.

Conclusions:

  • Potential β-hairpin-forming amyloidogenic segments can be identified across the human proteome.
  • These segments may contribute to both functional and disease-related amyloid formation.
  • The findings offer new insights into the structural diversity of amyloidogenesis.