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J Bacteriol. 1974 June; 118(3): 1090-1100
Copyright © 1974 American Society for Microbiology. All Rights Reserved.

Phenotypic Suppression of Phosphofructokinase Mutations in Escherichia coli by Constitutive Expression of the Glyoxylate Shunt

^a Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115

ABSTRACT

Fructose-6-phosphate kinase (pfkA) mutants have impaired growth on carbon sources which enter glycolysis at or above the level of fructose-6-phosphate, but the degree of impairment depends on the carbon source (e.g., growth on glucose is very much slower than growth on glucose-6-phosphate). The present report contains considerable data on this complicated growth phenotype and derives mainly from the finding of a class of partial revertants which grow as fast on glucose as on glucose-6-phosphate; the reversion mutation is shown to be constitutivity of the glyoxylate shunt (iclR^c). iclR^c does not increase the fructose-6-phosphate kinase level in the mutants, and the exact mechanism of the partial phenotypic suppression is not understood. However, iclR^c was already known to suppress some mutations which affected phosphoenolpyruvate levels, and H. L. Kornberg and J. Smith have suggested (1970) that the growth phenotype of pfkA mutants might be related to pathways of phosphoenolpyruvate formation. Surprisingly, the hexose-monophosphate shunt is not necessary for the suppression, which therefore must act to restore metabolism via the residual phosphofructokinase activity present in all pfkA mutants. A mutant totally lacking phosphofructokinase activity was not suppressed.

¹ Present address: Microbiology Section, Biological Sciences Group, University of Connecticut, Storrs, Conn. 06268.

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