Modelling cellular spreading and emergence of motility in the presence of curved membrane proteins and active cytoskeleton forces

TL;DR

This study presents a coarse-grained model showing how curved membrane proteins and active cytoskeleton forces promote vesicle spreading and motility, highlighting mechanisms relevant to cell adhesion and movement.

Contribution

It introduces a simplified model demonstrating how curved proteins and active forces drive cell-like spreading and motility, revealing minimal ingredients for these processes.

Findings

High concentration of curved proteins enhances spreading.

Curved proteins induce protrusive forces leading to lamellipodia formation.

Minimal set of factors can produce motile cell phenotypes.

Abstract

Eukaryotic cells adhere to extracellular matrix during the normal development of the organism, forming static adhesion as well as during cell motility. We study this process by considering a simplified coarse-grained model of a vesicle that has uniform adhesion energy with a flat substrate, mobile curved membrane proteins and active forces. We find that a high concentration of curved proteins alone increases the spreading of the vesicle, by the self-organization of the curved proteins at the high curvature vesicle-substrate contact line, thereby reducing the bending energy penalty at the vesicle rim. This is most significant in the regime of low bare vesicle-substrate adhesion. When these curved proteins induce protrusive forces, representing the actin cytoskeleton, we find efficient spreading, in the form of sheet-like lamellipodia. Finally, the same mechanism of spreading is found to include a minimal set of ingredients needed to give rise to motile phenotypes.