A plug release mechanism for membrane permeation by MLKL

Structure. 2014 Oct 7;22(10):1489-500. doi: 10.1016/j.str.2014.07.014. Epub 2014 Sep 11.

Abstract

MLKL is crucial for necroptosis, permeabilizing membranes through its N-terminal region upon phosphorylation of its kinase-like domain by RIP3. However, the mechanism underlying membrane permeabilization is unknown. The solution structure of the MLKL N-terminal region determined by nuclear magnetic resonance spectroscopy reveals a four-helix bundle with an additional helix at the top that is likely key for MLKL function, and a sixth, C-terminal helix that interacts with the top helix and with a poorly packed interface within the four-helix bundle. Fluorescence spectroscopy measurements indicate that much of the four-helix bundle inserts into membranes, but not the C-terminal helix. Moreover, we find that the four-helix bundle is sufficient to induce liposome leakage and that the C-terminal helix inhibits this activity. These results suggest that the four-helix bundle mediates membrane breakdown during necroptosis and that the sixth helix acts as a plug that prevents opening of the bundle and is released upon RIP3 phosphorylation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Membrane / chemistry
  • Cell Membrane / metabolism*
  • Humans
  • Models, Molecular
  • Mutation
  • Nuclear Magnetic Resonance, Biomolecular
  • Permeability
  • Phosphorylation
  • Protein Conformation
  • Protein Kinases / chemistry*
  • Protein Kinases / genetics
  • Protein Kinases / metabolism*
  • Spectrometry, Fluorescence

Substances

  • MLKL protein, human
  • Protein Kinases

Associated data

  • PDB/2MSV