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In response to molecular oxygen and/or fixed nitrogen, the product of the Klebsiella pneumoniae nitrogen fixation L (nifL) gene inhibits NifA-mediated transcriptional activation. Nitrogen regulation of NifL function occurs at two levels: transcription of the nifLA operon is regulated by the general Ntr system, and the activity of NifL is controlled by an unknown mechanism. We have studied the regulation of NifL activity in Escherichia coli and Salmonella typhimurium by monitoring its inhibition of NifA-mediated expression of a K. pneumoniae phi(nifH'-'lacZ) fusion. The activity of the NifL protein transcribed from the tac promoter is regulated well in response to changes of oxygen and/or nitrogen status, indicating that no nif- or K. pneumoniae-specific product is required. Unexpectedly, strains carrying ntrC (glnG) null alleles failed to release NifL inhibition, despite the fact that synthesis of NifL was no longer under Ntr control. Additional evidence indicated that it is indeed the transcriptional activation capacity of NtrC, rather than its repression capacity, that is needed, and hence it is a plausible hypothesis that NtrC activates transcription of a gene(s) whose product(s) in turn functions to relieve NifL inhibition under nitrogen-limiting conditions.

NtrC is required for control of Klebsiella pneumoniae NifL activity