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Ninjurin-1 (NINJ1) actively causes plasma membrane rupture (PMR) in cell death by forming filaments that solubilize membranes. Ninjurin-2 (NINJ2) filaments are curved, preventing PMR.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biophysics

Background:

  • Lytic cell death was traditionally considered a passive osmotic lysis event.
  • Ninjurin-1 (NINJ1) is identified as a key mediator of plasma membrane rupture (PMR).
  • Ninjurin-2 (NINJ2), a NINJ1 paralog, does not mediate PMR.

Purpose of the Study:

  • To elucidate the molecular mechanism of NINJ1-mediated PMR.
  • To understand the structural basis for the differing functions of NINJ1 and NINJ2.
  • To investigate the role of filament structure in NINJ1's execution of cell death.

Main Methods:

  • Cryogenic electron microscopy (cryo-EM) to determine filament structures.
  • Biophysical assays to study membrane interaction and solubilization.
  • Mutagenesis studies to probe functional domains and lipid interactions.

Main Results:

  • Both NINJ1 and NINJ2 form linear filaments with distinct hydrophobic and hydrophilic faces.
  • NINJ1 filaments are straight, facilitating membrane wrapping and solubilization or pore formation.
  • NINJ2 filaments are curved due to lipid interactions, preventing assembly and PMR.

Conclusions:

  • NINJ1 actively drives PMR by forming straight filaments that disrupt the plasma membrane.
  • NINJ2's inability to mediate PMR is due to its curved filament structure, influenced by lipid binding.
  • Filament geometry and lipid interactions are critical determinants of NINJ1/NINJ2 function in lytic cell death.