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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