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Sphingomyelin metabolism underlies Ras excitability for efficient cell migration and chemotaxis.

Da Young Shin1,2, Hiroaki Takagi2,3, Michio Hiroshima2,4

  • 1Laboratory of Single Molecule Biology, Department of Biological Sciences, Graduate School of Science, Osaka University.

Cell Structure and Function
|July 12, 2023
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Summary

Sphingomyelin metabolism is crucial for Ras excitability, enabling cell motility and chemotaxis. Inhibiting sphingomyelin metabolism disrupts Ras signaling, impairing cell migration and directionality.

Keywords:
Rascell migrationcell polarityexcitabilitysphingomyelin

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Biophysics

Background:

  • Eukaryotic cell motility relies on asymmetric Ras signaling, regulated by intracellular networks.
  • Membrane lipids like sphingomyelin influence Ras signaling, but their role in Ras excitability for cell motility is unclear.

Purpose of the Study:

  • To investigate the role of sphingomyelin metabolism in Ras excitability and cell motility.
  • To determine if sphingomyelin accumulation affects Ras signaling dynamics and cellular functions.

Main Methods:

  • Pharmacological inhibition of sphingomyelin metabolism using fendiline and other inhibitors.
  • Assessing Ras-GTP domain generation, cell motility, and chemotaxis under inhibited conditions.
  • Restoring cell function with exogenous sphingomyelinase or phosphatidylserine.

Main Results:

  • Inhibiting sphingomyelin metabolism suppressed Ras excitability and the formation of Ras-GTP domains.
  • Defects in Ras excitability led to reduced basal motility and impaired directed migration.
  • Sphingomyelin accumulation on the membrane was identified as the cause, reversible by exogenous enzymes.

Conclusions:

  • Normal sphingomyelin metabolism is essential for functional Ras excitability, supporting cell motility and chemotaxis.
  • Membrane lipid environment, specifically sphingomyelin levels, critically regulates Ras signaling dynamics.
  • This study reveals a novel mechanism linking membrane lipid metabolism to cellular excitability and migration.