Evolution of new information

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Creationists often claim that evolution cannot produce new information. This position, called infocreationism, lurks at the core of many creationist arguments on the subject of biological evolution, such as Stephen C. Meyer's allegedly peer-reviewed paper.[1]

The claim states that mutations do not ever introduce additional genetic "building plans", and that therefore evolution, dependent on mutations as its mechanism of change, cannot ever produce organisms better adapted to their environment.

First principles refutation[edit]

Perhaps the most remarkable aspect of this claim is that it can be refuted from first principles, without needing any specialized knowledge or evidence.

Suppose there exists a simple nucleotide sequence, Sequence A:


This sequence actually codes for the last five amino acids of the human insulin alpha-chain, but any other gene would suffice for this refutation. Suppose some particular mutation can transform sequence A into sequence B:


This will change the insulin product into one that features a threonine instead of an alanine as the final amino acid of the insulin alpha chain. This will probably decrease the binding of the insulin in humans, but not enough to actually render it ineffective (pigs and cows have a threonine instead of an alanine in this position, and insulin-dependant diabetics are able to utilise porcine and bovine insulin). In any case, if a human had such a mutation, it would be almost certainly considered a loss of information by any creationist.

Suppose that this human reproduces and the child has another particular mutation which transforms sequence B back into sequence A.


If the A-B mutation is one which subtracts information from a sequence, it follows that sequence A must contain more information than sequence B -- and the B-A mutation must, therefore, be one which adds information to a sequence. We have a mutation with a gain in information!

Finally, sequence A and sequence B could be any DNA sequence - even an entire genome. There is no known reason why mutations could not transform a gorilla genome into a human genome, or vice versa, given enough time. So, if it is assumed that one of these two animals has more information than the other, it could be said that there is no known reason why mutations cannot increase information. In fact, we have seen mutations turn non-coding DNA fragments into new proteins.[2] A fair complaint, though, would be that the required mutations are incredibly unlikely - but this means that mutations increasing information are possible, just improbable. This simple refutation merely reduces the argument from 'mutations cannot produce new information' to 'mutations rarely produce new information'. To properly deal with the argument, a less theoretical approach is required.

Expanded refutation[edit]

Information can be added to the genome in many different ways. Note that the total size of any organism's genome is not fixed - it can grow or shrink with mutation. Bases can be inserted or deleted, retroviruses can add genes, whole sections of the genome can be duplicated or deleted and even an entire chromosome or genome can be doubled or halved.

For instance, say a certain gene codes to produce the protein mentioned above (or any protein, for that matter). A duplication mutation causes duplication of this gene, resulting in two copies of this gene in the genome. This mutation is clearly not a harmful mutation, since it supplies a protein that is already there, and as such has little or no effect on the organism. Then assume a second mutation causes the copy to make a different version of the protein, which adds some new ability or function. That mutation would clearly be selected for, if beneficial. Now the "information" in the second gene has been added, without any loss in genome space. A similar mechanism can work by using some of the unused DNA that makes up the majority of all genomes.

List of studies showing increased genetic information[edit]

Quite apart from the fact that this claim is invalid in and of itself, this claim is refuted by many studies documenting the evolutionary origin of novel genes:

  1. Adami et al., 2000. (see below)
  2. Alves MJ, Coelho MM, Collares-Pereira MJ, 2001. Evolution in action through hybridisation and polyploidy in an Iberian freshwater fish: a genetic review. Genetica 111(1-3): 375-385. [1]
  3. Brown CJ, Todd KM, Rosenzweig RF, 1998. Multiple duplications of yeast hexose transport genes in response to selection in a glucose-limited environment. Mol. Biol. Evol. 15(8): 931-942. [2]
  4. Decadt, Y. JG, 2000. On the origin and impact of information in evolution paper available on the internet.
  5. Hughes AL, Friedman R, 2003. Parallel evolution by gene duplication in the genomes of two unicellular fungi. Genome Res. 13(6A): 1259-1264.
  6. Knox JR, Moews PC and Frere J-M, 1996. Molecular evolution of bacterial beta-lactam resistance. Chemistry & Biology 3: 937-947.
  7. Kuper, J., Doenges, C. & Wilmanns, M. (2005). "Two-fold repeated (beta alpha)4 half-barrels may provide a molecular tool for dual substrate specificity." EMBO reports, 6(2), 134–139. DOI
  8. Lang, D. et al, 2000. Structural evidence for evolution of the beta/alpha barrel scaffold by gene duplication and fusion. Science 289: 1546-1550. See also Miles, E.W. & Davies, D.R., 2000. On the ancestry of barrels. Science 289: 1490.
  9. Lenski, R.E., 1995. in Population Genetics of Bacteria, Society for General Microbiology, Symposium 52, eds. Baumberg, S., Young, J.P.W., Saunders, S.R. & Wellington, E.M.H., Cambridge University Press, UK., pp. 193-215.
  10. Lenski, R., Rose, M.R., Simpson, E.C. & Tadler, S.C., 1991. American Naturalist 138: 1315-1341.
  11. Long M. (2001). "Evolution of novel genes." Curr Opin Genet Dev. 11(6):673-80.
  12. Long, M., Betran, E., Thornton, K. and Wang, W. (2003). "The origin of new genes: glimpses from the young and old." Nature Reviews Genetics. 4(11): 865-875.
  13. Lynch M and Conery JS, 2000. The evolutionary fate and consequences of duplicate genes. Science 290: 1151-1155. See also Pennisi, E., 2000. Twinned genes live life in the fast lane. Science 290: 1065-1066.
  14. Nurminsky DI, Nurminskaya MV, De Aguiar D, Hartl DL. (1998). "Selective sweep of a newly evolved sperm-specific gene in Drosophila." Nature. 396(6711):572-5.
  15. Ohta T., 2003. Evolution by gene duplication revisited: differentiation of regulatory elements versus proteins. Genetica 118(2-3): 209-216.
  16. Park IS, Lin CH, and Walsh CT, 1996. Gain of D-alanyl-D-lactate or D-lactyl-D-alanine synthetase activities in three active-site mutants of the Escherichia coli D-alanyl-D-alanine ligase B. Biochemistry 35: 10464-10471.
  17. Prijambada ID et al., 1995. Emergence of nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through experimental evolution. Applied and Environmental Microbiology 61(5): 2020-2022.
  18. Schneider, T.D., 2000. Evolution of biological information. Nucleic Acids Res 28(14): 2794-2799. [3]
  19. Zhang J, Zhang YP, Rosenberg HF, 2002. Adaptive evolution of a duplicated pancreatic ribonuclease gene in a leaf-eating monkey. Nature Genetics 30(4):411-415. See also: Univ. of Michigan, 2002, How gene duplication helps in adapting to changing environments. [4]
  20. Whitman CP. (2002). "The 4-oxalocrotonate tautomerase family of enzymes: how nature makes new enzymes using a beta-alpha-beta structural motif." Arch Biochem Biophys. 402(1):1-13.PubMed DOI
  21. Bos DH. (2005). "Natural selection during functional divergence to LMP7 and proteasome subunit X (PSMB5) following gene duplication." J Mol Evol. 60(2):221-8. PubMed
  22. Ballicora MA, Dubay JR, Devillers CH, Preiss J. (2005). "Resurrecting the ancestral enzymatic role of a modulatory subunit." J Biol Chem. 280(11):10189-95. PubMed
  23. Todd AE, Orengo CA, Thornton JM. (2002)."Sequence and structural differences between enzyme and nonenzyme homologs." Structure (Camb). 10(10):1435-51. PubMed
  24. Todd AE, Orengo CA, Thornton JM. (2002). "Plasticity of enzyme active sites." Trends Biochem Sci. 27(8):419-26. PubMed
  25. Bartlett GJ, Borkakoti N, Thornton JM. (2003). "Catalysing new reactions during evolution: economy of residues and mechanism." J Mol Biol. 331(4):829-60. PubMed
  26. James LC, Tawfik DS. (2001). "Catalytic and binding poly-reactivities shared by two unrelated proteins: The potential role of promiscuity in enzyme evolution." Protein Sci. 10(12):2600-7. PubMed
  27. Todd AE, Orengo CA, Thornton JM. (2001). "Evolution of function in protein superfamilies, from a structural perspective." J Mol Biol. 307(4):1113-43. PubMed
  28. Raes, J., Van de Peer, Y. (2002). "Gene duplication, the evolution of novel gene functions, and detecting functional divergence of duplicates in silico." Appl Bioinformatics. 2(2):91-101. PubMed
  29. Van de Peer, Y., Taylor, J. S., Braasch, I., Meyer, A. "The ghost of selection past: rates of evolution and functional divergence of anciently duplicated genes." J Mol Evol. 53(4-5):436-446.
  30. Carginale, V., Trinchella, F., Capasso, C., Scudiero, R., Riggio, M., Parisi, E. (2004). "Adaptive evolution and functional divergence of pepsin gene family." Gene. 333:81-90. PubMed

Selected examples[edit]

Sdic is a new gene that evolved recently in the lineage of Drosophila melanogaster. It was formed from a duplication and fusion of the gene AnnX, which encodes annexin X, and Cdic, which encodes the intermediate polypeptide chain of the cytoplasmic dynein. The fusion joins AnnX exon 4 with Cdic intron 3, which brings together three putative promoter elements for testes-specific expression of Sdic: the distal conserved element (DCE) and testes-specific element (TSE) are derived from AnnX, and the proximal conserved element (PCE) from Cdic intron 3. Sdic transcription initiates within the PCE, and translation is initiated within the sequence derived from Cdic intron 3, continuing through a 10 base pair insertion that creates a new splice donor site that enables the new coding sequence derived from intron 3 to be joined with the coding sequence of Cdic exon 4. A novel protein is created lacking 100 residues at the amino end that contain sequence motifs essential for the function of cytoplasmic dynein intermediate chains. Instead, the amino end is a hydrophobic region of 16 residues that resembles the amino end of axonemal dynein intermediate chains from other organisms. The downstream portion of Sdic features large deletions eliminating Cdic exons v2 and v3, as well as multiple frameshift deletions or insertions. The new protein becomes incorporated into the tail of the mature sperm and may function as an axonemal dynein intermediate chain. The new Sdic gene is present in about 10 tandem repeats between the wildtype Cdic and AnnX genes located near the base of the X chromosome. The implications of these findings are discussed relative to the origin of new gene functions and the process of speciation.

Not long ago after the first living organisms appeared on earth about 3.5 billion years ago, they started undergoing mutations and adaptations. One of the very earliest of these created two enzymes, each with distinct but related functions, where only one previously existed. Using a combination of the modern techniques of structural biochemistry and protein engineering, combined with molecular phylogeny, the author recreates the story of this very ancient event.


Note on 'complex and specified' information[edit]

When confronted with explanations of how a mutation may increase 'raw' (Shannon) information content, creationists will change their goalposts and begin to talk about a new form of information - complex, specified information (also known as 'biological information') [5]. It is true that mutations do only create unspecified information, however it is a key point that selection is able to specify the information created by mutation (by selecting only those few mutations that happened to specify something useful - i.e. causing a decrease in the unspecified information). After many repeats of this process, the specificity will be very complex. After all, the adjective 'complex', as used by most creationists, simply means 'to a great degree', and 'complex information' means only 'lots of information'. Therefore, to argue that evolution is impossible because mutations cannot create both information and specificity (thus ignoring selection) is akin to arguing that aircraft cannot fly because the engine doesn't provide both the required thrust and lift (thus ignoring the wings).

In fact, many creationists argue that selection decreases information. This is probably true but irrelevant, as selection is increasing the specificity of the information that is already present, rather than creating it anew. To use the above example again, one could argue that wings increase air resistance (therefore opposing the thrust force), but this ignores the fact that wings are the part of the plane that provides the lift, not the thrust. Mutations provide the raw (unspecified) information, and selection acts to specify it. Therefore in any discussion of complex or specified information, both must be considered.

See also[edit]

External links[edit]

Further reading[edit]

  • Adami, C., Ofria, C. & Collier, T.C., 2000. Evolution of biological complexity. Proceedings of the National Academy of Science USA 97(9): 4463-4468. [13]
  • Hillis DM, Bull JJ, White ME, Badgett MR, Molineux IJ. 1992. Experimental phylogenetics: generation of a known phylogeny. Science 255: 589-92.