N-terminal acetylation of α-synuclein induces increased transient helical propensity and decreased aggregation rates in the intrinsically disordered monomer

Protein Sci. 2012 Jul;21(7):911-7. doi: 10.1002/pro.2088. Epub 2012 Jun 11.

Abstract

The conformational properties of soluble α-synuclein, the primary protein found in patients with Parkinson's disease, are thought to play a key role in the structural transition to amyloid fibrils. In this work, we report that recombinant 100% N-terminal acetylated α-synuclein purified under mild physiological conditions presents as a primarily monomeric protein, and that the N-terminal acetyl group affects the transient secondary structure and fibril assembly rates of the protein. Residue-specific NMR chemical shift analysis indicates substantial increase in transient helical propensity in the first 9 N-terminal residues, as well as smaller long-range changes in residues 28-31, 43-46, and 50-66: regions in which the three familial mutations currently known to be causative of early onset disease are found. In addition, we show that the N-terminal acetylated protein forms fibrils that are morphologically similar to those formed from nonacetylated α-synuclein, but that their growth rates are slower. Our results highlight that N-terminal acetylation does not form significant numbers of dimers, tetramers, or higher molecular weight species, but does alter the conformational distributions of monomeric α-synuclein species in regions known to be important in metal binding, in association with membranes, and in regions known to affect fibril formation rates.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Acetylation
  • Amyloid / chemistry*
  • Amyloid / metabolism
  • Amyloid / ultrastructure
  • Humans
  • Mass Spectrometry
  • Nuclear Magnetic Resonance, Biomolecular
  • Parkinson Disease / metabolism*
  • Protein Multimerization
  • Protein Structure, Secondary
  • alpha-Synuclein / chemistry*
  • alpha-Synuclein / metabolism
  • alpha-Synuclein / ultrastructure

Substances

  • Amyloid
  • alpha-Synuclein