Involved in the catabolism of short chain fatty acids (SCFA) via the tricarboxylic acid (TCA)(acetyl degradation route) and probably via the 2-methylcitrate cycle I (propionate degradation route). Catalyzes the reversible isomerization of citrate to isocitrate via cis-aconitate (PubMed:21984793, PubMed:20647021). Could catalyze the hydration of 2-methyl-cis-aconitate to yield (2R,3S)-2-methylisocitrate. The apo form of AcnA functions as a RNA-binding regulatory protein (By similarity). citrate = D-threo-isocitrate (2S,3R)-3-hydroxybutane-1,2,3-tricarboxylate = 2-methyl-cis-aconitate + H2O Binds 1 [4Fe-4S] cluster per subunit. kcat is 19.6 sec(-1) for aconitase activity with citrate as substrate (at pH 8). kcat is 28.9 sec(-1) for aconitase activity with isocitrate as substrate (at pH 8). kcat is 71 sec(-1) for aconitase activity with cis-aconitate as substrate (at pH 8). Optimum pH is between 7.5 and 7.75. Optimum temperature is 50 degrees Celsius. Carbohydrate metabolism; tricarboxylic acid cycle; isocitrate from oxaloacetate: step 2/2. Organic acid metabolism; propanoate degradation. Monomer. Repressed by AcnR, RipA, GlxR and activated by RamA. Repression by RipA is part of iron homeostasis and serves to reduce the iron demand under iron limitation. The activation of acn transcription by RamA serves to allow the increased carbon flux through the TCA cycle during growth on acetate. GlxR is a global regulator that binds to the acn promoter and presumably represses its transcription in the presence of cyclic AMP (cAMP). Cells lacking this gene are glutamate auxotrophic in glucose minimal medium, show a strong growth defect, and secret large amounts of acetate. Deletion causes a strong selection pressure for secondary mutations within the gltA gene, which might be caused by a growth-inhibitory level of cytoplasmic citrate. Belongs to the aconitase/IPM isomerase family. Extended N-terminus. Extended N-terminus.