Inhibition of growth by imadazol(on)e propionic acid: Evidence in vivo for coordination of histidine catabolism with the catabolism of other amino acids

Barry R. Bochner, Michael A. Savageau

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Imidazole propionic acid (ipa), a gratuitous inducer of the histidine-utilization (hut) system in Salmonella typhimurium, inhibits the organism's growth on succinate minimal medium. Induction of the hut system is necessary, but not sufficient, to cause inhibition. A study of the ability of single amino acids to relieve ipa-restricted growth suggests that insufficient glutamate is the cause of slow growth. The inhibition of growth by imidazolone propionic acid (iopa), an intermediate in the catabolism of histidine to glutamate, is similar to that by ipa. Studies using 2, 3, 5-triphenyl tetrazolium chloride plates to examine amino acid catabolism suggest that accumulation of ipa or iopa leads to inactivation of aspartate amino-transferase (AAT). This interpretation is supported by studies of an Escherichia coli mutant lacking AAT. The mutant grows poorly on succinate minimal medium, and the poor growth is relieved by the same amino acids that relieve ipa- and iopa-restricted growth. These and other findings are discussed in terms of coordination of the histidine-utilization system with enzymatic activities involved in the catabolism of other amino acids.

Original languageEnglish (US)
Pages (from-to)87-95
Number of pages9
JournalMGG Molecular & General Genetics
Volume168
Issue number1
DOIs
StatePublished - Jan 1979
Externally publishedYes

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Histidine
Amino Acids
Growth
Succinic Acid
Transferases
Aspartic Acid
Glutamic Acid
propionic acid
Salmonella typhimurium
Chlorides
imidazole
Escherichia coli
imidazolone

ASJC Scopus subject areas

  • Genetics

Cite this

Inhibition of growth by imadazol(on)e propionic acid : Evidence in vivo for coordination of histidine catabolism with the catabolism of other amino acids. / Bochner, Barry R.; Savageau, Michael A.

In: MGG Molecular & General Genetics, Vol. 168, No. 1, 01.1979, p. 87-95.

Research output: Contribution to journalArticle

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