The role of membrane tension in clathrin-mediated endocytosis

TITLE:

The role of membrane tension in clathrin-mediated endocytosis

DATE:

Friday, April 22nd, 2016

TIME:

3:30 PM

LOCATION:

GMCS 214

SPEAKER:

Dr. Padmini Rangamani. Assistant Professor in Mechanical Engineering, University of California, San Diego

ABSTRACT:

In clathrin-mediated endocytosis (CME), clathrin and various adaptor proteins coat a patch of the plasma membrane, which is reshaped to

form a budded vesicle. Experimental studies have demonstrated that elevated membrane tension can inhibit bud formation by a clathrin coat. I will

first discuss recent results that show that membrane tension can be heterogeneous along the surface of the membrane and depend on protein

concentration. Then I will discuss the mechanics of membrane budding across a range of membrane tensions by simulating clathrin coats that either

grow in area or progressively induce greater curvature. At low membrane tension, progressively increasing the area of a curvature-generating coat

causes the membrane to smoothly evolve from a flat to budded morphology, whereas the membrane remains essentially flat at high membrane tensions.

Interestingly, at physiologically relevant, intermediate membrane tensions, the shape evolution of the membrane undergoes a ‘’snapthrough

instability” in which increasing coat area causes the membrane to “snap” from an open, U-shaped bud to a closed, √鬩-shaped bud. This instability is

accompanied by a large energy barrier, which could cause a developing endocytic pit to stall if the binding energy of additional coat is insufficient

to overcome this barrier. Similar results were found for a coat of constant area in which the spontaneous curvature progressively increases.

Additionally, we found that a pulling force on the bud, simulating a force from actin polymerization, is sufficient to drive a transition from an

open to closed bud, overcoming the energy barrier opposing this transition.

HOST:

Dr. Parag Katira

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