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7.10: Evolution of Metabolism

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    Many models have been proposed to describe the mechanisms by which novel metabolic pathways evolve. These include the sequential addition of novel enzymes to a short ancestral pathway, the duplication and then divergence of entire pathways as well as the recruitment of pre-existing enzymes and their assembly into a novel reaction pathway. [1] The relative importance of these mechanisms is unclear, but genomic studies have shown that enzymes in a pathway are likely to have a shared ancestry, suggesting that many pathways have evolved in a step-by-step fashion with novel functions created from pre-existing steps in the pathway.[2] An alternative model comes from studies that trace the evolution of proteins' structures in metabolic networks, this has suggested that enzymes are pervasively recruited, borrowing enzymes to perform similar functions in different metabolic pathways (evident in the MANET database).[3] These recruitment processes result in an evolutionary enzymatic mosaic. [4]. A third possibility is that some parts of metabolism might exist as "modules" that can be reused in different pathways and perform similar functions on different molecules.[5].

    As well as the evolution of new metabolic pathways, evolution can also cause the loss of metabolic functions. For example, in some parasites metabolic processes that are not essential for survival are lost and preformed amino acids, nucleotides and carbohydrates may instead be scavenged from the host [6]. Similar reduced metabolic capabilities are seen in endosymbiotic organisms. [7]

    A striking feature of metabolism is the similarity of the basic metabolic pathways among vastly different species[8]. For example, the set of carboxylic acids that are best known as the intermediates in the citric acid cycle are present in all known organisms, being found in species as diverse as the unicellular bacterium Escherichia coli and huge multicellular organisms like elephants.[9]. These similarities in metabolic pathways are likely due to their early appearance in evolutionary history, and their retention is likely due to their efficacy.[10,11]. In various diseases, such as type II diabetes, metabolic syndrome, and cancer, normal metabolism is disrupted.[12]. The metabolism of cancer cells is also different from the metabolism of normal cells, and these differences can be used to find targets for therapeutic intervention in cancer.[13]

    Excerpted from Wikipedia: Metabolism Accessed 14. November 2023


    1.  Schmidt S, Sunyaev S, Bork P, Dandekar T (June 2003). "Metabolites: a helping hand for pathway evolution?". Trends in Biochemical Sciences28 (6): 336–41. doi:10.1016/S0968-0004(03)00114-2PMID 12826406.
    2. ^ Light S, Kraulis P (February 2004). "Network analysis of metabolic enzyme evolution in Escherichia coli"BMC Bioinformatics5: 15. doi:10.1186/1471-2105-5-15PMC 394313PMID 15113413. Alves R, Chaleil RA, Sternberg MJ (July 2002). "Evolution of enzymes in metabolism: a network perspective". Journal of Molecular Biology320 (4): 751–70. doi:10.1016/S0022-2836(02)00546-6PMID 12095253.
    3. ^ Kim HS, Mittenthal JE, Caetano-Anollés G (July 2006). "MANET: tracing evolution of protein architecture in metabolic networks"BMC Bioinformatics7: 351. doi:10.1186/1471-2105-7-351PMC 1559654PMID 16854231.
    4. ^ Teichmann SA, Rison SC, Thornton JM, Riley M, Gough J, Chothia C (December 2001). "Small-molecule metabolism: an enzyme mosaic". Trends in Biotechnology19 (12): 482–6. doi:10.1016/S0167-7799(01)01813-3PMID 11711174.
    5. ^ Spirin V, Gelfand MS, Mironov AA, Mirny LA (June 2006). "A metabolic network in the evolutionary context: multiscale structure and modularity"Proceedings of the National Academy of Sciences of the United States of America103 (23): 8774–9.  Bibcode:2006PNAS..103.8774Sdoi:10.1073/pnas.0510258103PMC 1482654PMID 16731630.
    6. ^ Lawrence JG (December 2005). "Common themes in the genome strategies of pathogens". Current Opinion in Genetics & Development15 (6): 584–8. doi:10.1016/j.gde.2005.09.007PMID 16188434. Wernegreen JJ (December 2005). "For better or worse: genomic consequences of intracellular mutualism and parasitism". Current Opinion in Genetics & Development15 (6): 572–83. doi:10.1016/j.gde.2005.09.013PMID 16230003.
    7. ^ Pál C, Papp B, Lercher MJ, Csermely P, Oliver SG, Hurst LD (March 2006). "Chance and necessity in the evolution of minimal metabolic networks". Nature440 (7084): 667–70. Bibcode:2006Natur.440..667Pdoi:10.1038/nature04568PMID 16572170S2CID 4424895.
    8.  Pace NR (January 2001). "The universal nature of biochemistry"Proceedings of the National Academy of Sciences of the United States of America98 (3): 805–8. Bibcode:2001PNAS...98..805Pdoi:10.1073/pnas.98.3.805PMC 33372PMID 11158550.
    9. Smith E, Morowitz HJ (September 2004). "Universality in intermediary metabolism"Proceedings of the National Academy of Sciences of the United States of America101 (36): 13168–73. Bibcode:2004PNAS..10113168Sdoi:10.1073/pnas.0404922101PMC 516543PMID 15340153.
    10. Ebenhöh O, Heinrich R (January 2001). "Evolutionary optimization of metabolic pathways. Theoretical reconstruction of the stoichiometry of ATP and NADH producing systems". Bulletin of Mathematical Biology63 (1): 21–55. doi:10.1006/bulm.2000.0197PMID 11146883S2CID 44260374.
    11. Meléndez-Hevia E, Waddell TG, Cascante M (September 1996). "The puzzle of the Krebs citric acid cycle: assembling the pieces of chemically feasible reactions, and opportunism in the design of metabolic pathways during evolution". Journal of Molecular Evolution43 (3): 293–303. Bibcode:1996JMolE..43..293Mdoi:10.1007/BF02338838PMID 8703096S2CID 19107073.
    12. Smith RL, Soeters MR, Wüst RC, Houtkooper RH (August 2018). "Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease"Endocrine Reviews39 (4): 489–517. doi:10.1210/er.2017-00211PMC 6093334PMID 29697773.
    13. Vander Heiden MG, DeBerardinis RJ (February 2017). "Understanding the Intersections between Metabolism and Cancer Biology"Cell168 (4): 657–669. doi:10.1016/j.cell.2016.12.039PMC 5329766PMID 28187287.

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