AI Article Synopsis
- Application of mild shear stress to Dictyostelium discoideum cells leads to active actin cytoskeleton remodeling, enhancing cell movement speed but not directionality.
- External calcium significantly boosts cell speed, with a concentration 10 times higher than what is needed for cell adhesion to surfaces.
- Calcium effects on cell movement are linked to changes in the amplitude, rather than frequency, of cell edge dynamics, and certain mutants show altered responses to calcium.
Article Abstract
Application of hydrodynamic mild shear stress to adherent Dictyostelium discoideum vegetative cells triggers active actin cytoskeleton remodeling resulting in net cell movement along the flow. The average cell speed is strongly stimulated by external calcium (Ca2+, K50%=22 microM), but the directionality of the movement is almost unaffected. This calcium concentration is ten times higher than the one promoting cell adhesion to glass surfaces (K50%=2 microM). Addition of the calcium chelator EGTA or the Ca2+-channel blocker gadolinium (Gd3+) transiently stops cell movement. Monitoring the evolution of cell-surface contact area with time reveals that calcium stimulates cell speed by increasing the amplitude of both protrusion and retraction events at the cell edge, but not the frequency. As a consequence, with saturating external calcium concentrations, cells are sensitive to very low shear forces (20 pN; sigma=0.1 Pa). Moreover, a null-mutant lacking the unique Gbeta subunit does not respond to external Ca2+ changes (K50%>1000 microM), although the directionality of the movement is comparable with that of wild-type cells. Furthermore, cells lacking the inositol 1,4,5-trisphosphate receptor (IP3-receptor) exhibit a markedly reduced Ca2+ sensitivity. Thus, calcium release from internal stores and calcium entry through the plasma membrane modulate cell speed in response to shear stress.
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| http://dx.doi.org/10.1242/jcs.02461 | DOI Listing |
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