Open AccessStudies on the roles of GlnK and GlnB in regulating Klebsiella pneumoniae NifL‐dependent nitrogen control
Author(s) -
Arcondéguy Tania,
Heeswijk Wally C.,
Merrick Mike
Publication year - 1999
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.1999.tb08805.x
Subject(s) - klebsiella pneumoniae , intracellular , biology , nitrogen fixation , mutant , escherichia coli , biochemistry , signal transduction , microbiology and biotechnology , activator (genetics) , gene , bacteria , genetics
In Klebsiella pneumoniae , nitrogen fixation ( nif ) genes are regulated in response to fixed nitrogen and oxygen. The activity of the nif ‐specific transcriptional activator NifA is modulated by NifL, which mediates both oxygen and nitrogen control. The signal transduction protein GlnK is required to relieve the inhibitory effect of NifL on NifA that occurs when the intracellular N status is high and in a wild‐type cell, the action of GlnK cannot be substituted by the structurally related protein PII. We have studied the modulation of NifA activity by NifL in an heterologous system in which the host organism is Escherichia coli . Using a Δ glnB ,Δ glnK mutant, we have shown that the modulation of NifA activity by NifL is dependent on the concentration of GlnK in the cell and that when overproduced, PII can substitute for GlnK. Furthermore, our data suggest that PII can counteract the positive action of GlnK in relieving NifL‐dependent inhibition of NifA activity. This negative effect of PII may be physiologically important in establishing repression of nif gene expression when the intracellular nitrogen status rises.