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PubMed1974

Effect of dicyclohexylcarbodiimide on growth and membrane-mediated processes in wild type and heptose-deficient mutants of Escherichia coli K-12.

The effects of N,N'-dicyclohexylcarbodiimide (DCCD) on the growth of Streptococcus faecalis, and on the growth, beta-galactosidase synthesis, and various membrane-mediated processes, were studied in wild-type Escherichia coli JE1011 and its lipopolysaccharide-defective mutant NS1. DCCD (0.1 mM) completely inhibited the growth of S. faecalis and E. coli NS1 but had little effect on strain JE1011. The same amount of DCCD with E. coli NS1, but not with E. coli JE1011, inhibited the induction of beta-galactosidase, increased the permeability of the cells to o-nitrophenyl-beta-d-galactoside without causing extensive cell lysis or release of ultraviolet-absorbing materials, and inhibited the oxidation of certain intermediates of the tricarboxylic acid cycle. Inhibition of the oxidation of malate, fumarate, and alpha-ketoglutarate by DCCD appeared to be at the level of the transport system for these compounds. Inhibition of the membrane-bound adenosine triphosphatase by DCCD was not entirely responsible for these effects, since oxidation of these substances, and transport of [(14)C]succinate and [(14)C]fumarate, was inhibited by DCCD in a mutant, N(144), which lacked adenosine triphosphatase activity. It is concluded that lipopolysaccharide forms a barrier to DCCD in wild-type E. coli, and that DCCD can inhibit several processes in the cell.

Adenosine Triphosphatases↗