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Missing-in-metastasis and IRSp53 deform PI(4,5)P2-rich membranes by an inverse BAR domain-like mechanism

Pieta K Mattila1, Anette Pykäläinen, Juha Saarikangas

  • 1Institute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland.

The Journal of Cell Biology
|March 21, 2007
PubMed

Insights

Actin-binding proteins MIM and IRSp53 deform PI(4,5)P(2) membranes into tubules via their IMD, promoting cell motility. This novel membrane-deformation activity is crucial for filopodia formation.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Biophysics

Background:

  • The actin cytoskeleton is essential for cell motility and morphogenesis.
  • Membrane dynamics are critical for these cellular processes.
  • Proteins like MIM and IRSp53 are known to interact with the actin cytoskeleton.

Purpose of the Study:

  • To investigate the role of MIM and IRSp53 in membrane deformation.
  • To elucidate the mechanism by which these proteins induce membrane curvature.
  • To determine the contribution of membrane-deformation activity to filopodia formation.

Main Methods:

  • In vitro membrane-binding and deformation assays.
  • Structural analysis of the IRSp53/MIM domain (IMD).
  • Cell-based assays to observe filopodia/microspike induction.

Main Results:

  • MIM and IRSp53 directly bind PI(4,5)P(2)-rich membranes and induce tubular structures.
  • The N-terminal IRSp53/MIM domain (IMD) is responsible for this membrane-deforming activity.
  • IMDs induce membrane curvature opposite to BAR domains by binding the tubule interior, leading to protrusions.
  • Membrane-deforming activity, not F-actin bundling, is critical for filopodia induction.

Conclusions:

  • MIM and IRSp53 possess a novel membrane-deformation activity mediated by their IMDs.
  • This activity drives plasma membrane protrusions and filopodia formation.
  • The interplay between actin dynamics and IMD-mediated membrane deformation promotes cell motility and morphogenesis.

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