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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.
Azorhizobium caulinodans PII
and GlnK Proteins Control Nitrogen Fixation and Ammonia
Assimilation
Nathalie
Michel-Reydellet
and
P. Alexandre
Kaminski*
Unité 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.
*
Corresponding author. Mailing address: Unité de
Biochimie Cellulaire, Département de Biochimie et
Génétique Moléculaire, Institut Pasteur, 28 rue de
Dr. Roux, 75724 Paris Cedex 15, France. Phone: (33) 1 45 68 83 88. Fax:
(33)1 40 61 30 43. E-mail: akaminsk{at}pasteur.fr.

Present address: Laboratory of Biochemical Engineering, Department
of Chemical Engineering, Stanford University, Stanford,
CA 94305-5025.
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.
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