Key result
The absence of Myo1g decreased cell stiffness, affecting cell adhesion, cell spreading, phagocytosis, and endocytosis in B-lymphocytes.
Myo1g is identified as a key mediator regulating cell stiffness and related cellular processes in B-lymphocytes.
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Myo1g regulates B-lymphocyte mechanics in mice; leaves open any role in human immune disorders.
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.
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López‐Ortega et al. (2016) studied this question. Absence of Myo1g was evaluated on Cell stiffness, cell adhesion, cell spreading, phagocytosis, and endocytosis. The absence of Myo1g decreased cell stiffness, affecting cell adhesion, cell spreading, phagocytosis, and endocytosis in B-lymphocytes.
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