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Volume 137, Issue 12

Examination of the role of Na in the physiology of the Na-dependent soil bacterium Free

Abstract

The growth of the Na-dependent soil bacterium strain 184 was inhibited only 36% by 50 μ-carbonyl cyanide -chlorophenylhydrazone (CCCP) at alkaline pH, whereas other species of this genus were inhibited 80–90% under the same conditions. Growth of strain 184 at alkaline pH was inhibited 66% by 50 μ-monensin and 100% by monensin plus CCCP. The majority of the ATPase activity on everted membrane vesicles prepared from strain 184 grown at alkaline pH was sensitive to azide and ,′-dicyclohexylcarbodiimide (DCCD), but ATPase was less sensitive to these inhibitors when Na was present. The respiratory activity of strain 184 was neither dependent on nor activated by Na and was unaffected by the antagonistic Na-analogues K and Rb. A Na -dependent, 2-heptyl-4-hydroxyquinoline -oxide (HQNO) supersensitive NADH oxidase was not present in strain 184. Na was required in the growth medium to promote optimal cell yields. Limiting the amount of Na available caused a lag phase in which cell viability was lost. Viability was maintained by the addition of Li or Mg to Na-limited medium, but only Li appeared to promote growth. K appeared to be a competitive inhibitor of a Na/Li site required for cell growth. Rb was a more complex competitor and affected the final yield and the growth rate of strain 184. Rb-tolerant mutants of strain 184 were selected and the majority of these were found to be defective in the Na-dependent acid excretion normally observed with . . Analysis of an acid over-producing strain showed that Rb appeared to be an uncompetitive inhibitor of Na-dependent growth and in competition with Na as a promoter of acidification.

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© Society for General Microbiology 1991
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1991-12-01
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Examination of the role of Na+ in the physiology of the Na+-dependent soil bacterium Azotobacter salinestris
Microbiology 137, 2891 (1991); https://doi.org/10.1099/00221287-137-12-2891
/content/journal/micro/10.1099/00221287-137-12-2891
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