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     One of the many major disputes  between creationists and evolutionists concerns whether or not sufficient enough new information can arise in the genome through mutation to account for phenotypic changes.  Evolutionists define evolution as the change in the genotype of a population over time.  Darwin is generally credited with discovering natural selection which has been considered the driving force behind evolution.  But in order for complex organisms such as man to have evolved over time from less complex organisms, massive amounts of entirely new information had to be added to the genome of these less complex biological systems.  
     These less complex systems would not have had the genetic material to code for arms and legs, much less muscles, nervous systems, or brains.  Natural selection alone cannot account for the variety we see in the world.  Natural selection selects, it does not create.  It is a highly effective quality control system.  In order for a comparatively simple, one celled organism to become a 30 trillion celled, complex organism, natural selection had to have extremely massive amounts of genetic information from which to select over time.
   The only known natural means of getting us to this new information is mutation. If mutations are not capable of producing new genetic material that code for new phenotypes, then the case for evolution is fatally weakened.  This series of articles will argue that, in fact, mutation has not been seen to provide the kind of new information necessary for evolution to occur.
    Before the advent of molecular biology, evolutionary change was seen as mere morphological change.  Ernst Haeckel viewed the cell as kind of microscopic piece of Jell-O, a “simple little lump of albuminous combination of carbon.”1  Just based on the external shape of the structure, it could easily be theorized that a flaky piece of skin could  transform into a scale.  It could further be theorized that a scale morphed into a feather.  A fin could easily be imagined to transform into an appendage like a leg, a primitive amphibian to reptile, a primitive “hominid” into a modern human.  Elaborate and convincing drawings and modern computer graphics make it easy to visualize such changes occurring.  In fact, very little effort needs to be expended imagining this because it is already imagined for us.  
    But as scientists have come to better understand life at the molecular level, it has become increasingly apparent that the biochemical paths that these changes would have to take are significantly more complex than previously imagined.  A reptilian scale differs greatly from an avian feather.  It is easy to imagine that an eye-spot might appear on a primitive organism, but the actual genetic information for the formation of such an organ is extremely complex, not to mention the complexity involved in it transforming into a marvel such as the trilobite or human eye.  More about the eye later.

What is a Mutation?

    Mutations are changes in the genetic material of the cell.  There are many types of mutations.  Some involve small numbers of base pairs while others involve larger numbers.  The smallest of these is the nucleotide substitution (a point mutation), where one amino acid is replaced by another amino acid.  Transposition is where an amino acid sequence changes location, usually through breakage and fusion of chromosomes.  
    There are insertional mutations, were a series of amino acids are inserted into another series.  A frameshift mutation shifts the amino acids, which, because they are read in sequences of threes, changes the genetic meaning of the sequence.  Nonsense mutations might involve a premature stop codon which will change the genetic meaning of sequence, shortening the protein.  A missense mutation is point mutation that can cause serious effects, such as sickle cell anemia.  Some mutations occur at the chromosome level, where parts of chromosomes break off and reattach to another chromosome.  Mutations could be broadly categorized, however, as deletions, insertions, and duplications.2  The list of specifics could go on but the point is that mutations change the genetic structure of the genome.  Mutations which occur in somatic cells are relevant only to the organism.  Gametic mutations are the ones which can be passed on to offspring, thus effecting evolution.
    Houle and Kondrosho categorize mutations as either lethal, deleterious, neutral or advantageous.  Nearly all agree that by far the rarest type of mutation is the one which is advantagous.3  These are the mutations which evolutionists believe are liable to produce accumulative, beneficial change. The vast majority of mutations, however, are either harmful or neutral to the organism but are usually repaired.
     One of the many amazing things that biologists have discovered about living organisms is that genetic material is more often than not self-correcting.  There are multiple mechanisms in a cell, and in the DNA, which tend to correct the mutations that often occur.  Our bodies are bombarded every day by mutagens of every sort including radioactive rays from the sun and chemical agents which cause deleterious effects in our genetic material.  If it were not for the corrective action of the DNA, our physical bodies would deteriorate more quickly than they already do.  
However, “mutations that effect fitness are more likely to be deleterious than advantageous.”  Macro-mutations deleteriously effect the organism or else result in its death.   Clearly, “substantial indirect evidence derived from molecular studies supports the contention that most mutations in natural populations are deleterious.”4  Horrible diseases that afflict mankind are the result of these mutations which are left uncorrected and that survive  copying errors.  
    If evolution is true, we are largely who we are because of mutations.  According to the doctrine of evolution, we have eyes, ears, noses, mouths, feet, hearts, lungs, etc., every physical thing which make us who we are, because we are the result of a long series of mistakes and copying errors.  Evolutionists, however, believe that some of these mistakes can be advantageous to us, ultimately providing us with new abilities.  However, “the basic challenge is that discrete mutations of large effects, such as lethals, visibles, or human genetic diseases, can be readily observed, but these are irrelevant to long-term evolution as they have extremely large deleterious fitness effects.  Mutations with small positive or negative effects on fitness are the ones that we need to understand, and it
In-Depth Mutation and Evolution Part One

Information Decrease

     Bacteria, because they reproduce every half hour or so and because they are so very prolific, are thought to be just the idea specimens for studying mutations and evolution which would, according to theory, normally take billions of years to occur.  One example of a beneficial error that is often used to support the theory of evolution is the ability of bacteria to assimilate new sources of nutrients, which in general terms effect its fitness.  One example of this is found in a 1982 study reported by R. P. Mortlock.  He subjected soil bacteria to strong selective pressure by denying them their normal nutrient of ribitol.  The bacterial cell transports ribitol, a sugar residue found in soil, into the cell and breaks it down in a series of steps, the first of which uses ribitol dehydrogenase (RDH) .  He tried to get them to assimilate an unnatural substitute.  After trying several other unnatural sugars xylitol was used.  It is very similar to ribitol but it does not grow in nature.  Though the chemical differences between ribitol and xylitol are very small, the cells RDH enzyme is specific to ribitol.  And though, because they are so similar, RDH can assimilate xylitol at a very low rate by osmosis through the cell wall, RDH is only made when a specific gene is turned on and this gene is turned on only in the presence of ribitol.  From the wild-type bacteria, Mortlock found a mutant, called X1, that could grow on xylitol.  This mutant could grow on xylitol at about one ninth the rate of the wild type.  When this strain was cultured another mutation (called X2)  appeared which could grow two times as fast on xylitol as X1.  In strain X2 another mutation was found that allowed it to grow almost twice as fast as X2.  This mutation was called X3.  

      On the surface this looks very much as if this represents the kind of incremental changes needed for evolution to occur.  A new ability was indeed the result of a mutation, just as evolutionists say would occur.  The problem with using this as an example of macro-evolutionary change is that the whole process involves the loss or destruction of information not the addition of new information.  

      The first mutation did not change the permease enzyme transport system itself but rather destroyed the represser protein, consequently allowing RDH to be made in such great quantity that it counteracted the low activity on xylitol as it oozed through the cell wall.  Therefore, it grew, but more slowly on xylitol than on ribitol.  The mutation in the X1 strain (which led to the X2 strain) did change the enzyme and raised its activity level on both xylitol and L-aribitol, another non-naturally growing substrate, but because the new enzyme accepted a wider range of molecules as substrates the enzyme became less specific and reduced the information in the genome.  This is an important point I’ll reiterate later.  Also, the mutation which produced the X2 strain reduced the information in the genome because it weakened the bond at the active site by degrading  the enzyme to which the substrate bonded. The mutation which led to the X3 strain disabled the gene that regulates the transcription of the transport enzyme that carries the nutrient into the cell.  All of these are examples of decrease in information.  

     “Enzymes are highly specific in that each catalyzes only a single reaction or set of closely related reactions...Since nearly every biological reaction is catalyzed by an enzyme, a very large number of distinct enzyme molecules is required.”6  When an enzyme mutates to catalyze multiple substrates, it destabilizes the molecule.  It is helpful to think of the process here as similar to a combination lock.  The lock works because it answers to only one specific, series of digits.  Just any numbers won’t do.  If a combination lock opened with any set of digits, it would cease to function efficiently.   Because it would answer to a broader set of digits, it loses specificity, thereby losing information.  If an enzyme were to catalyze any molecule as a substrate, it could be harmful to the cell.

       But more important than this is the problem that the example above does not demonstrate increase in information, even though it may have permitted a new trait.  The process above could never explain how a single cell, low complexity organism became a thirty trillion cell, complex creature, such as ourselves.  It simply cannot explain increased complexity. Theoretically there be mutations which might increase information, but the cost of such grand mutations is often too high. However, it is important to understand that what we are getting at here is the creation of new genetic information not merely a new function.  A gain of a function is not the same thing as the gain of new genetic information.  Losing the genetic information for wings might be beneficial to an insect living on a very windy island, but it is a loss nonetheless and cannot explain Darwinian evolution. --ELP


1. Behe, Michael J., Darwin’s Black Box, The Biochemical challenge to Evolution, The Free Press, NY: 1996, p. 22.

2. Lynch, Michael, The Origins of Genome Architecture, Sinauer Associates, Inc., Sunderland, Massachusetts: 2007, p. 370.

3. Fox, Charles W., and Jason B. Wolf, editors, Evolutionary Genetics, Concepts and Case Studies, Oxford University Press, 2006, p.  43.

4. Keightley, Peter D. and Michael Lynch, Evolution, 57(3), 2003, pp. 683–685.

5. Fox, p. 41.

6. Freifelder, David, Molecular Biology, 2nd edition, Jones and Bartlett Publishers, Inc. Boston: 1983. P. 164.

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Copyright Eric L. Padgett  03-30-2012
Christian Apologist