Membrane Mechanics of Endocytosis in Cells with Turgor

TL;DR

This study models the mechanical forces and shapes involved in endocytosis in cells with turgor pressure, revealing how membrane rigidity, curvature, and actin contribute to the process.

Contribution

The paper introduces a physical model of membrane mechanics in endocytosis under turgor pressure, highlighting the roles of curvature and actin in membrane invagination and scission.

Findings

Actin machinery peaks at deformation onset, preventing stalling.

Coat proteins influence curvature but not initiation force.

Isotropic curvature inducers can trigger neck formation.

Abstract

Endocytosis is an essential process by which cells internalize a piece of plasma membrane and material from the outside. In cells with turgor, pressure opposes membrane defor- mations, and increases the amount of force that has to be generated by the endocytic machinery. To determine this force, and calculate the shape of the membrane, we used physical theory to model an elastic surface under pressure. Accurate fits of experimental profiles are obtained assuming that the coated membrane is highly rigid and preferentially curved at the endocytic site. The forces required from the actin machinery peaks at the onset of deformation, indicating that once invagination has been initiated, endocytosis is unlikely to stall before completion. Coat proteins do not lower the initiation force but may affect the process by the curvature they induce. In the presence of isotropic curvature inducers, pulling the tip of the invagination can trigger the formation of a neck at the base of the invagination. Hence direct neck constriction by actin may not be required, while its pulling role is essential. Finally, the theory shows that anisotropic curvature effectors stabilize membrane invaginations, and the loss of crescent-shaped BAR domain proteins such as Rvs167 could therefore trigger membrane scission.