Azorhizobium caulinodans PII and GlnK Proteins Control Nitrogen Fixation and Ammonia Assimilation
AUTOR(ES)
Michel-Reydellet, Nathalie
FONTE
American Society for Microbiology
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=93699Documentos Relacionados
- Characterization of Azorhizobium caulinodans glnB and glnA genes: involvement of the P(II) protein in symbiotic nitrogen fixation.
- Context-Dependent Functions of the PII and GlnK Signal Transduction Proteins in Escherichia coli
- The Escherichia coli signal transducers PII (GlnB) and GlnK form heterotrimers in vivo: Fine tuning the nitrogen signal cascade
- Streptococcus mutans GlnK protein: an unusual PII family member
- Characterization of GlnK1 from Methanosarcina mazei Strain Gö1: Complementation of an Escherichia coli glnK Mutant Strain by GlnK1
