Journal of Bacteriology, April 1999, p. 2655-2658, Vol. 181, No. 8
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
andUnité de Physiologie Cellulaire, Centre National de la Recherche Scientifique, Unité Recherche Associée 1300, Département des Biotechnologies, Institut Pasteur, 75724 Paris Cedex 15, France
Received 15 October 1998/Accepted 5 February 1999
We herein report that Azorhizobium caulinodans PII and GlnK are not necessary for glutamine synthetase (GS) adenylylation whereas both proteins are required for complete GS deadenylylation. The disruption of both glnB and glnK resulted in a high level of GS adenylylation under the condition of nitrogen fixation, leading to ammonium excretion in the free-living state. PII and GlnK also controlled nif gene expression because NifA activated nifH transcription and nitrogenase activity was derepressed in glnB glnK double mutants, but not in wild-type bacteria, grown in the presence of ammonia.
Present address: Laboratory of Biochemical Engineering, Department
of Chemical Engineering, Stanford University, Stanford, CA 94305-5025.
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 |