Abstract
Changes in membrane potential during bacterial chemotaxis were studied by measuring the membrane potential of Escherichia coli indirectly by use of the permeating, lipid-soluble cation triphenylmethylphosphonium. Addition of attractants or repellents to the bacteria caused a hyperpolarizing peak and additional, later changes in membrane potential. This peak was a part of the chemotactic mechanism, because all attractants and repellents tested gave this peak while chemotactically inert chemicals did not; mutants lacking galactose taxis failed to give the peak with galactose but did with another attractant and with repellents; methionine, required for chemotaxis, is also required for production of this peak; a mutant in a control gene (flaI), unable to synthesize flagella and cytoplasmic membrane proteins related to motility and chemotaxis, failed to give the peak; and paralyzed (mot) mutants gave little or none of the peak, while generally nonchemotactic (che) mutants did give this peak. Very likely there are ion fluxes that cause this change in membrane potential. The possible role of the mot gene product as an ion gate controlled by a methylation-demethylation process in response to attractants and repellents acting through their chemoreceptors is discussed.