Disease relevance of rpoC

• They are organized in gene clusters in the order above, which corresponds to the order of the homologous rpoB and rpoC genes in the corresponding operon of the Escherichia coli genome [1].
• The role of this hypervariable region was studied by deletion mutagenesis of the cloned E. coli rpoC, encoding beta'. Long deletions mimicking beta' from Gram-positive bacteria failed to assemble into RNAP [2].
• Escherichia coli 397c is temperature sensitive for growth at 43.5 degrees C and unable to plate bacteriophage P2 at 33 degrees C. The mutation conferring these phenotypes was mapped to the rpoC gene [3].
• Salmonella typhimurium rpoB and rpoC genes cloned on lambda phages [4].

High impact information on rpoC

• The terminator for the operon is located on a fragment which spans the 3' end of the rpoC gene [5].
• In these plasmids trpR is positioned between the strong regulated tac promoter and the rpoC transcription terminator [6].
• (3) The antiterminator had less effect on fragments containing Rho-independent terminators; the rpoC t fragment and three fragments derived from the rrnB terminator region stopped antiterminated transcription [7].
• RfaH is also required for the transcription of wild-type levels of mRNA from promoter-distal genes in the rfaQ-K, traY-Z, and rplK-rpoC gene clusters, supporting the role for RfaH in transcriptional elongation [8].
• This has now been confirmed in vitro where the lack of coordinate expression has been shown to be correlated with the selective inhibition of rpoB and rpoC gene expression by RNa polymerase [9].

Biological context of rpoC

• The phenotype of the mutant was dependent on a mutation in the RNA polymerase gene rpoC [10].
• The rpoC deletion and the point mutation cause over 20- and 10-fold reductions, respectively, in the copy number of ColE1 [11].

Analytical, diagnostic and therapeutic context of rpoC

• The locations of four of the eleven rpoB amber mutations that are strongly polar on expression of the downstream rpoC gene have been determined through a combination of MaeI mapping, PCR amplification and DNA sequencing [12].

References