Pathways

Vitamin C (ascorbate) is a vitamin found in food and used as a dietary supplement. The vast majority of animals and plants are able to synthesize vitamin C, through a sequence of enzyme-driven steps, which convert monosaccharides to vitamin C. In plants, this is accomplished through the conversion of mannose or galactose to ascorbic acid starting in the cytosol and ending in the mitochondrial matrix . First, GDP-mannose 3,5-epimerase catalyzes the reversible epimerization of GDP-D-mannose into either GDP-L-gulose or GDP-L-galactose. It also can reversibly epimerize GDP-L-gulose into GDP-L-galactose and vice versa. It requires NAD as a cofactor. Second, GDP-L-galactose phosphorylase catalyzes the conversion of GDP-L-galactose into L-galactose 1-phosphate. Third, L-galactose 1-phosphate phosphatase catalyzes the conversion of L-galactose 1-phosphate into L-galactose. It requires magnesium ion as a cofactor. Fourth, L-galactose dehydrogenase catalyzes the conversion of L-galactose into L-galactono-1,4-lactone. L-galactono-1,4-lactone must then be imported into the mitochondrial matrix by a predicted innermitochondrial membrane transporter to complete ascorbate synthesis. L-galactono-1,4-lactone dehydrogenase, localized to the innermitochondrial membrane (coloured dark green in the image), catalyzes two reactions in ascorbate metabolism: the conversion of L-galactono-1,4-lactone into L-ascorbate and the subsequent conversion of L-ascorbate into L-dehydroascorbate. It requires FAD as a cofactor. Ascorbate can then be converted into monodehydroascorbate radical by the mitochondrial L-ascorbate peroxidase S (this plays a key role in hydrogen peroxide removal). Monodehydroascorbate reductase 5 then can convert monodehydroascorbate radical back into L-ascorbate.

E. coli is able to utilize L-ascorbate (vitamin C) as the sole source of carbon under anaerobic and aerobic conditions. Ascorbic acid in the cytoplasm is processed through a spontaneous reaction with a hydrogen ion and hydrogen peroxide, producing water, dehydroascorbic acid and ascorbic acid. Dehydroascorbic acid reacts with water spontaneously producing an isomer, dehydroascorbate (bicyclic form). The compound then loses a hydrogen ion resulting in a 2,3-Diketo-L-gulonate which is then reduced through a NADH dependent 2,3 diketo-L-gulonate reductase, releasing a NAD and 3-Dehydro-L-gulonate. 3-Dehydro-L-gulonate is phosphorylated through an ATP mediated L-xylulose/3-keto-L-gulonate kinase resulting in an ADP, hydrogen ion and a 3-Keto-L-gulonate 6 phosphate. L-ascorbate can also be imported and converted to L-ascorbate-6-phosphate by the L-ascorbate PTS transporter. L-ascorbate-6-phosphate reacts with a probable L-ascorbate-6-phosphate lactonase ulaG, resulting in a 3-keto-L-gulonate 6-phosphate. The compound 3-keto-L-gulonate 6-phosphate can then be processed aerobically or anaerobically. Aerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by a 3-keto-L-gulonate-6-phosphate decarboxylase ulaD, releasing carbon dioxide and L-xylulose-5-phosphate, which is then changed into an isomer by L-ribulose-5-phosphate 3-epimerase ulaE, resulting in L-ribulose 5-phosphate. The product also changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase ulaF resulting in Xylulose 5-phosphate, which is finally used as part of the pentose phosphate pathway. Anaerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by 3-keto-L-gulonate 6-phosphate decarboxylase sgbH, releasing carbon dioxide and L-xylulose-5-phosphate, which is changed into an isomer by predicted L-xylulose 5-phosphate 3-epimerase, resulting in L-ribulose 5-phosphate. The product again changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase resulting in Xylulose 5-phosphate. Xylulose 5-phosphate then continues as part of the pentose phosphate pathway. Expression of the ula regulon is regulated by the L-ascorbate 6-phosphate-binding repressor UlaR and by cAMP-CRP. Under aerobic conditions, metabolism of L-ascorbate is hindered by the special reactivity and toxicity of this compound in the presence of oxygen.

E. coli is able to utilize L-ascorbate (vitamin C) as the sole source of carbon under anaerobic and aerobic conditions. Ascorbic acid in the cytoplasm is processed through a spontaneous reaction with a hydrogen ion and hydrogen peroxide, producing water, dehydroascorbic acid and ascorbic acid. Dehydroascorbic acid reacts with water spontaneously producing an isomer, dehydroascorbate (bicyclic form). The compound then loses a hydrogen ion resulting in a 2,3-Diketo-L-gulonate which is then reduced through a NADH dependent 2,3 diketo-L-gulonate reductase, releasing a NAD and 3-Dehydro-L-gulonate. 3-Dehydro-L-gulonate is phosphorylated through an ATP mediated L-xylulose/3-keto-L-gulonate kinase resulting in an ADP, hydrogen ion and a 3-Keto-L-gulonate 6 phosphate. L-ascorbate can also be imported and converted to L-ascorbate-6-phosphate by the L-ascorbate PTS transporter. L-ascorbate-6-phosphate reacts with a probable L-ascorbate-6-phosphate lactonase ulaG, resulting in a 3-keto-L-gulonate 6-phosphate. The compound 3-keto-L-gulonate 6-phosphate can then be processed aerobically or anaerobically. Aerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by a 3-keto-L-gulonate-6-phosphate decarboxylase ulaD, releasing carbon dioxide and L-xylulose-5-phosphate, which is then changed into an isomer by L-ribulose-5-phosphate 3-epimerase ulaE, resulting in L-ribulose 5-phosphate. The product also changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase ulaF resulting in Xylulose 5-phosphate, which is finally used as part of the pentose phosphate pathway. Anaerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by 3-keto-L-gulonate 6-phosphate decarboxylase sgbH, releasing carbon dioxide and L-xylulose-5-phosphate, which is changed into an isomer by predicted L-xylulose 5-phosphate 3-epimerase, resulting in L-ribulose 5-phosphate. The product again changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase resulting in Xylulose 5-phosphate. Xylulose 5-phosphate then continues as part of the pentose phosphate pathway. Expression of the ula regulon is regulated by the L-ascorbate 6-phosphate-binding repressor UlaR and by cAMP-CRP. Under aerobic conditions, metabolism of L-ascorbate is hindered by the special reactivity and toxicity of this compound in the presence of oxygen.

E. coli is able to utilize L-ascorbate (vitamin C) as the sole source of carbon under anaerobic and aerobic conditions. Ascorbic acid in the cytoplasm is processed through a spontaneous reaction with a hydrogen ion and hydrogen peroxide, producing water, dehydroascorbic acid and ascorbic acid. Dehydroascorbic acid reacts with water spontaneously producing an isomer, dehydroascorbate (bicyclic form). The compound then loses a hydrogen ion resulting in a 2,3-Diketo-L-gulonate which is then reduced through a NADH dependent 2,3 diketo-L-gulonate reductase, releasing a NAD and 3-Dehydro-L-gulonate. 3-Dehydro-L-gulonate is phosphorylated through an ATP mediated L-xylulose/3-keto-L-gulonate kinase resulting in an ADP, hydrogen ion and a 3-Keto-L-gulonate 6 phosphate. L-ascorbate can also be imported and converted to L-ascorbate-6-phosphate by the L-ascorbate PTS transporter. L-ascorbate-6-phosphate reacts with a probable L-ascorbate-6-phosphate lactonase ulaG, resulting in a 3-keto-L-gulonate 6-phosphate. The compound 3-keto-L-gulonate 6-phosphate can then be processed aerobically or anaerobically. Aerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by a 3-keto-L-gulonate-6-phosphate decarboxylase ulaD, releasing carbon dioxide and L-xylulose-5-phosphate, which is then changed into an isomer by L-ribulose-5-phosphate 3-epimerase ulaE, resulting in L-ribulose 5-phosphate. The product also changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase ulaF resulting in Xylulose 5-phosphate, which is finally used as part of the pentose phosphate pathway. Anaerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by 3-keto-L-gulonate 6-phosphate decarboxylase sgbH, releasing carbon dioxide and L-xylulose-5-phosphate, which is changed into an isomer by predicted L-xylulose 5-phosphate 3-epimerase, resulting in L-ribulose 5-phosphate. The product again changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase resulting in Xylulose 5-phosphate. Xylulose 5-phosphate then continues as part of the pentose phosphate pathway. Expression of the ula regulon is regulated by the L-ascorbate 6-phosphate-binding repressor UlaR and by cAMP-CRP. Under aerobic conditions, metabolism of L-ascorbate is hindered by the special reactivity and toxicity of this compound in the presence of oxygen.

E. coli is able to utilize L-ascorbate (vitamin C) as the sole source of carbon under anaerobic and aerobic conditions. Ascorbic acid in the cytoplasm is processed through a spontaneous reaction with a hydrogen ion and hydrogen peroxide, producing water, dehydroascorbic acid and ascorbic acid. Dehydroascorbic acid reacts with water spontaneously producing an isomer, dehydroascorbate (bicyclic form). The compound then loses a hydrogen ion resulting in a 2,3-Diketo-L-gulonate which is then reduced through a NADH dependent 2,3 diketo-L-gulonate reductase, releasing a NAD and 3-Dehydro-L-gulonate. 3-Dehydro-L-gulonate is phosphorylated through an ATP mediated L-xylulose/3-keto-L-gulonate kinase resulting in an ADP, hydrogen ion and a 3-Keto-L-gulonate 6 phosphate. L-ascorbate can also be imported and converted to L-ascorbate-6-phosphate by the L-ascorbate PTS transporter. L-ascorbate-6-phosphate reacts with a probable L-ascorbate-6-phosphate lactonase ulaG, resulting in a 3-keto-L-gulonate 6-phosphate. The compound 3-keto-L-gulonate 6-phosphate can then be processed aerobically or anaerobically. Aerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by a 3-keto-L-gulonate-6-phosphate decarboxylase ulaD, releasing carbon dioxide and L-xylulose-5-phosphate, which is then changed into an isomer by L-ribulose-5-phosphate 3-epimerase ulaE, resulting in L-ribulose 5-phosphate. The product also changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase ulaF resulting in Xylulose 5-phosphate, which is finally used as part of the pentose phosphate pathway. Anaerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by 3-keto-L-gulonate 6-phosphate decarboxylase sgbH, releasing carbon dioxide and L-xylulose-5-phosphate, which is changed into an isomer by predicted L-xylulose 5-phosphate 3-epimerase, resulting in L-ribulose 5-phosphate. The product again changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase resulting in Xylulose 5-phosphate. Xylulose 5-phosphate then continues as part of the pentose phosphate pathway. Expression of the ula regulon is regulated by the L-ascorbate 6-phosphate-binding repressor UlaR and by cAMP-CRP. Under aerobic conditions, metabolism of L-ascorbate is hindered by the special reactivity and toxicity of this compound in the presence of oxygen.

E. coli is able to utilize L-ascorbate (vitamin C) as the sole source of carbon under anaerobic and aerobic conditions. Ascorbic acid in the cytoplasm is processed through a spontaneous reaction with a hydrogen ion and hydrogen peroxide, producing water, dehydroascorbic acid and ascorbic acid. Dehydroascorbic acid reacts with water spontaneously producing an isomer, dehydroascorbate (bicyclic form). The compound then loses a hydrogen ion resulting in a 2,3-Diketo-L-gulonate which is then reduced through a NADH dependent 2,3 diketo-L-gulonate reductase, releasing a NAD and 3-Dehydro-L-gulonate. 3-Dehydro-L-gulonate is phosphorylated through an ATP mediated L-xylulose/3-keto-L-gulonate kinase resulting in an ADP, hydrogen ion and a 3-Keto-L-gulonate 6 phosphate. L-ascorbate can also be imported and converted to L-ascorbate-6-phosphate by the L-ascorbate PTS transporter. L-ascorbate-6-phosphate reacts with a probable L-ascorbate-6-phosphate lactonase ulaG, resulting in a 3-keto-L-gulonate 6-phosphate. The compound 3-keto-L-gulonate 6-phosphate can then be processed aerobically or anaerobically. Aerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by a 3-keto-L-gulonate-6-phosphate decarboxylase ulaD, releasing carbon dioxide and L-xylulose-5-phosphate, which is then changed into an isomer by L-ribulose-5-phosphate 3-epimerase ulaE, resulting in L-ribulose 5-phosphate. The product also changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase ulaF resulting in Xylulose 5-phosphate, which is finally used as part of the pentose phosphate pathway. Anaerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by 3-keto-L-gulonate 6-phosphate decarboxylase sgbH, releasing carbon dioxide and L-xylulose-5-phosphate, which is changed into an isomer by predicted L-xylulose 5-phosphate 3-epimerase, resulting in L-ribulose 5-phosphate. The product again changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase resulting in Xylulose 5-phosphate. Xylulose 5-phosphate then continues as part of the pentose phosphate pathway. Expression of the ula regulon is regulated by the L-ascorbate 6-phosphate-binding repressor UlaR and by cAMP-CRP. Under aerobic conditions, metabolism of L-ascorbate is hindered by the special reactivity and toxicity of this compound in the presence of oxygen.

E. coli is able to utilize L-ascorbate (vitamin C) as the sole source of carbon under anaerobic and aerobic conditions. Ascorbic acid in the cytoplasm is processed through a spontaneous reaction with a hydrogen ion and hydrogen peroxide, producing water, dehydroascorbic acid and ascorbic acid. Dehydroascorbic acid reacts with water spontaneously producing an isomer, dehydroascorbate (bicyclic form). The compound then loses a hydrogen ion resulting in a 2,3-Diketo-L-gulonate which is then reduced through a NADH dependent 2,3 diketo-L-gulonate reductase, releasing a NAD and 3-Dehydro-L-gulonate. 3-Dehydro-L-gulonate is phosphorylated through an ATP mediated L-xylulose/3-keto-L-gulonate kinase resulting in an ADP, hydrogen ion and a 3-Keto-L-gulonate 6 phosphate. L-ascorbate can also be imported and converted to L-ascorbate-6-phosphate by the L-ascorbate PTS transporter. L-ascorbate-6-phosphate reacts with a probable L-ascorbate-6-phosphate lactonase ulaG, resulting in a 3-keto-L-gulonate 6-phosphate. The compound 3-keto-L-gulonate 6-phosphate can then be processed aerobically or anaerobically. Aerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by a 3-keto-L-gulonate-6-phosphate decarboxylase ulaD, releasing carbon dioxide and L-xylulose-5-phosphate, which is then changed into an isomer by L-ribulose-5-phosphate 3-epimerase ulaE, resulting in L-ribulose 5-phosphate. The product also changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase ulaF resulting in Xylulose 5-phosphate, which is finally used as part of the pentose phosphate pathway. Anaerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by 3-keto-L-gulonate 6-phosphate decarboxylase sgbH, releasing carbon dioxide and L-xylulose-5-phosphate, which is changed into an isomer by predicted L-xylulose 5-phosphate 3-epimerase, resulting in L-ribulose 5-phosphate. The product again changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase resulting in Xylulose 5-phosphate. Xylulose 5-phosphate then continues as part of the pentose phosphate pathway. Expression of the ula regulon is regulated by the L-ascorbate 6-phosphate-binding repressor UlaR and by cAMP-CRP. Under aerobic conditions, metabolism of L-ascorbate is hindered by the special reactivity and toxicity of this compound in the presence of oxygen.

E. coli is able to utilize L-ascorbate (vitamin C) as the sole source of carbon under anaerobic and aerobic conditions. Ascorbic acid in the cytoplasm is processed through a spontaneous reaction with a hydrogen ion and hydrogen peroxide, producing water, dehydroascorbic acid and ascorbic acid. Dehydroascorbic acid reacts with water spontaneously producing an isomer, dehydroascorbate (bicyclic form). The compound then loses a hydrogen ion resulting in a 2,3-Diketo-L-gulonate which is then reduced through a NADH dependent 2,3 diketo-L-gulonate reductase, releasing a NAD and 3-Dehydro-L-gulonate. 3-Dehydro-L-gulonate is phosphorylated through an ATP mediated L-xylulose/3-keto-L-gulonate kinase resulting in an ADP, hydrogen ion and a 3-Keto-L-gulonate 6 phosphate. L-ascorbate can also be imported and converted to L-ascorbate-6-phosphate by the L-ascorbate PTS transporter. L-ascorbate-6-phosphate reacts with a probable L-ascorbate-6-phosphate lactonase ulaG, resulting in a 3-keto-L-gulonate 6-phosphate. The compound 3-keto-L-gulonate 6-phosphate can then be processed aerobically or anaerobically. Aerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by a 3-keto-L-gulonate-6-phosphate decarboxylase ulaD, releasing carbon dioxide and L-xylulose-5-phosphate, which is then changed into an isomer by L-ribulose-5-phosphate 3-epimerase ulaE, resulting in L-ribulose 5-phosphate. The product also changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase ulaF resulting in Xylulose 5-phosphate, which is finally used as part of the pentose phosphate pathway. Anaerobic: 3-keto-L-gulonate 6-phosphate is decarboxylated by 3-keto-L-gulonate 6-phosphate decarboxylase sgbH, releasing carbon dioxide and L-xylulose-5-phosphate, which is changed into an isomer by predicted L-xylulose 5-phosphate 3-epimerase, resulting in L-ribulose 5-phosphate. The product again changes into a different isomer through a L-ribulose-5-phosphate 4-epimerase resulting in Xylulose 5-phosphate. Xylulose 5-phosphate then continues as part of the pentose phosphate pathway. Expression of the ula regulon is regulated by the L-ascorbate 6-phosphate-binding repressor UlaR and by cAMP-CRP. Under aerobic conditions, metabolism of L-ascorbate is hindered by the special reactivity and toxicity of this compound in the presence of oxygen.