Speaker
Description
Interactions between actin filaments and myosin molecular motors generate the forces required for muscle contraction, cell division, and cell movement. The mechanism of contraction is well understood in muscle cells, where actin and myosin adopt a regular sarcomeric structure. In contrast, understanding contractility in the disordered networks of the cell cortex remains an open problem. Non-muscle actomyosin networks can also contain contractile filament bundles, known as stress fibres.
We use a 2D agent-based model to investigate how 4 simplified models for filament turnover (uniform, biased, branching, and treadmilling) influence actomyosin contraction and bundle formation~\cite{Tam2026}. Without turnover, there is negative feedback between bundle formation and contractility. Uniform turnover and branching disrupt bundle formation allowing contraction to persist, whereas treadmilling disrupts the trade-off between bundle formation and contractility. Conversely, biased turnover increases bundle formation and reduces contractility. Our results suggest that cells could tune contractility and bundle formation by varying actin turnover pathways.
Bibliography
@article{Tam2026,
title = {Non-uniform filament turnover, contractility, and bundle formation in disordered actomyosin networks},
author = {Tam, A. K. Y. and Mogilner, A. and Oelz, D. B.},
date = {2026},
journaltitle = {Biophys. J.},
doi = {10.1016/j.bpj.2026.02.032}
}
