Calcium-calmodulin dependence of actin accretion and lethality in cultured HEp-2 cells infected with enteropathogenic Escherichia coli

Abstract

Infection of cultured HEp-2 cells with enteropathogenic Escherichia coli causes substantial actin accretion at points of bacterial contact and cell death. Loss of viability was delayed by chelating intracellular free calcium. Actin accretion was partially inhibited by preventing elevation of free cytosolic calcium and prevented by treatment with a calmodulin inhibitor.