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. Author manuscript; available in PMC: 2019 Aug 3.
Published in final edited form as: J Mol Biol. 2018 Apr 5;430(16):2293–2308. doi: 10.1016/j.jmb.2018.03.024

Figure 2.

Figure 2

Protein crowding provides a stochastic driving force for membrane bending and fission. (A) Collisions among membrane-bound proteins densely covering the membrane surface generate steric pressure. The membrane takes on curvature to relieve steric pressure until crowding energy is balanced by the bending energy of the membrane. (B) When wild-type ENTH domain is bound to giant unilamellar vesicles at sufficient coverage, the resulting steric pressure drove membrane tubulation. Image from Stachowiak et al, Nature Cell Biology 2012 [76]. (C) Wild-type ENTH drove membrane fission in addition to membrane curvature, as evidenced by the presence of highly curved membrane tubules (black arrows) and fission vesicles (red arrowheads) after exposure of initially low-curvature vesicles to protein. (D) A version of the ENTH domain lacking the membrane-inserting amphipathic helix (his-ENTH) and recruited to membranes by a histidine-NTA interaction formed highly curved fission vesicles when crowded at membrane surfaces. (E) Histidine-tagged green fluorescent protein (his-GFP) also drove potent membrane fission by protein crowding, despite lacking any structural feature traditionally associated with fission. Data in (C – E) from Snead et al, PNAS 2017 [12].