Disease relevance of fixK

• In Rhizobium meliloti, transcription of the key nitrogen-fixation regulatory genes nifA and fixK is induced in response to microaerobiosis through the action of the FixL and FixJ proteins [1].
• In a similar manner to its Escherichia coli crp and fnr homologues, R. meliloti fixK regulates its own expression negatively [2].
• R. leguminosarum bv. viciae possesses a second fnr-like gene, designated fixK, whose encoded gene product is very similar to Rhizobium meliloti and Azorhizobium caulinodans FixK [3].
• The "two-component" FixLJ system activates nitrogen fixation genes via nifA and fixK in Sinorhizobium meliloti [4].
• We describe the cloning, sequencing, regulation, and mutational analysis of a Bradyrhizobium japonicum fixK-like gene whose product belongs to the family of Fnr-Crp-related regulatory proteins [5].

High impact information on fixK

• In addition fixK negatively regulates expression of the nif-specific activator nifA as well as its own expression by autoregulation [6].
• Here we show that the isolated carboxyl-terminal domain of FixJ, FixJC, binds the fixK promoter, whereas binding of the full-length FixJ protein requires its phosphorylation [7].
• Phosphorylation of the Rhizobium meliloti FixJ protein induces its binding to a compound regulatory region at the fixK promoter [7].
• In contrast, those in helices alpha4 and alpha5 constitutively bound to the fixK promoter in a monomeric form, suggesting that the alpha4 and alpha5 helices may be involved in the post-phosphorylation/dimerization signal transfer to liberate the DNA-binding activity of the C-terminal domain, not only serving as a dimerization interface [8].
• One recurrent function of fixK genes in rhizobia is to activate the transcription of operons required for respiration in the microoxic environment of the nodule [2].

Chemical compound and disease context of fixK

• Similar to the situation in Rhizobium meliloti, expression of the fixK gene in B. japonicum was shown to be induced at low O2 tension and this induction was dependent on the two-component regulatory system FixLJ [5].
• A purine-related metabolite negatively regulates fixNOQP expression in Sinorhizobium meliloti by modulation of fixK expression [9].

Biological context of fixK

• Here we use an in vitro transcription system to prove that FixJ is a transcriptional activator of both nifA and fixK and that phosphorylation of FixJ markedly increases its activity [1].
• Dimerization was required for high-affinity binding to fixK promoter DNA [10].
• Molecular genetic analysis of the Rhizobium meliloti fixK promoter: identification of sequences involved in positive and negative regulation [11].
• Individual R. leguminosarum bv. viciae fixK and fixL insertion mutants displayed a Fix+ phenotype [3].
• The fixK-fixL region is located upstream of the fixNOQP operon on the non-nodulation plasmid pRleVF39c [3].

Regulatory relationships of fixK

• A sequence comparison of the -54 to -39 region of nifAp with the upstream sequences of fixKp does not reveal a block of identical nucleotides that could account for the fixJ-dependent microaerobic induction of both promoters [12].

Other interactions of fixK

• Thus nifA and fixK are subject to a mixed regulation, positive (by fixLJ) and negative (by fixK) [6].
• Another orf was identified down-stream of fixK-fixL and encodes a product which has homology to pseudoazurins from different species [3].
• In Sinorhizobium meliloti, the FixL-FixJ couple controls the expression of the nitrogen fixation genes through the binding of the two-domains response regulator FixJ to the fixK and nifA promoters [13].

Analytical, diagnostic and therapeutic context of fixK

• A fixK-lacZ fusion presented 14-fold-reduced induction levels in microaerobic cell cultures in the presence of AICAr [9].

References