Disease relevance of phoB

• The expression of alkaline phosphatase (the product of the phoA gene) in Escherichia coli is believed to be subject to both positive control by the phoB gene product and negative control by the phoR gene product [1].
• Hence, accumulation of polyP requires a functional phoB gene and elevated levels of (p)ppGpp [2].
• To determine if stalk elongation is regulated by the Pho regulon, the Caulobacter phoB gene that encodes the transcriptional activator of the Pho regulon was cloned and mutated [3].

High impact information on phoB

• The synthesis of these proteins is controlled by two genes (the phoB-phoR operon), involving both negative and positive functions [4].
• The phoB gene was cloned and sequenced and in the deduced amino acid sequence two deviations from that of E. coli PhoB were detected [5].
• Using low micromolar concentrations we observed dose- and sequence-dependent inhibition of the reporter gene gfp and endogenous gene phoB [6].
• Together with the DNA sequence of the upstream phoB gene that we determined previously, this region shows the following features [7].
• The plasmid was introduced into various regulatory mutants related to the phosphate regulon, and phoB gene expression in these strains was studied under limited and excess phosphate conditions [8].

Chemical compound and disease context of phoB

• Characterization of the ugp region containing the genes for the phoB dependent sn-glycerol-3-phosphate transport system of Escherichia coli [9].

Biological context of phoB

• (1974) that phoRc mutants represent a cistron (phoB) different from phoR [10].
• The S. meliloti phoB gene was required for the activation of exp gene expression under phosphate limitation, but not for induction of exp expression by MucR or ExpG [11].
• Of a variety of well-characterized Pi transport mutants, only phoB mutants were equally resistant to TeO3(2-), and susceptibility could also be restored in strains carrying an F' plasmid for the phoB region and lost once more after F' curing [12].
• In-frame deletions were generated within the phoB gene, and the phenotypes of the mutants were analyzed [13].
• The fusion gene product interfered with phoB and phoA expression in the phoR mutants [14].

Other interactions of phoB

• The transcriptome profiles of the wild-type and the phoB mutant strains were compared at the time point showing the highest expression levels of the phoB and phoR genes under a P-limiting condition [15].

References