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A coarse-grained model for polyglutamine aggregation modulated by amphipathic flanking sequences.

Kiersten M Ruff¹, Siddique J Khan², Rohit V Pappu²

¹Department of Biomedical Engineering and Center for Biological Systems Engineering, Washington University in St. Louis, St. Louis, Missouri; Division of Biology and Biomedical Sciences, Computational and Systems Biology Program, Washington University in St. Louis, St. Louis, Missouri.

Biophysical Journal

|September 5, 2014

Summary

The N17 sequence in huntingtin protein aggregation reduces interchain entanglements and association barriers. This finding helps explain protein clumping in Huntington

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Area of Science:

Biochemistry
Molecular Biology
Neuroscience

Background:

Protein aggregation with expanded polyglutamine (polyQ) tracts is central to Huntington's disease pathogenesis.
Flanking sequences modulate polyQ aggregation mechanisms, influencing disease progression.

Purpose of the Study:

To investigate the impact of the N17 sequence on polyQ aggregation dynamics.
To rationalize in vitro observations of N17's effects on polyQ aggregation using computational simulations.

Main Methods:

Reanalysis of atomistic simulation data to identify N17's effects on intermolecular association and interchain entanglements.
Development of phenomenological pair potentials incorporating N17's effects.
Coarse-grained Brownian dynamics simulations to study large-scale aggregation.

Main Results:

The N17 module decreases solubility, destabilizes nonfibrillar aggregates, and accelerates fibril formation.
N17 reduces both the frequency of intermolecular association and interchain entanglements between polyQ domains.
In the absence of N17, entanglements lead to distinct timescales for small and large aggregate formation; N17 synchronizes these timescales.

Conclusions:

N17's combined effects of reducing entanglements and introducing association barriers provide a minimalist explanation for observed polyQ aggregation.
Understanding these molecular mechanisms is crucial for developing therapeutic strategies for Huntington's disease.