Myo1g is an active player in maintaining cell stiffness in B-lymphocytes

Cytoskeleton (Hoboken). 2016 May;73(5):258-68. doi: 10.1002/cm.21299. Epub 2016 May 9.

Abstract

B-lymphocytes are migrating cells that specialize in antigen presentation, antibody secretion, and endocytosis; these processes implicate the modulation of plasma membrane elasticity. Cell stiffness is a force generated by the interaction between the actin-cytoskeleton and the plasma membrane, which requires the participation of several proteins. These proteins include class I myosins, which are now considered to play a role in controlling membrane-cytoskeleton interactions. In this study, we identified the motor protein Myosin 1g (Myo1g) as a mediator of this phenomenon. The absence of Myo1g decreased the cell stiffness, affecting cell adhesion, cell spreading, phagocytosis, and endocytosis in B-lymphocytes. The results described here reveal a novel molecular mechanism by which Myo1g mediates and regulates cell stiffness in B-lymphocytes. © 2016 Wiley Periodicals, Inc.

Keywords: B-lymphocyte; cell stiffness; cytoskeleton; myosin.

MeSH terms

  • Actin Cytoskeleton / genetics
  • Actin Cytoskeleton / metabolism*
  • Animals
  • B-Lymphocytes / cytology
  • B-Lymphocytes / metabolism*
  • Cell Adhesion / physiology
  • Cell Membrane / genetics
  • Cell Membrane / metabolism*
  • Endocytosis / physiology*
  • Female
  • Mice
  • Mice, Knockout
  • Minor Histocompatibility Antigens / genetics
  • Minor Histocompatibility Antigens / metabolism*
  • Myosins / genetics
  • Myosins / metabolism*
  • Phagocytosis / physiology*

Substances

  • Minor Histocompatibility Antigens
  • Myo1g protein, mouse
  • Myosins