THE EFFECT OF pH ON THE STABILITY OF CIS-ACONITIC ACID IN DILUTE SOLUTION

Ambler, J. A.; Roberts, E. J.

doi:10.1021/jo01161a013

Cited by 27 publications

(20 citation statements)

References 3 publications

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“…1B). If cis-aconitate is released from the enzyme-substrate complex, it can spontaneously be converted to the more stable isomer trans-aconitate (Ambler and Roberts, 1948). Trans-aconitate is an efficient inhibitor of aconitase and if this toxic by-product accumulates, it inhibits the citrate isomerization step (Saffran and Prado, 1949;Lauble et al, 1994;Cai and Clarke, 1999;Cai et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

The transcriptional regulator TamR from Streptomyces coelicolor controls a key step in central metabolism during oxidative stress

Huang

Grove

2013

Molecular Microbiology

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Section: Introductionmentioning

confidence: 99%

The transcriptional regulator TamR from Streptomyces coelicolor controls a key step in central metabolism during oxidative stress

Huang

Grove

2013

Molecular Microbiology

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“…5). It has been speculated that the intracellular trans-aconitate might be generated spontaneously from the cis form because of its instability (28). With regard to trans-aconitate metabolism, two enzymes are known to react with trans-aconitate as the substrate.…”

Section: Discussionmentioning

confidence: 99%

Functional analysis of cis-aconitate decarboxylase and trans-aconitate metabolism in riboflavin-producing filamentous Ashbya gossypii

Sugimoto

Kato

Park

2014

Journal of Bioscience and Bioengineering

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In Ashbya gossypii, isocitrate lyase (ICL1) is a very crucial enzyme for riboflavin production. Itaconate, the inhibitor of ICL1, has been used as an antimetabolite for mutagenic studies in A. gossypii. It has been reported that itaconate is produced from cis-aconitate by cis-aconitate decarboxylase (CAD1) in Aspergillus terreus. In this study, identification of CAD1 gene and determination of the presence of itaconate in the riboflavin biosynthetic pathway in A. gossypii were carried out to confirm itaconate metabolism. Although no CAD1 candidate gene was found and no itaconate production was observed, cis- and trans-aconitate were detected in the riboflavin production phase. It is known that trans-aconitate inhibits aconitase (ACO1) in the tricarboxylic acid cycle. In A. gossypii, the transcription level of AGR110Wp, the homolog of trans-aconitate 3-methyltransferase (TMT1), was enhanced by almost threefold during riboflavin production than that during its growth phase. TMT1 catalyzes the methylation reaction of trans-aconitate in Saccharomyces cerevisiae. Thus, these results suggest that the enhancement of the transcription level of this TMT1 homolog decreases the trans-aconitate level, which may mitigate the inhibition of ACO1 by oxidative stress in the riboflavin biosynthetic pathway in A. gossypii. This is a novel finding in A. gossypii, which may open new metabolic engineering ideas for improving riboflavin productivity.

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“…The TCA cycle enzyme aconitase catalyzes the conversion of citrate to isocitrate via the intermediate formation of cis ‐aconitate. This compound is not always released from the enzyme complex [90], but when released, it is readily converted to the more stable trans ‐aconitate isomer [91,92]. trans ‐Aconitate inhibits the TCA cycle enzyme FH [93,94] and aconitase [95,96].…”

Section: Spontaneous Formation Of Trans‐aconitatementioning

confidence: 99%

Enzyme promiscuity, metabolite damage, and metabolite damage control systems of the tricarboxylic acid cycle

Niehaus

Hillmann

2020

The FEBS Journal

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Promiscuous enzymes and spontaneous chemical reactions can convert normal cellular metabolites into noncanonical or damaged metabolites. These damaged metabolites can be a useless drain on metabolism and may be inhibitory and/or reactive, sometimes leading to toxicity. Thus, mechanisms to prevent metabolite damage from occurring (metabolite damage preemption) or to convert damaged metabolites back to physiological forms (metabolite repair) are essential for sustained operation of metabolic networks. Some iconic examples of metabolite damage and its repair or preemption are associated with the tricarboxylic acid (TCA) cycle, and other metabolite damage control systems are likely to exist here due to the inherent promiscuity of TCA cycle enzymes and reactivity of TCA cycle intermediates. Here, we review known metabolite damage reactions and metabolite damage control systems associated with the TCA cycle. This includes a previously unrecognized metabolite damage control system – an oxaloacetate (OAA) enol‐keto tautomerase activity that is ‘built‐in’ to the TCA cycle. This activity is required to remove the highly inhibitory enol form of OAA and is likely to be critical for TCA cycle operation. By cataloging these instances, we show that metabolite damage and its repair or preemption is a prevalent feature of the TCA cycle and suggest many more metabolite damage control systems are likely to exist.

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THE EFFECT OF pH ON THE STABILITY OF CIS-ACONITIC ACID IN DILUTE SOLUTION

Cited by 27 publications

References 3 publications

The transcriptional regulator TamR from Streptomyces coelicolor controls a key step in central metabolism during oxidative stress

The transcriptional regulator TamR from Streptomyces coelicolor controls a key step in central metabolism during oxidative stress

Functional analysis of cis-aconitate decarboxylase and trans-aconitate metabolism in riboflavin-producing filamentous Ashbya gossypii

Enzyme promiscuity, metabolite damage, and metabolite damage control systems of the tricarboxylic acid cycle

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