TY - JOUR
AU - Hasecke, Filip
AU - Miti, Tatiana
AU - Perez, Carlos
AU - Barton, Jeremy
AU - Schölzel, Daniel
AU - Gremer, Lothar
AU - Grüning, Clara S. R.
AU - Matthews, Garrett
AU - Meisl, Georg
AU - Knowles, Tuomas P. J.
AU - Willbold, Dieter
AU - Neudecker, Philipp
AU - Heise, Henrike
AU - Ullah, Ghanim
AU - Hoyer, Wolfgang
AU - Muschol, Martin
TI - Origin of metastable oligomers and their effects on amyloid fibril self-assembly
JO - Chemical science
VL - 9
IS - 27
SN - 2041-6539
CY - Cambridge
PB - RSC
M1 - FZJ-2018-07275
SP - 5937 - 5948
PY - 2018
AB - Assembly of rigid amyloid fibrils with their characteristic cross-β sheet structure is a molecular signature of numerous neurodegenerative and non-neuropathic disorders. Frequently large populations of small globular amyloid oligomers (gOs) and curvilinear fibrils (CFs) precede the formation of late-stage rigid fibrils (RFs), and have been implicated in amyloid toxicity. Yet our understanding of the origin of these metastable oligomers, their role as on-pathway precursors or off-pathway competitors, and their effects on the self-assembly of amyloid fibrils remains incomplete. Using two unrelated amyloid proteins, amyloid-β and lysozyme, we find that gO/CF formation, analogous to micelle formation by surfactants, is delineated by a “critical oligomer concentration” (COC). Below this COC, fibril assembly replicates the sigmoidal kinetics of nucleated polymerization. Upon crossing the COC, assembly kinetics becomes biphasic with gO/CF formation responsible for the lag-free initial phase, followed by a second upswing dominated by RF nucleation and growth. RF lag periods below the COC, as expected, decrease as a power law in monomer concentration. Surprisingly, the build-up of gO/CFs above the COC causes a progressive increase in RF lag periods. Our results suggest that metastable gO/CFs are off-pathway from RF formation, confined by a condition-dependent COC that is distinct from RF solubility, underlie a transition from sigmoidal to biphasic assembly kinetics and, most importantly, not only compete with RFs for the shared monomeric growth substrate but actively inhibit their nucleation and growth.
LB - PUB:(DE-HGF)16
C6 - pmid:30079208
UR - <Go to ISI:>//WOS:000438391900009
DO - DOI:10.1039/C8SC01479E
UR - https://juser.fz-juelich.de/record/858389
ER -