Disease relevance of acnA

• Transcriptional regulation of the aconitase genes (acnA and acnB) of Escherichia coli [1].
• The tricarboxylic acid (TCA) cycle aconitase gene acnA from Streptomyces viridochromogenes Tü494 was cloned and analyzed [2].
• Phages containing the acn gene were isolated from a lambda-E. coli gene bank by immunoscreening with an antiserum raised against purified bacterial enzyme [3].

High impact information on acnA

• This strain was correspondingly less motile and possessed fewer flagella than either the parental strain or the acnA and acnAB mutants [4].
• 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 [5].
• AcnA catalyzes the isomerization of citrate to isocitrate in the TCA cycle, as indicated by the ability of acnA to complement the aconitase-deficient Escherichia coli mutant JRG3259 [2].
• An acnA mutant was unable to develop aerial mycelium and to sporulate, resulting in a bald phenotype [2].
• Inactivation of prpD abolished the residual aconitase activity of an AcnAB-null strain, whereas inactivation of ybhJ, an unidentified acnA paralogue, had no significant effect on AcnC activity [6].

Chemical compound and disease context of acnA

• Here it is shown that E. coli acn mutants are hypersensitive to the redox-stress reagents H(2)O(2) and methyl viologen [7].

Biological context of acnA

• In the study described here, an overexpression promoter (pBAD promoter) and two comparatively weak promoters (sodA and acnA in Escherichia coli SoxRS regulon) were studied in both endpoint and kinetics formats [8].
• The acn gene was located at 28 min (1350 kb) in the physical map of the E. coli chromosome by probing Southern blots with a fragment of the gene [3].

Associations of acnA 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 [9].

Regulatory relationships of acnA

• In addition to being activated by the SoxRS oxidative stress regulatory system, the acnA gene appeared to be activated by the ferric uptake regulator (Fur) [10].

Other interactions of acnA

• 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].
• Enzymological and regulatory studies with acn-lacZ fusions indicated that AcnB is the major aconitase, which is synthesized earlier in the growth cycle than AcnA, and subject to catabolite and anaerobic repression [9].
• Two transposon mutants with increased susceptibility to POA were found to harbor mutations in acnA encoding aconitase-1 and ygiY encoding a putative two-component sensor protein [11].

Analytical, diagnostic and therapeutic context of acnA

• Southern and Western blotting confirmed that the acnA gene had been replaced by the disrupted gene and that the aconitase A protein was no longer expressed [10].
• The aconitase of Escherichia coli: purification of the enzyme and molecular cloning and map location of the gene (acn) [3].

References