Open AccessThe effects of extracellular calcium on motility, pseudopod and uropod formation, chemotaxis, and the cortical localization of myosin II in Dictyostelium discoideum
Author(s) -
Lusche Daniel F.,
Wessels Deborah,
Soll David R.
Publication year - 2009
Publication title -
cell motility and the cytoskeleton
Language(s) - English
Resource type - Journals
eISSN - 1097-0169
pISSN - 0886-1544
DOI - 10.1002/cm.20367
Subject(s) - dictyostelium discoideum , extracellular , chemotaxis , biology , motility , microbiology and biotechnology , pseudopodia , myosin , dictyostelium , cytoskeleton , biophysics , actin , cell , biochemistry , receptor , gene
Extracellular Ca ++ , a ubiquitous cation in the soluble environment of cells both free living and within the human body, regulates most aspects of amoeboid cell motility, including shape, uropod formation, pseudopod formation, velocity, and turning in Dictyostelium discoideum . Hence it affects the efficiency of both basic motile behavior and chemotaxis. Extracellular Ca ++ is optimal at 10 mM. A gradient of the chemoattractant cAMP generated in the absence of added Ca ++ only affects turning, but in combination with extracellular Ca ++ , enhances the effects of extracellular Ca ++ . Potassium, at 40 mM, can partially substitute for Ca ++ . Mg ++ , Mn ++ , Zn ++ , and Na + cannot. Extracellular Ca ++ , or K + , also induce the cortical localization of myosin II in a polar fashion. The effects of Ca ++ , K + or a cAMP gradient do not appear to be similarly mediated by an increase in the general pool of free cytosolic Ca ++ . These results suggest a model, in which each agent functioning through different signaling systems, converge to affect the cortical localization of myosin II, which in turn effects the behavioral changes leading to efficient cell motility and chemotaxis. Cell Motil. Cytoskeleton 2009. © 2009 Wiley‐Liss, Inc.