GLUCOSE INHIBITION AND THE DIAUXIE PHENOMENON

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Abstract
Salmonella typhimurium, strain LT2 (C+dgs) gives rise to mutants (C-dgs) that are unable to utilize glucose (or other carbohydrates), glycerol, or pyruvate as sole sources of carbon and energy for growth, although they still behave like the parent strain in being able to use various Krebs cycle compounds. Although excellent growth of these mutants occurs in a mineral-citrate medium, the addition of glucose severely inhibits growth. Glucose resistant (dgr) mutants are isolated, which are still unable to use glucose, glycerol, or pyruvate as sole sources of carbon and energy for growth (C-dgr-1). By transduction with phage PLT 22, previously grown on the wild type (C+dgs), it was possible to convert C-dgr-1 to C+dgr-1. A study of the wild type and of these variants has demonstrated the following The glucose inhibition is a ramification of the glucose-citrate diauxie phenomenon exhibited by the wild type, and mutation to glucose resistance is actually mutation to diauxie resistance, when specifically glucose is a member of a pair of compounds to which the wild type exhibits diauxie. The dgr-1 marker in an otherwise wild-type genetic background acts as a modifier, resulting in a lowering of the growth rate specifically with glucose as substrate and causing a 2 to 3-fold increase in activity of an acid phosphatase. Glucose does not inhibit directly the penetration of citrate into the cell, but rather the synthesis of some factor or factors required for citrate "permeation".