Pearling instability of membrane tubes driven by curved proteins and actin polymerization

TL;DR

This paper investigates how membrane tubes can become unstable and undergo pearling due to the combined effects of curved proteins and actin polymerization, which may lead to vesicle formation.

Contribution

It introduces a theoretical model showing how actin polymerization can induce pearling instability in membrane tubes with curved proteins, suggesting a mechanism for membrane fission.

Findings

Actin polymerization enhances membrane tube instability.

Curved proteins alone tend to stabilize tubes.

Theoretical results relate to in-vivo and in-vitro experiments.

Abstract

Membrane deformation inside living cells is crucial for the proper shaping of various intracellular organelles and is necessary during the fission/fusion processes that allow membrane recycling and transport (e.g. endocytosis). Proteins that induce membrane curvature play a key role in such processes, mostly by adsorbing to the membrane and forming a scaffold that deforms the membrane according to the curvature of the proteins. In this paper we explore the possibility of membrane tube destabilisation through a pearling mechanism enabled by the combined effects of the adsorbed curved proteins and the actin polymerization they may recruit. The pearling instability can furthermore serve as the initiation for fission of the tube into vesicles. We find that adsorbed proteins are more likely to stabilise the tubes, while the actin polymerization can provide the additional constrictive force needed for the robust instability. We discuss the relevance of the theoretical results to in-vivo and in-vitro experiments.