Disease relevance of rpoB

• DNA segments of various sizes, which cover the rifd allele of the rpoB gene, were cloned into lambda vector phages [1].
• Thus, the B. subtilis rpoB region differs from its E. coli counterpart in both genetic and transcriptional organization [2].
• Cloning and physical mapping of the Staphylococcus aureus rplL, rpoB and rpoC genes, encoding ribosomal protein L7/L12 and RNA polymerase subunits beta and beta' [3].
• The resulting protein chip was used to detect the mismatched and unpaired mutations in the synthesized oligonucleotides, as well as a single-base mutation in rpoB gene from Mycobacterium tuberculosis, with high specificity [4].
• Primers were designed to amplify the rpoB gene of Neisseria meningitidis [5].

High impact information on rpoB

• Systematic dissection of a approximately 1 kb fragment determined that the rpoB promoter is contained in a 15-nucleotide segment (-14 to +1) upstream of the transcription initiation site (+1) [6].
• Particular mutations in the rpoB gene were able to suppress negative effects that certain dnaA mutations had on the replication of lambda plasmids; this suppression was allele-specific [7].
• An element that reduces the level of distal gene expression to one-sixth is located on a fragment which spans the rplL-rpoB intercistronic region [8].
• Interaction between mutations of ribosomes and RNA polymerase: a pair of strA and rif mutants individually temperature-insensitive but temperature-sensitive in combination [9].
• Introduction of the nonpermissive rif allele to the permissive strA strain reduces or abolishes the transcription of T7 genome [10].

Chemical compound and disease context of rpoB

• Molecular characterization of rpoB mutations conferring cross-resistance to rifamycins on methicillin-resistant Staphylococcus aureus [11].
• In addition, the expression of some Orf135 mutants in orf135(-) E. coli reduced the level of formation of rpoB mutants elicited by H(2)O(2) [12].
• An isogenic pair of relA+ and relA strains of Escherichia coli B/r with a mutation in the RNA polymerase subunit gene rpoB (Rifr) was isolated in which the relationship between guanosine tetraphosphate (ppGpp) concentration and stable RNA (rRNA, tRNA) gene activity was altered [13].
• Effect of dnaA and rpoB mutations on attenuation in the trp operon of Escherichia coli [14].
• Either a multicopy supply of the rof gene or bicyclomycin, both of which inhibit the transcription termination Rho factor, suppressed the increased sensitivity to oxidative stress of the rifampicin-resistant rpoB mutation in Escherichia coli [15].

Biological context of rpoB

• Both transcriptional (operon) and translational (gene) fusions of either rpoB or rpoC to the lacZ reporter were used to monitor their in vivo expression by inserting single copies of these fusions into the bacterial chromosome on integration-proficient lambda vectors [16].
• The rpoB and rpoC mutants suggested that zwittermicin A might inhibit transcription, DNA replication, DNA gyrase or topoisomerase I; however, we found no further evidence to support any of these as the target for zwittermicin A [17].
• The results suggest that deltapsi drives zwittermicin A uptake, and that, unlike other antibiotics for which resistance maps in rpoB or rpoC, zwittermicin A does not cause the rapid cessation of DNA or RNA synthesis, suggesting a unique mechanism of antibiosis [17].
• Furthermore, experiments with the overexpressing plasmids confirm the requirement for a portion of the rplL-rpoB intercistronic region in the vicinity of the RNaseIII processing site for the efficient translation of the beta subunit mRNA [18].
• A series of transcriptional and translational fusions of the gene for the beta subunit of RNA polymerase (rpoB) to the lacZ reporter gene have been constructed on lambda vectors [18].

Anatomical context of rpoB

• rpoB mutation in Escherichia coli alters control of ribosome synthesis by guanosine tetraphosphate [13].

Associations of rpoB with chemical compounds

• A second class of zwittermicin A-resistant mutants was aminoglycoside sensitive and was affected in rpoB and rpoC, genes that encode subunits of RNA polymerase [17].
• Here, we have shown that the introduction of a certain Rif(r) rpoB mutation into a B. subtilis strain resulted in cells that overproduce an aminosugar antibiotic 3,3'-neotrehalosadiamine (NTD), the production of which is dormant in the wild-type strain [19].
• These three mutations are of particular interest because, unlike rpoB8, they do not increase termination at all rho-dependent and rho-independent terminators. rpoB211 and rpoB212 both change Asn-1072 to His in conserved region H of rpoB (betaN1072H), whereas rpoC214 changes Arg-352 to Cys in conserved region C of rpoC (beta'R352C) [20].
• Two rpoB mutations that suppress the temperature defect of the dnaA46 mutation in initiation of replication were tested for effects on attenuation in the tryptophan operon [14].
• Such strains may contain as many as four or five different mutations, and M. tuberculosis strains that are resistant to both streptomycin and rifampin contain mutations in the rpsL and rpoB genes, respectively [21].

Other interactions of rpoB

• This region is almost certainly equivalent to the rif locus, located near to fus at interval 12/13 on the S. aureus linkage map [3].
• Sequenced spontaneous extragenic suppressors of dksA polyauxotrophy are frequently the same T563P rpoB allele that suppresses a ppGpp(0) phenotype [22].
• The gene was designated coaA and localized between argEH and rpoB near min 90 of the chromosome [23].
• The chloroplast genome contains sequences homologous to the Escherichia coli rpoA, rpoB and rpoC genes [24].
• The second case involves suppression of a temperature-sensitive gyrB mutation by a rifampin-resistant allele of rpoB, the gene encoding the beta subunit of RNA polymerase [25].

Analytical, diagnostic and therapeutic context of rpoB

• Experiments using promoter probe vectors and site-directed mutagenesis located a major rpoB promoter overlapping the 3'-coding region of orf23, 250 nucleotides upstream from the beta initiation codon [2].
• Transformation, via homologous recombination, was demonstrated by DNA sequencing of PCR products containing the three mutations in the Rifr region of rickettsial rpoB [26].
• Complementation tests established that the mutations were in rpoB, the structural gene for the beta subunit of ribonucleic acid polymerase [27].
• Sequence analysis of rpoB, both from these isolates of S. pneumoniae and from two strains of S. mitis, reveals that, among a number of clinical isolates, resistance to rifampicin in S. pneumoniae has arisen by point mutation [28].
• Restriction enzyme analysis indicated that this DNA fragment was located on the B. burgdorferi chromosomal map between rpoB and p22A; its direction of transcription was towards p22A [29].

References