Previous Article | Next Article ![]()
Journal of Bacteriology, August 1998, p. 4278-4286, Vol. 180, No. 16
Department of Molecular and Cell Biology, The
University of Texas at Dallas, Richardson, Texas 75083-0688
Received 11 September 1997/Accepted 3 June 1998
Arginine catabolism produces ammonia without transferring nitrogen
to another compound, yet the only known pathway of arginine catabolism
in Escherichia coli (through arginine decarboxylase) does
not produce ammonia. Our aims were to find the ammonia-producing pathway of arginine catabolism in E. coli and to examine
its function. We showed that the only previously described pathway of
arginine catabolism, which does not produce ammonia, accounted for only 3% of the arginine consumed. A search for another arginine catabolic pathway led to discovery of the ammonia-producing arginine
succinyltransferase (AST) pathway in E. coli. Nitrogen
limitation induced this pathway in both E. coli and
Klebsiella aerogenes, but the mechanisms of activation
clearly differed in these two organisms. We identified the E. coli gene for succinylornithine aminotransferase, the third enzyme of the AST pathway, which appears to be the first of an astCADBE operon. Its disruption prevented arginine
catabolism, impaired ornithine utilization, and affected the synthesis
of all the enzymes of the AST pathway. Disruption of astB
eliminated succinylarginine dihydrolase activity and prevented arginine
utilization but did not impair ornithine catabolism. Overproduction of
AST enzymes resulted in faster growth with arginine and aspartate. We
conclude that the AST pathway is necessary for aerobic arginine catabolism in E. coli and that at least one enzyme of this
pathway contributes to ornithine catabolism.
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Arginine Catabolism and the Arginine
Succinyltransferase Pathway in Escherichia coli

*
Corresponding author. Mailing address: Department of
Molecular and Cell Biology, Mail Station FO 3.1, The University of
Texas at Dallas, P.O. Box 830688, Richardson, TX 75083-0688. Phone: (972) 883-2523. Fax: (972) 883-2409. E-mail:
reitzer{at}utdallas.edu.
Present address: Department of Biology, University of California at
San Diego, La Jolla, CA 92093-0116.
This article has been cited by other articles:
| Appl. Environ. Microbiol. | Infect. Immun. | Eukaryot. Cell |
|---|---|---|
| Mol. Cell. Biol. | J. Virol. | Microbiol. Mol. Biol. Rev. |
| ALL ASM JOURNALS |