A second mutant of Escherichia coli B (strain RD-2) with impaired K transport has been isolated with nitro guanidine as the mutagenic agent. Except for its K requirement, RD-2 manifests the same nutritional requirements as the parent strain and contrasts with RD-1, which was shown to be deficient both in K transport and in methionine biosynthesis (1). RD-2 will not grow in a low K media (20 μM. K) Which supports growth of the parent strain? Electron microscopic examination of the two strains reveals no differences in surface layer ultrastructure to account for the transport-t impairment. Potassium accumulation studies demonstrate that the mutant low K growth failure is attributable to a K accumulation impairment. In contrast to the parent strain, RD-2 cannot accumulate K from the low K media. Addition of K to a no accumulating low K suspension of RD-2 stimulates uptake of K, thus establishing viability of the cells. Measurement of low K steady state tracer fluxes yields flux values for RD-2, which are one-third those of the parent strain, and the calculated influx rate constants are consistent with the interpretation that RD-2's accumulation failure is due to influx impairment.
展开▼
