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Journal of Bacteriology, August 2002, p. 4636-4639, Vol. 184, No. 16
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.16.4636-4639.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Mutations in the Bacillus subtilis glnRA Operon That Cause Nitrogen Source-Dependent Defects in Regulation of TnrA Activity

Susan H. Fisher* and Lewis V. Wray, Jr.

Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts 02118

Received 28 March 2002/ Accepted 16 May 2002

The Bacillus subtilis nitrogen transcriptional factor TnrA is inactive in cells grown with excess nitrogen, e.g., glutamine or glutamate plus ammonium, because feedback-inhibited glutamine synthetase (product of glnA) binds to TnrA and blocks its DNA-binding activity. Two conditional mutations that allow TnrA-dependent gene expression in cells grown with glutamate plus ammonium, but not in glutamine-grown cells, were characterized. One mutant contained a mutation in the glnA ribosome binding site, while the other mutant synthesized a truncated GlnR protein that constitutively repressed glnRA expression. The levels of glutamine synthetase were reduced in both mutants. As a result, when these mutants are grown with excess nitrogen in the absence of glutamine, there is insufficient production of the feedback inhibitors necessary to convert glutamine synthetase into its feedback-inhibited form and TnrA-activated genes are expressed at high levels.


* Corresponding author. Mailing address: Department of Microbiology, Boston University School of Medicine, 715 Albany St., Boston, MA 02118. Phone: (617) 638-5498. Fax: (617) 638-4286. E-mail: shfisher{at}bu.edu.


Journal of Bacteriology, August 2002, p. 4636-4639, Vol. 184, No. 16
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.16.4636-4639.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




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