Trpml controls actomyosin contractility and couples migration to phagocytosis in fly macrophages

Sandra Sofía Edwards-Jorquera1, Floris Bosveld2, Yohanns A Bellaïche2

  • 1Centro de Regulación del Genoma, Facultad de Ciencias, Universidad de Chile, Santiago, Chile.

Insights

The lysosomal calcium channel Trpml (Transient Receptor Potential Mucolipin) is crucial for linking immune cell movement and phagocytosis. It controls actomyosin contractility for migration and aids in phagocytic processing near the cell membrane.

Area of Science:

  • Cell Biology
  • Immunology
  • Molecular Biology

Background:

  • Phagocytes, like macrophages, utilize their actomyosin cytoskeleton for migration and engulfing materials (phagocytosis/macropinocytosis).
  • The precise mechanisms coupling cell migration and extracellular material uptake in immune cells remain largely unelucidated.

Purpose of the Study:

  • To identify key molecular players involved in coupling cell locomotion and phagocytosis in Drosophila hemocytes.
  • To elucidate the distinct subcellular roles of identified molecules in migration and phagocytic processing.

Main Methods:

  • Utilized time-lapse imaging to observe cellular dynamics.
  • Employed genetic approaches to investigate gene function in Drosophila hemocytes.

Main Results:

  • Identified the lysosomal calcium channel Trpml (Transient Receptor Potential Mucolipin) as essential for coupling hemocyte migration and phagocytosis.
  • Trpml regulates hemocyte migration via actomyosin contractility at the cell rear.
  • Trpml functions in a myosin-independent manner near the phagocytic cup for phagocytic processing.
  • Vamp7 also influences phagocytic processing and locomotion through distinct pathways.

Conclusions:

  • Trpml plays dual, spatially distinct roles in regulating immune cell migration and phagocytic efficiency.
  • Multiple evolutionary mechanisms likely exist to coordinate phagocytic processing with cell migration for immune surveillance.
  • This study provides novel insights into the molecular basis of immune cell motility and environmental interaction.

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