Browsing Pathways

Palmitate is synthesized by stepwise condensation of C2 units to a growing acyl chain. Each elongation cycle results in the addition of two carbons to the acyl chain, and consists of four separate reactions. The pathway starts with acetyl-CoA interacting with hydrogen carbonate through an ATP driven acetyl-CoA carboxylase resulting in a phosphate, an ADP , a hydrogen ion and a malonyl-CoA. The latter compound interacts with a holo-[acp] through a malonyl-CoA-ACP transacylase resulting in a CoA and a malonyl-[acp]. This compound interacts with hydrogen ion, acetyl-CoA through a KASIII resulting in a CoA, carbon dioxide and an acetoacetyl-[acp]. The latter compound interacts with a hydrogen ion through a NADPH driven 3-oxoacyl-[acyl-carrier-protein] reductase resulting in an NADP and a (R) 3-Hydroxybutanoyl-[acp](1). This compound is then dehydrated by a 3-hydroxyacyl-[acyl-carrier-protein] dehydratase resulting in the release of water and a crotonyl-[acp](2). The crotonyl-[acp] interacts with a hydrogen ion through a NADH enoyl-[acyl-carrier-protein] reductase(NAD) resulting in NAD and a butyryl-[acp](3). The butyryl-[acp] interacts with a hydrogen ion, a malonyl-[acp] through a KASI resulting in a holo-[acp],carbon dioxide and a 3-oxo-hexanoyl-[acp](4). The 3-oxo-hexanoyl-[acp] interacts with a hydrogen ion through a NADPH driven 3-oxoacyl-[acyl-carrier-protein] reductase resulting in an NADP and a (R) 3-Hydroxyhexanoyl-[acp](1). This compound is then dehydrated by a 3-hydroxyacyl-[acyl-carrier-protein] dehydratase resulting in the release of water and a trans hex-2-enoyl-[acp](2). The trans hex-2-enoyl-[acp] interacts with a hydrogen ion through a NADH enoyl-[acyl-carrier-protein] reductase(NAD) resulting in NAD and a hexanoyl-[acp](3). The hexanoyl-[acp] interacts with a hydrogen ion, a malonyl-[acp] through a KASI resulting in a holo-[acp],carbon dioxide and a 3-oxo-octanoyl-[acp](4). The 3-oxo-octanoyl-[acp] interacts with a hydrogen ion through a NADPH driven 3-oxoacyl-[acyl-carrier-protein] reductase resulting in an NADP and a (R) 3-Hydroxyoctanoyl-[acp](1). This compound is then dehydrated by a 3-hydroxyacyl-[acyl-carrier-protein] dehydratase resulting in the release of water and a trans oct-2-enoyl-[acp](2). The trans oct-2-enoyl-[acp] interacts with a hydrogen ion through a NADH enoyl-[acyl-carrier-protein] reductase(NAD) resulting in NAD and a octanoyl-[acp](3). The octanoyl-[acp] interacts with a hydrogen ion, a malonyl-[acp] through a KASI resulting in a holo-[acp],carbon dioxide and a 3-oxo-decanoyl-[acp](4). The 3-oxo-decanoyl-[acp] interacts with a hydrogen ion through a NADPH driven 3-oxoacyl-[acyl-carrier-protein] reductase resulting in an NADP and a (R) 3-Hydroxydecanoyl-[acp](1). This compound is then dehydrated by a 3-hydroxyacyl-[acyl-carrier-protein] dehydratase resulting in the release of water and a trans-delta2-decenoyl-[acp](2). The a trans-delta2-decenoyl-[acp] interacts with a hydrogen ion through a NADH enoyl-[acyl-carrier-protein] reductase(NAD) resulting in NAD and a decanoyl-[acp](3). The decanoyl-[acp] interacts with a malonyl-[acp] through a KASI resulting in a holo-[acp],carbon dioxide and a 3-oxo-dodecanoyl-[acp](4). The 3-oxo-dodecanoyl-[acp ]interacts with a hydrogen ion through a NADPH driven 3-oxoacyl-[acyl-carrier-protein] reductase resulting in an NADP and a (R) 3-Hydroxydodecanoyl-[acp](1). This compound is then dehydrated by a 3-hydroxyacyl-[acyl-carrier-protein] dehydratase resulting in the release of water and a trans dodec-2-enoyl-[acp](2). The trans dodec-2-enoyl-[acp] interacts with a hydrogen ion through a NADH enoyl-[acyl-carrier-protein] reductase(NAD) resulting in NAD and a dodecanoyl-[acp](3). This compound can either react with water spontaneously resulting in a hydrogen ion, a holo-[acp] and a dodecanoic acid or it interacts with a hydrogen ion, a malonyl-[acp] through a KASI resulting in a holo-[acp],carbon dioxide and a 3-oxo-myristoyl-[acp](4). The 3-oxo-myristoyl-[acp] interacts with a hydrogen ion through a NADPH driven 3-oxoacyl-[acyl-carrier-protein] reductase resulting in an NADP and a (3R) 3-Hydroxymyristoyl-[acp](1). This compound is then dehydrated by a 3-hydroxyacyl-[acyl-carrier-protein] dehydratase resulting in the release of water and a trans tetradec-2-enoyl-[acp](2). This compound interacts with a hydrogen ion, through a NADH-driven KASI resulting in a NAD and a myristoyl-[acp]. Myristoyl-[acp] with a hydrogen ion, a malonyl-[acp] through a KASI resulting in a holo-[acp],carbon dioxide and a 3-oxo-palmitoyl-[acp](4). The 3-oxo-palmitoyl-[acp] interacts with a hydrogen ion through a NADPH driven 3-oxoacyl-[acyl-carrier-protein] reductase resulting in an NADP and a (3R) 3-Hydroxypalmitoyl-[acp](1). This compound is then dehydrated by a 3-hydroxyacyl-[acyl-carrier-protein] dehydratase resulting in the release of water and a trans hexadecenoyl-[acp](2). The trans hexadecenoyl-[acp] interacts with a hydrogen ion through a NADH enoyl-[acyl-carrier-protein] reductase(NAD) resulting in NAD and a palmitoyl-[acp](3). Palmitoyl then reacts with water spontaneously resulting in a hydrogen ion, a holo-[acp] and palmitic acid. No integral membrane protein required for long chain fatty acid uptake has been identified in E. coli. The transport of long chain fatty acids across the cytoplasmic membrane is dependent on fatty acyl-CoA synthetase. An energised membrane is necessary for fatty acid transport and it has been suggested that uncharged fatty acids flip across the inner membrane by diffusion.

L-Carnitine can stimulate anaerobic growth of E.coli when exogenous electron acceptors (i.e. nitrate, etc.) are absent. During anaerobic growth, E.coli can reduce L-carnitine to γ-butyrobetaine by CoA-linked intermediates when carbon and nitrogen are present in the system. Therefore, L-carnitine may act as external electron acceptor for anaerobic growth as well as generation of an osmoprotectant for cell.

Allantoin can be degraded in anaerobic conditions. The first step involves allantoin being degraded by an allantoinase resulting in an allantoate. This compound in turn is metabolized by reacting with water and 2 hydrogen ions through an allantoate amidohydrolase resulting in the release of a carbon dioxide, ammonium and an S-ureidoglycine. The latter compund is further degrades through a S-ureidoglycine aminohydrolase resulting in the release of an ammonium and an S-ureidoglycolate. S-ureidoglycolate can be metabolized into oxalurate by two different reactions. The first reactions involves a NAD driven ureidoglycolate dehydrogenase resulting in the release of a hydrogen ion , an NADH and a oxalurate. On the other hand S-ureidoglycolate can react with NADP resulting in the release of an NADPH, a hydroge ion and an oxalurate. It is hypothesized that oxalurate can interact with a phosphate and release a a carbamoyl phosphate and an oxamate. The carbamoyl phosphate can be further degraded by reacting with an ADP, and a hydrogen ion through a carbamate kinase resulting in the release of an ammonium , ATP and carbon dioxide

The degradation of deoxycytidine starts with deoxycytidine being introduced into the cytosol through either a nupG or nupC symporter. Once inside, it can can be degrade through water,a hydrogen ion and a deoxycytidien deaminsa resultin in the release of a ammonium and a a deoxyuridine. The deoxyuridine is then degraded through a uracil phosphorylase resulting in the release of a deoxyribose 1-phosphate and a uracil. The degradation of thymidine starts with thymidine being introduced into the cytosol through either a nupG or nupC symporter. Thymidine is then degrades through a phosphorylase resulting in the release of a thymine and a deoxyribose 1-phosphate.

The reaction of pyruvate to cytochrome bd terminal oxidase electron transfer starts with 2 pyruvate and 2 water molecules reacting in a pyruvate oxidase resulting in the release of 4 electrons into the inner membrane, and releasing 2 carbon dioxide molecules , 2 acetate and 4 hydrogen ion into the cytosol. 2 ubiquinone,4 hydrogen ion and 4 electron ion react resulting in the release of 2 ubiquinol . The 2 ubiquinol in turn release 4 hydrogen ions into the periplasmic space through a cytochrome bd-I terminal oxidase and releasing 4 electrons through the enzyme. Oxygen and 4 hydrogen ion reacts with the 4 electrons resulting in 2 water molecules.

Ethanolamine, in E. coli, is produced through phospholipid biosynthesis. Once in the cytosol it can be used to produce acetaldehyde by reacting with ethanolamine ammonia-lyase resulting in the release of ammonium and acetaldehyde.

The cyanate degradation pathway begins with the transportation of cyanate into the cytosol through a cynX transporter. Once inside the cytosol cyanate reacts with hydrogen carbonate and a hydrogen ion through a cyanase resulting in the release of carbon dioxide and carbamate. Carbamate reacts spontaneously with hydrogen resulting in the release of ammonium and carbon dioxide. Carbon dioxide reacts with water through carbonic anhydrase resulting in the release of hydrogen ion and hydrogen carbonate.

The mevalonate pathway, also known as the isoprenoid pathway, plays an essential role in creating the chemicals needed for many plants to function. This pathway, combined with the MEP/DOXP pathway give many plants their scents, such as cinnamon and ginger, and are responsible for the red colour in tomatoes. The pathway begins with acetyl-CoA, having come from the glycolysis pathway. Acetyl-CoA immediately becomes acetoacetyl-CoA through the enzyme acetyl-CoA acetyltransferase 1/2. Combined, acetoacetyl-CoA and acetyl-CoA react with hydroxymethylglutaryl-CoA synthase to create 3-hydroxy-3methylglutaryl-CoA. From here, this compound is catalyzed by 3-hydroxy-3-methylglutaryl-coenzyme A reductase 1 and becomes (R)-mevalonate. Mevalonate is paired with mevalonate kinase to produce mevalonic acid-5P. In turn, mevalonic acid-5P reacts with phosphomevalonate kinase, and entering the peroxisome and becoming (R)-mevalonic acid-5-pyrophosphate. Remaining in the peroxisome, diphosphomevalonate decarboxylase MVD1 is used alongside (R)-mevalonic acid-5-pyrophosphate to create isopentenyl pyrophosphate, bringing the pathway into the chloroplast. Dimethylallylpyrophosphate is produced after isopentenyl pyrophosphate and isopentenyl diphosphate delta-isomerase II team up to catalyze it. Dimethylallylpyrophosphate then joins forces with isopentenyl again, this time adding geranylgeranyl pyrophosphate synthase 6 and moving into the mitochondria to produce geranyl-PP. This is followed by monoterpenoid biosynthesis.

The methionine metabolism starts from aspartate-produced homoserine. Homoserine reacts with HSK resulting in the release of O-phospho-L-homoserine. The latter compound interacts with cysteine through CGS resulting in the release of phosphate and cystathionine. The latter compound reacts with COI3 resulting in the release of 2-aminoprop-2-enoate, hydrogen ion and homocysteine. Homocysteine can react with S-adenosyl-L-methionine through a HMT protein complex resulting in the release of methionine. Methionine can be used to generate S-adenosyl-L-methionine or it can generate oxobutanoate

Gibberellins (GAs) are a large class of tetracyclic diterpenoid plant hormones that regulate numerous growth and developmental processes, such as seed germination, organ elongation, and flowering induction. All known gibberellins share an ent-gibberellane skeleton and follow the same synthesis pathway. Biosynthesis begins in the plasmids via the terpenoid pathway and finishes in the endoplasmic reticulum and cytosol where they undergo modification until a biologically-active form is reached (GA1, GA3, GA4, or GA7). Gibberellins are named in the order that they are discovered (GA1 through GAn). Gibberellin biosynthesis via non C-3, non C-13 hydroxylation occurs in the cytosol and converts the inactive GA12 to the active GA4, and inactive GA36 and GA13. The first two reactions are catalyzed by gibberellin 20-oxidase, requiring Fe2+ and L-ascorbate as cofactors. It first converts gibberellin A12 into gibberellin A15 and then into gibberellin A24. Gibberellin A24 has three different fates. The first route involves the conversion of gibberellin A24 into gibberellin A9 by gibberellin 20-oxidase and then the subsequent conversion of gibberellin A9 into the active gibberellin A4 by gibberellin 3-oxidase. It requires Fe2+ and L-ascorbate as cofactors. The second route involves the conversion of gibberellin A24 into gibberellin A36 by gibberellin 3-oxidase. The third route involves the conversion of gibberellin A24 into gibberellin A25 by gibberellin 20-oxidase and then the subsequent conversion of gibberellin A25 into gibberellin A13 by a not yet elucidated gibberellin oxidase (coloured orange in the image).