Structural stability of paired helical filaments requires microtubule-binding domains of tau: a model for self-association

Neuron. 1991 May;6(5):717-28. doi: 10.1016/0896-6273(91)90169-z.

Abstract

Highly purified and SDS-soluble paired helical filaments (PHFs) were immunogold labeled and immunoblotted with antibodies to tau: Tau 14 (N-terminal half), AH-1 (microtubule-binding domain), and Tau 46 (C-terminal end). The main component of PHFs was modified tau of 68, 64, and 60 kd, also called A68 or PHF-tau. Trypsin digestion reduced the maximum width of PHFs by 10%-20%, increased aggregation of filaments, and abolished the binding of Tau 14, but had no effect on the binding of AH-1. The smallest tau-reactive tryptic fragments were 13 and 7-8 kd, positive with AH-1, and negative with Tau 46. Our results and the model of Crowther and Wischik suggest that by self-association and anti-parallel arrangement of the microtubule-binding domains, PHF-tau forms the backbone of PHFs.

Publication types

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

MeSH terms

  • Alzheimer Disease / metabolism
  • Animals
  • Blotting, Western
  • Brain / metabolism
  • Chymotrypsin / metabolism
  • Epitopes
  • Humans
  • Immunohistochemistry
  • Microtubule-Associated Proteins / metabolism*
  • Microtubules / metabolism*
  • Nerve Tissue Proteins / metabolism*
  • Neurofibrils / metabolism*
  • Peptide Fragments / metabolism
  • Trypsin / metabolism
  • tau Proteins

Substances

  • Epitopes
  • Microtubule-Associated Proteins
  • Nerve Tissue Proteins
  • Peptide Fragments
  • tau Proteins
  • Chymotrypsin
  • Trypsin