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The Ragulator complex and lysosomal calcium release are crucial for cell migration.

Tatsunori Jo1,2,3, Kohei Tsujimoto1,2,3, Takeshi Nakatani1,4

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Lysosomes facilitate immune cell migration by releasing calcium via TRPML1 channels, activating myosin IIA. This process enhances leukocyte trafficking and reduces inflammatory conditions like gouty arthritis and lung injury.

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Area of Science:

  • Cell Biology
  • Immunology
  • Molecular Medicine

Background:

  • Immune cell migration relies on actomyosin contractility driven by myosin IIA activation.
  • The Ragulator complex-MPRIP interaction is vital for this process, but the lysosome's role in myosin IIA activation remains unclear.

Purpose of the Study:

  • To elucidate the mechanism of lysosome-mediated myosin IIA activation in immune cell migration.
  • To investigate the role of the TRPML1 channel and calcium efflux in leukocyte trafficking.

Main Methods:

  • Investigated the interaction between the Ragulator complex, MPRIP, and lysosomes.
  • Utilized TRPML1 channel function and Lamtor1 disruption to study leukocyte migration.
  • Administered ouabain, a cardiac glycoside, to assess its effects on cell migration and inflammatory models.

Main Results:

  • Calcium efflux from the lysosomal TRPML1 channel enhances Ragulator complex-MPRIP interaction, promoting leukocyte trafficking.
  • Disrupting Lamtor1 impairs Ragulator complex lysosomal localization and TRPML1-mediated migration.
  • Ouabain dissociates Lamtor1, inhibits Ragulator complex interaction with myosin IIA, and suppresses cell migration.
  • Ouabain treatment ameliorated gouty arthritis and lung injury in mice by reducing leukocyte infiltration.

Conclusions:

  • Lysosomes, via TRPML1-mediated calcium release, facilitate Ragulator complex and MPRIP interaction, activating myosin IIA and promoting leukocyte migration.
  • Targeting this lysosomal pathway with agents like ouabain shows therapeutic potential for inflammatory diseases.