Affiliation:
1. Department of Biological Chemistry, Harvard Medical School, Boston, Massachusetts
Abstract
Cozzarelli
, N. R. (Harvard Medical School, Boston, Mass.), J. P.
Koch, S. Hayashi, and E. C. C. Lin
. Growth stasis by accumulated
l
-α-glycerophosphate in
Escherichia coli
. J. Bacteriol.
90:
1325–1329.1965.—Cells of
Escherichia coli
K-12 can grow on either glycerol or
l
-α-glycerophosphate as the sole source of carbon and energy. The first step in the dissimilation of glycerol requires a kinase, and the initial process of utilization of
l
-α-glycerophosphate involves an active transport system. In either case, intracellular
l
-α-glycerophosphate is an intermediate whose further metabolism depends upon a dehydrogenase. When this enzyme is lost by mutation, the cells not only fail to grow on glycerol or
l
-α-glycerophosphate, but are subject to growth inhibition in the presence of either compound. Resistance to inhibition by glycerol can be achieved by the loss of glycerol kinase. Such cells are still susceptible to growth inhibition by
l
-α-glycerophosphate. Similarly, in dehydrogenase-deficient cells, immunity to exogenous
l
-α-glycerophosphate can be achieved by genetic blocking of the active transport system. Such cells are still sensitive to free glycerol in the growth medium. Reversal of inhibition by glycerol or
l
-α-glycerophosphate in cells lacking the dehydrogenase can also be brought about by the addition of glucose. Glucose achieves this effect without recourse to catabolite repression. Our results suggest that growth stasis associated with the over-accumulation of
l
-α-glycerophosphate is due to interference with other cellular processes by competition with physiological substrates rather than to depletion of cellular stores of adenosine triphosphate or inorganic phosphate.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
99 articles.
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