  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.
