Disease relevance of rpoB

• The genes encoding the beta- and beta'-subunits of RNA polymerase (rpoB and rpoC respectively) are fused as one continuous open reading frame in Helicobacter pylori and in other members of this genus, but are separate in other bacterial taxonomic groups, including the closely related genus Campylobacter [1].
• We found the fusion to be specific to Helicobacter and Wolinella genera; rpoB and rpoC overlap in the other genera [2].

High impact information on rpoB

• H. pylori containing these separated rpoB and rpoC genes in place of the native fusion gene produced non-tethered beta and beta' RNAP subunits, grew well in culture and colonized and proliferated well in conventional C57BL/6 mice [1].
• To test whether this beta-beta' tethering is essential, we used polymerase chain reaction-based cloning to separate the rpoB and rpoC moieties of the H. pylori rpoB-rpoC fusion gene with a non-polar chloramphenicol resistance cassette containing a new translational start, and introduced this construct into H. pylori by electro-transformation [1].
• Analysis of spontaneous Rif(r), Cla(r), and Cip(r) mutants confirmed previous results indicating that mutations within the rpoB gene, the 23S rRNA gene, and the gyrA gene, respectively, are responsible; also, several new mutant alleles were identified [3].
• Mutagenesis of the rpoB gene at codon position 701 (R701H) induced low-level resistance [4].
• Geographical differences in the genetic diversity of Helicobacter pylori isolates were examined by analyzing rpoB sequences [5].

Biological context of rpoB

• The fusion may have arisen by a frameshift mutation at the site of rpoB and rpoC overlap [2].

Other interactions of rpoB

• Most of the mutations that occurred in H. pylori mutY mutants, as examined by rpoB sequence changes that confer rifampicin resistance, are GC to TA transversions [6].

References