In response to molecular oxygen and/or fixed nitrogen, the product of
the Klebsiella pneumoniae nitrogen fixation L (nifL) gene inhibits Nif
A-mediated transcriptional activation. Nitrogen regulation of NifL fun
ction occurs at two levels: transcription of the nifLA operon is regul
ated by the general Ntr system, and the activity of NifL is controlled
by an unknown mechanism. We have studied the regulation of NifL activ
ity in Escherichia coli and Salmonella typhimurium by monitoring its i
nhibition of NifA-mediated expression of a K. pneumoniae Phi(nifH'-'la
cZ) fusion. The activity of the NifL protein transcribed from the tac
promoter is regulated well in response to changes of oxygen and/or nit
rogen status, indicating that no nif- or K. pneumoniae-specific produc
t 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 t
hat it is indeed the transcriptional activation capacity of NtrC, rath
er than ifs repression capacity, that is needed, and hence it is a pla
usible hypothesis that Ntr-C activates transcription of a gene(s) whos
e product(s) in term functions to relieve NifL inhibition under nitrog
en-limiting conditions.