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Myo1g is an active player in maintaining cell stiffness in B‐lymphocytes
Author(s) -
LópezOrtega O.,
OvalleGarcía E.,
OrtegaBlake I.,
Antillón A.,
ChávezMunguía B.,
PatiñoLópez G.,
FragosoSoriano R.,
SantosArgumedo L.
Publication year - 2016
Publication title -
cytoskeleton
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.95
H-Index - 86
eISSN - 1949-3592
pISSN - 1949-3584
DOI - 10.1002/cm.21299
Subject(s) - endocytosis , biology , microbiology and biotechnology , myosin , cytoskeleton , cell membrane , actin , cell , actin cytoskeleton , biochemistry
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.