Disease relevance of acnB

• Transcriptional regulation of the aconitase genes (acnA and acnB) of Escherichia coli [1].
• Aconitase specific activities were amplified up to fivefold by infection with lambdaacnB phages from the Kohara lambda-E. coli gene library, and up to 120-fold (50% of soluble protein) by inducing transformants containing a plasmid (pGS783) in which the acnB coding region is expressed from a regulated T7 promoter [2].

High impact information on acnB

• The acnB lesion did not alter fliC transcription, nor did apo-AcnB select the fliC transcript from a library of S. enterica transcripts; thus, the effect of AcnB on FliC is indirect [3].
• These revealed that the levels of the flagellum protein FliC were much lower for the acnB mutant [3].
• On the basis of the differential expression of the acnA and acnB genes, AcnA has been designated as an aerobic-stationary-phase enzyme that is specifically induced by iron and oxidative stress, whereas AcnB functions as the major citric-acid-cycle enzyme during exponential growth [4].
• Proteomic analyses further revealed that the level of superoxide dismutase (SodA) is enhanced in acnB and acnAB mutants, and by exposure to methyl viologen [5].
• Northern-blot experiments showed expression of acnB under all conditions tested, whereas the RNA of enzymes of the prp operon (PrpE, a propionyl-CoA synthetase, and PrpD) was exclusively present during growth on propionate [6].

Biological context of acnB

• The acnB gene was located at 2 center dot 85 min (131 center dot 6 kb) in a region of the chromosome previously assigned to two unidentified ORFs [2].

Associations of acnB with chemical compounds

• A 2.8 kb acnA monocistronic transcript was detected by Northern blot hybridization, but only in redox-stressed (methyl-viologen-treated) cultures, and a 2.5 kb acnB monocistronic transcript was detected in exponential- but not stationary-phase cultures [1].
• Aerobic and anaerobic growth in glucose minimal medium were impaired but not abolished by the acnB mutation, indicating that the lesion is partially complemented by the acnA+ gene, and growth was enhanced by glutamate [7].

Other interactions of acnB

• These findings are consistent with previous observations that acnA is specifically subject to SoxRS-mediated activation, whereas acnB encodes the major aconitase that is synthesized earlier in the growth cycle than AcnA [1].

Analytical, diagnostic and therapeutic context of acnB

• Affinity chromatography and gel retardation analysis showed that the AcnA and AcnB apo-proteins each interact with the 3' untranslated regions (3'UTRs) of acnA and acnB mRNA at physiologically significant protein concentrations [8].
• Western blotting confirmed that the AcnA and AcnB proteins were no longer produced by the corresponding mutants and PCR analysis showed that the chromosomal acnB gene had been replaced by the disrupted gene [7].

References