Home | Feedback | Links | Books

Evolutionists' Confusion over Mutations
and Information Put to Rest

omeone recently brought to my attention a list of 'refutations' of 'creationist arguments' against evolution posted on http://www.talkorigins.org/indexcc/CB/CB102.html. The 'creationist arguments' cited there are distortions and the 'refutations' are misinformed, incompetent, and easily demolished. Here I address Claim CB102 of the post dealing with information gain in Darwinian evolution. The author of this argument (Mark Isaak) made four major points and I shall deal with each of them in turn.

Many years ago I published a paper that pointed out that the evolutionary process can be characterized as a transmission of information from the environment to the genome (Spetner 1964). Somewhat later I wrote that there is no known random mutation that adds information to the genome (Spetner 1997). This statement in one form or another has found its way into the debate on evolution versus creation. Evolutionists have distorted the statement to attack it, as in Claim CB102, where Isaak has written his target for attack as, 'Mutations are random noise; they do not add information. Evolution cannot cause an increase in information.' Perhaps something like this statement was indeed made in an argument by someone, but Isaak has distorted its meaning. For his 'refutation' he writes the following 4 points (the references are his citations):

1. It is hard to understand how anyone could make this claim, since anything mutations can do, mutations can undo. Some mutations add information to a genome; some subtract it. Creationists get by with this claim only by leaving the term 'information' undefined, impossibly vague, or constantly shifting. By any reasonable definition, increases in information have been observed to evolve. We have observed the evolution of

• increased genetic variety in a population (Lenski 1995; Lenski et al. 1991)
• increased genetic material (Alves et al. 2001; Brown et al. 1998; Hughes and Friedman 2003; Lynch and Conery 2000; Ohta 2003)
• novel genetic material (Knox et al. 1996; Park et al. 1996)
• novel genetically-regulated abilities (Prijambada et al. 1995)

If these do not qualify as information, then nothing about information is relevant to evolution in the first place.

2. A mechanism that is likely to be particularly common for adding information is gene duplication, in which a long stretch of DNA is copied, followed by point mutations that change one or both of the copies. Genetic sequencing has revealed several instances in which this is likely the origin of some proteins. For example:

• Two enzymes in the histidine biosynthesis pathway that are barrel-shaped, structural and sequence evidence suggests, were formed via gene duplication and fusion of two half-barrel ancestors (Lang et al. 2000).
• RNASE1, a gene for a pancreatic enzyme, was duplicated, and in langur monkeys one of the copies mutated into RNASE1B, which works better in the more acidic small intestine of the langur. (Zhang et al. 2002)
• Yeast was put in a medium with very little sugar. After 450 generations, hexose transport genes had duplicated several times, and some of the duplicated versions had mutated further. (Brown et al. 1998)

The biological literature is full of additional examples. A PubMed search (at http://www.ncbi.nlm.nih.gov/entrez/query.fcgi) on "gene duplication" gives more than 3000 references.

3. According to Shannon-Weaver information theory, random noise maximizes information. This is not just playing word games. The random variation that mutations add to populations is the variation on which selection acts. Mutation alone will not cause adaptive evolution, but by eliminating nonadaptive variation, natural selection communicates information about the environment to the organism so that the organism becomes better adapted to it. Natural selection is the process by which information about the environment is transferred to an organism's genome and thus to the organism (Adami et al. 2000).

4. The process of mutation and selection is observed to increase information and complexity in simulations (Adami et al. 2000; Schneider 2000).

I shall deal with these points one by one. But first there are a few introductory statements to be made. For the past three quarters of a century, the Modern Synthesis (MS) has been the paradigm of evolutionary theory and it remains so today. It is still the most widely accepted version of evolutionary theory (Mayr 1993, Pigliucci 2009). I must presume that this is the theory that Isaak is attempting to defend. The MS hypothesizes that evolution occurs in small steps in each of which a random mutation appears by chance and endows the organism with a heritable reproductive advantage. Through natural selection this mutant form gradually, over many generations, takes over the population. I contend that such a process has never been shown, neither theoretically nor observationally, to lead to the addition of any new information in the genome.

There are random mutations that are principally errors in DNA replication. These, together with genetic recombination, have been chosen by the architects of the MS to play the role of the variation that Darwin proposed to be the raw material on which natural selection works.

There are also nonrandom (or directed) mutations, which have been ignored and even denied by the MS. These have been seen to be important to evolution only in the past two or three decades, but whose importance is not acknowledged by the MS. Nonrandom genetic changes form the core of the Nonrandom Evolutionary Hypothesis (NREH), which I introduced in my book (Spetner, 1997) and on which I expounded further in a later book (Spetner, 2014). Transposable elements (TE) in the genome are known to cause complex mutations when they are activated. Their activation is not random; they are activated by stress. Stress, most often environmental stress, is known to induce TEs to become active and produce an adaptive response that tends to relieve that stress. The mechanism for the activation of a TE, and its ability to produce an adaptive response is endogenous in the organism. How this mechanism could have evolved is unknown, but its presence in many organisms is undeniable and it is likely to be universal.

Various types of stress have been reported to stimulate TE activity in a wide variety of organisms: in bacteria (Chou et al., 2009; Stoebel et al., 2009; Stoebel and Dorman, 2010; Drevinek et al.. 2010; Gaffé et al., 2011), in yeast (Rolfe et al., 1986; Bradshaw and McEntee, 1989), in plants (Wessler, 1996; Grandbastien, 1998; Lin et al., 2007), in Drosophila (Strand and McDonald, 1985; Aminetzach et al., 2005; Chung, 2007), in mosquitos (Chénais et al., 2012) and in mammals (Liu et al., 1995). It is widely acknowledged that TEs play an important role in the evolution of genomes (Kazazian, 2004; Feschotte and Pritham, 2007). The mutations induced by environmental stress have in most of the above cases been reported to be adaptive to that stress. The ability of an organism to call on TEs to adapt to an environmental stress is widespread if not universal.

Point 1. I return now to Isaak's first point and its four bullets, which I here designate by the letters A through D:

1. Lenski has not shown that the increase in variety comes from random mutations. Indeed, Lenski had not yet sequenced the DNA of the bacteria in the study Isaak cited. In a later study of Lenski's (Maddamsetti et al., 2015) he and his colleagues did sequence the DNA and they found TEs in the genome. They did not realize that TEs are responsible for most of genetic diversity (Kidwell and Lisch 1997), and they ignored them. The (nonrandom) activity of these TEs was the likely cause of the observed genetic diversity, and not random mutation. Isaak's first bullet therefore fails to show that random mutations can cause an increase of information in the genome.
   


2. The claim in the second bullet is that gene duplication represents an increase of information. That is like saying that two copies of a newspaper provide more information than does one. The role that evolutionists customarily assign to gene duplication is not that the duplication itself adds information, but that the duplication makes available a free copy of a gene (or even the whole genome), which is released from its normal function and is permitted to mutate in the hope of achieving an adaptive mutation. Any added information would then come from mutations. So the question reverts back to whether random mutations can add information, and I claim there is no evidence for it. But Isaak in his second bullet cites what he thinks is evidence of information having been added through the process of gene (or even full genome) duplication followed by what he assumed to be random mutations. There is no evidence that the diversity thus produced was the result of random mutations. There is good reason to believe that TEs played that role as nonrandom players in directed evolution. Apparently Isaak thinks that gene duplication happens spontaneously and at random. This is not so. Gene duplications are the result of the activity of TEs that cause gene duplication by effecting the insertion of gene copies in one or more specific sites (Morgante et al. 2005). This does not happen randomly, but it occurs when more copies of the gene product are needed such as when the cell has to synthesize the gene product more rapidly. Although there is no evidence that random mutations lead to genetic diversity, it has long been known that TEs do (Kidwell and Lisch, 1997). The second bullet fails to show that gene duplication adds information through random mutations or other random processes.
   


3. In this bullet, the acquisition of antibiotic resistance by pathogenic micro-organsims is cited as evidence for 'novel genetic material' and is supposed to be evidence of an increase of information in evolution. This is an old shopworn argument used by evolutionists for more than half a century and has been refuted long ago. A refutation can be found in two of my books (Spetner, 1997, 2014). Almost all antibiotic resistance acquired by bacteria comes not from random mutations but through horizontal gene transfer (HGT) from bacteria in the environment that are already resistant (Davies and Davies 2010; Forsberg et al 2012). None of it is evidence of MS evolution! All our antibiotics have been extracted from, or copied from, bacteria that synthesize them. Naturally occurring antibiotics have been estimated to date back as far as 2 billion years ago, and it is suspected that the history of resistance enzymes goes back that far as well (D'Costa et al. 2011). Bacteria make these antibiotics to defend themselves. They are endowed with the resistance enzymes to protect themselves against their own antibiotics. Antibiotic resistance is not an example of MS evolution and is not an example of the origin of 'new genetic material'.
   


4. In his fourth bullet, Isaak argues for random evolution by invoking the appearance of what he calls 'novel genetic regulation' in the appearance of a newly acquired ability of bacteria to synthesize new enzymes that allow them to metabolize a new nutrient found in the wastewater from a nylon factory. In 1975 a bacterial strain (Flavobacterium) was reported thriving in the wastewater of a Japanese nylon factory (Kinoshita et al. 1975). Although nylon (and the waste products from manufacturing) were new to the biosphere, having only appeared some thirty years earlier, these bacteria were able to synthesize three new enzymes to metabolize this new nutrient. All three of these enzymes were necessary; one or two alone would not help. It is incredible that these three new enzymes could have been produced by random processes alone in less than thirty years. Moreover, the Flavobacterium is not the only bacterium that evolved to synthesize the enzymes to metabolize the nylon waste. A strain of Pseudomonas was cultured in the presence of the nylon waste and it synthesized the same enzymes (Kanagawa et al. 1989). To ensure that the Pseudomonas did not obtain the enzymes by HGT from the Flavobacterium, the experimenters took a strain of Pseudomonas from 10,000 miles away and cultured it in the presence of the nylon waste. It too developed the enzymes to metabolize the waste. More reasonable than suggesting the three nylonase enzymes were the result of random mutations, would be a suggestion that they resulted from nonrandom mutations triggered by a TE. TEs in the form of insertion sequences were indeed reported to have appeared multiple times on the plasmid containing the three nylon-degrading genes (Kato et al. 1994). The TEs were likely activated by the stress of a paucity of normal nutrients and a plethora of nylon waste. It is ironic that Isaak cited Prijambada et al. (1995) to illustrate his point here, because those authors wrote, 'Though a molecular basis for the emergence of nylon oligomer metabolism in [the bacteria] is still unknown, it is probable that the basic mechanisms acting during environmental stress are involved in this adaptation.' They are suggesting here what my NREH predicts. It may well be that this unknown mechanism involves nonrandom mutations triggered by an insertion sequence. In this bullet too, Isaak failed to show any evidence that information has been increased by random mutations.

I have here shown that the first point in Isaak's argument for an increase of information in evolution according to the MS is a failure. I have demolished all four parts of Isaak's point 1.

Point 2. Isaak's second point is no more than a repetition of the second bullet of his first point and I have already demolished that argument.

Point 3. In this point Isaak shows he misunderstands the role of random noise. He claims that random noise maximizes information. Random noise added to a signal does not increase the information in the signal and certainly does not maximize it. This is rather obvious to anyone except to someone who tries to pontificate on a subject he does not understand. What is true about random noise in the context of maximizing information is the following. A message usually contains redundancy, which means that the ratio of information/message-length is lower than it could be. Redundancy can be recognized in a symbol string if knowledge of some symbols allow the prediction of others. This feature is evident in the auto-complete function in a word processor. Appropriate coding can remove redundancy. If the coding succeeds in yielding a symbol string that does not permit prediction of future symbols from past symbols, then all redundancy has been removed and the ratio of information/message-length is maximized. If this has been done, then the symbol string appears random. It appears random but it is not random because it contains information and a truly random string of symbols does not contain information. It appears as random noise but it is not random noise! Isaak's statement that random mutations can maximize information shows his confusion of this subject. This demolishes Isaak's point 3.

Point 4. In this point Isaak invokes published computer simulations of evolution to show that simulations of an evolutionary process (random mutations with selection) show that information can be built up in the process. There is a fallacy in invoking simulations to show that evolution can generate information, and in my book (Spetner 2014) I have exposed the fallacy of the claim of Schneider (2000), which is one of Isaak's references. Random mutation with selection can indeed generate information. Saying otherwise is a straw man that evolutionists like to erect so they can knock it down. Let me give here an example of information generated by random mutation. The B lymphocytes of the vertebrate immune system do indeed generate information through random mutations and selection. They do it through a super high mutation rate about a million times the average mutation rate in humans. This hypermutation is confined to a small portion of the B-cell genome where it randomly generates an enormous number of potential antibodies until it yields one that matches an invading pathogen. Once a match is found, the matching antibody is cloned millions of times to be attached to the invading pathogens to mark them selectively for destruction. Note that the hypermutation is under strict cellular control and is not random. It is activated by a special enzyme, which occurs only when an invasion of pathogens is detected (Di Noia and Neuberger 2007). The hypermutation is controlled so that the high mutation rate is confined to just the B cells and just to the small portion of its genome where it can do its creative job without disrupting other parts of the genome. I introduce the hypermutation of the B cells at this point because it is related to the evolution simulations that purport to show that random mutations can build information in evolution. The simulations rely on an exceedingly high mutation rate that can yield all combinations of nucleotide strings of length 3, or 4 or more. These strings can match to prescribed targets and therefore can represent information. But if this mutation rate were spread across the genome in real life, the cell would perish. The high mutation rate, on which these simulations rely to build information, cannot happen randomly in living cells because it would be lethal. This demolishes point 4.

I have now demolished all the arguments given in the above-cited website that were intended to refute a supposed creationist argument that claims evolution cannot increase information. The target of the 'refutation' was not a real argument. The correct statement is that there are no examples of random mutations increasing information in the genome. I made this statement more than twenty years ago and I repeated it in my recent book (Spetner 2014). More important, in that book I have noted that the central claim of the MS, that evolution proceeds through random mutation and natural selection, has never been justified. It has never been shown that MS-type evolutionary events could happen. Probability analyses are the tools for analyzing random events. No calculation has ever shown that the probabilities of MS-type evolutionary events are anything but negligibly small. Moreover, of the countless billions of random mutations that are supposed to add information, which are the crucial elements of the MS, none have ever been observed. So the MS has neither theoretical nor observational support. It is therefore not a valid theory. The evolution that has been observed to occur is driven not by random mutations but by nonrandom genetic changes caused by transposable elements that are triggered by stress on the organism. The mechanism that produces adaptation of an organism to environmental changes is built into the organism and how that mechanism arose is unknown.

Literature Cited

Aminetzach Y. T. et al. (2005) Pesticide resistance via transposition-mediated adaptive gene truncation in Drosophila. Science 309: 764-767.

Bradshaw, V. and K. McEntee (1989) DNA damage activates transcription and transposition of yeast Ty retrotransposons. Molecular and General Genetics 218 (3): 465-474.

Chénais, B. et al. (2012) The impact of TEs on eukaryotic genomes: From genome size increase to genetic adaptation to stressful environments. Gene 509: 7-15.

Chou, H. H., Berthet J. and Marx C, J. (2009) Fast growth increases the selective advantage of a mutation arising recurrently during evolution under metal limitation. PLoS Genetics 5: e1000652.

Chung, H., et al. (2007) Cis-regulatory elements in the Accord retrotransposon result in tissue-specific expression of the Drosophila melanogaster insecticide resistance gene Cyp6g1. Genetics 175: 1071-1077.

D'Costa, V.M. et. al. (2011) Antibiotic Resistance is Ancient. Nature 477: 457-461.

Davies, J. and D. Davies (2010) Origins and Evolution of Antibiotic Resistance. Microbiology and Molecular Biology Reviews 74: 417-433.

Di Noia, J. M. and M. S. Neuberger (2007) Molecular Mechanisms of Antibody Somatic Hypermutation. Annual Review of Biochemistry 76: 1-22.

Drevinek P. et al. (2010) Oxidative stress of Burkholderia cenocepacia induces insertion sequencemediated genomic rearrangements that interfere with macrorestriction- based genotyping. Journal of Clinical Microbiology 48: 34-40.

Feschotte, C., and E. J. Pritham (2007) DNA transposons and the evolution of eukaryotic genomes. Annual Reviews of Genetics 41: 331-368.

Forsberg, K. J. et al. (2012) The Shared Antibiotic Resistome of Soil Bacteria and Human Pathogens. Science 337: 1107-1111.

Gaffé J. et al. (2011) Insertion sequence-driven evolution of Escherichia coli in chemostats. Journal of Molecular Evolution 72: 398-412.

Grandbastien, M-A. et al. (1998) Activation of plant retrotransposons under stress conditions. Trends in Plant Science 3(5): 181-187.

Kanagawa. K et al. (1989) Plasmid dependence of Pseudomonas sp. Strain NK87 Enzymes that degrade 6-aminohexanoate-cyclic dimer. Journal of Bacteriology 171: 3181-3186.

Kato, Ko, Kinya Ohtsuki, Yuji Koda, Tohru Maekawa, Tetsuya Yomo, Seiji Negoro & ltaru Urabe (1995) A plasmid encoding enzymes for nylon oligomer degradation: nucleotide sequence and analysis of pOAD2 Microbiology 141: 2585-2590

Kazazian, H. H. Jr. (2004) Mobile elements: Drivers of genome evolution. Science 303: 1626-1632.

Kidwell, M. and D. Lisch (1997) TEs as sources of variation in animals and plants. Proceedings of the National Academy of Sciences USA 94: 7704-7711.

Kinoshita, S. et al. (1975). Utilization of a cyclic dimer and linear oligomers of e-aminocaproic acid by Achromobacter guttatus KI72. Agricultural and Biological Chemistry 39: 1219-1223.

Lin R. et al. (2007) Transposase-derived transcription factors regulate light signaling in Arabidopsis. Science 318: 1302-1305.

Liu, W-M et al. (1995) Cell stress and translational inhibitors transiently increase the abundance of mammalian SINE transcripts. Nucleic Acids Research 23 (10): 1758-1765.

Maddamsetti, R. et al. (2015) Adaptation, Clonal Interference, and Frequency-Dependent Interactions in a Long-Term Evolution Experiment with Escherichia coli. Genetics 200: 619-631.

Mayr, E. (1993) What Was the Evolutionary Synthesis? TREE 8 (7): 31-34.

Morgante, M. et al. (2005) Gene duplication and exon shuffling by helitron-like transposons generate intraspecies diversity in maize. Nature Genetics 37: 997-1002.

Pigliucci, M. (2009) An Extended Synthesis for Evolutionary Biology. Annals New York Academy of Science 1168: 218-228.

Prijambada, I. D. et al. (1995) Emergence of Nylon Oligomer Degradation Enzymes in Pseudomonas aeruginosa PAO through Experimental Evolution. Applied and Environmental Microbiology 61 (5): 2020-2022.

Rolfe, M. et al. (1986) Induction of yeast Ty element transcription by ultraviolet light. Nature 319: 339-340.

Schneider, T. D. (2000) Evolution of biological information. Nucleic Acids Research 28: 2794-2799.

Spetner, L. M. (1964). Natural selection: an information-transmission mechanism for evolution. Journal of Theoretical Biology 7: 412 419.

Spetner. L. M. (1997). Not by chance. Shattering the Modern Theory of Evolution. Brooklyn: Judaica Press. [First published in Israel in 1996.]

Spetner, L. M. (2014) The Evolution Revolution Brooklyn: Judaica Press.

Stoebel, D. M. and C. J. Dorman (2010) The effect of mobile element IS10 on experimental regulatory evolution in Escherichia coli. Molecular Biology and Evolution 27: 2105-2112.

Stoebel, D. M. et al. (2009) Compensatory evolution of gene regulation in response to stress by Escherichia coli lacking RpoS. PLoS Genetics 5: e1000671

Strand, D. J. and J. F. McDonald (1985) Copia is transcriptionally responsive to environmental stress. Nucleic Acids Research 13 (12): 4401-4410.

Wessler, S. R. (1996) Plant retrotransposons: Turned on by stress. Current Biology 6 (8):959-961.