Mutation



A mutation is any spontaneous heritable change in DNA sequence that contributes to genetic variability. It results from 2 possible mechanisms.
 * 1) Cellular accidents during processes like replication, recombination, or transposition.
 * 2) Exposures to foreign mutagens, such as chemicals or ultra violet rays.

If even one of the nucleotides in a gene is changed to another, then a new variation of the allele has been added to the population, and a different amino acid may be assembled into the protein during gene expression.

Types
Mutations are classified as harmful, beneficial, or neutral.
 * Harmful - spontaneous changes to genes will render proteins dysfunctional, and can lead to physical deformation, cancer, or death.
 * Beneficial - mutations that produce some benefit can theoretically happen, even though the protein loses all or some of its function.
 * Neutral - mutation where there is no effect (also known as a silent mutation). A neutral mutation either results from a codon that is translated into the same amino acid during gene expression, or a changed amino acid that has no effect on protein function. The following table shows several codons that are each translated into the same amino acid. In each case, the 3rd nucleotide in the codon would be a neutral mutation if changed.

It is however difficult to say that a given mutation which is considered to be neutral has no negative effect upon an organism if it is fixed in the genome because genomes are highly compressed, and that genetic sequences are often overlapping or nested. Anuj Kumar has stated in 'An Overview of Nested Genes in Eukaryotic Genomes',

For more than 30 years, we have understood that genes may be organized within genomic DNA in complex spatial arrangements. In particular, gene-coding sequences can overlap: a given segment of genomic DNA can encode more than one gene product, with the overlapping genes often oriented on opposite strands. In some cases, the overlapping genes are organized such that one gene is entirely contained within the chromosomal region occupied by another gene. In such instances, the internal gene is referred to as a “nested” gene.

Furthermore, sequences of information in a genome may be comprised of nucleotides which are at different loci on the DNA molecule, and may be part of other sequences which may or many not be directly related in function, as stated by Elizabeth Pennisi,

According to a painstaking new analysis of 1% of the human genome, genes can be sprawling, with far-flung protein-coding and regulatory regions that overlap with other genes.

Since the base pairs of a sequence may be part of one or more other sequences, if a mutation substitutes a nucleotide with a different one, entropy may result to any sequences that share the nucleotide. For example, it is common in eukaryotic cells that a given genetic sequence may code for multiple proteins or mRNAs, such as the human cSlo sequence which codes for 576 variants. . It may also be that a sequence which expresses a protein may share nucleotide with a sequence which functions to regulate gene expression, causing entropy to both genes simultaneously, which can be understood by the statement of Dr. John Stamatoyannopoulos, a genome scientist who led a team that discovered a second code hidden in DNA,

The fact that the genetic code can simultaneously write two kinds of information means that many DNA changes that appear to alter protein sequences may actually cause disease by disrupting gene control programs or even both mechanisms simultaneously.

This poses a great conundrum for evolution theory. Evolutionists claim that the base mechanism of evolution is mutations which increase genetic information and ultimately define new anatomical structures and biological function. Yet many mutations cause genetic entropy which is compound because of the compressed nature of genomes. Therefore, to believe that accruing mutation designs new information, features and functions is like believing that one can walk uphill by taking one step forward and two steps backward, and any mutation which is fixed in a genome should be carefully considered before it is said to be truly neutral.

New information
It is clear that new gene alleles are accumulating in populations today, but there are two possible sources for these changes; mutations, and intentional changes introduced by genetic recombination. The theory of evolution attributes the continued production of genetic diversity to mutations, but evolutionists overlook the fact that the cell was intelligently designed. The cellular machinery was programmed to perform a level of self genetic engineering, and is editing genes systematically so that organisms can adapt to a wide variety of environmental conditions.

Evolutionists contend that mutation, acted upon by natural selection is the mechanism for evolutionary advancement. While this mechanism has the power to change the genome over time, most biological evolution is actually due to genetic recombination followed by natural selection. There are many examples put forward by evolutionary biologists that attempt to show how new genes have been introduced into the genome of an organism. However, in most documented cases it merely illustrates the built-in plasticity or variation within the original created kind. Merely shuffling of already existing genes becomes woefully inadequate if the observational science is followed.

Despite the few examples of beneficial genetic mutations it is unrealistic to assume that this information produced through changing already existing DNA would then be acted on again many more times by other related mutations to build radically different and complex structures than what was there previously. This is to say that mutations are not a reasonable means of producing cascading morphological change from one kind of animal to another but merely speciation.

Obviously mutations can indeed cause dramatic phenotype change from environmental pressures. Many experiments have been performed on fruit flies (Drosophila) where poisons and radiation induced mutations. However, the problem is that they are always deleterious. The Drosophila experiments showed an extra pair of wings on a fly, but these were a hindrance to flying because there are no accompanying muscles. Therefore, these flies would be eliminated by natural selection. Even in the case of mutations which can change the amount of DNA possessed by an organism, an increase in the amount of DNA does not result in increased function. Biophysicist Dr. Lee Spetner in his book, Not by Chance: Shattering the Modern Theory of Evolution, analyzed examples of mutational changes that evolutionists claimed were increases in information, and demonstrated that they were actually examples of loss of specificity, meaning loss of information.

In all the reading I've done in the life-sciences literature, I've never found a mutation that added information. … All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it." - Spetner

and

We see then that the mutation reduces the specificity of the ribosome protein and that means a loss of genetic information. ... Rather than saying the bacterium gained resistance to the antibiotic, it is more correct to say that is lost sensitivity to it. ... All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it.

Georgia Purdom from AiG, Ph.D. of molecular genetics, has stated,

Mutations only alter current genetic information; they have never, ever been observed to add genetic information; they can only change what is there. I have a lot of papers come across my desk of supposedly mutations that have added genetic information, and I've read them all, and I've looked at them all, and never, once have I seen one that has added genetic information; they just don't do that.

Mathematical challenge
Mutations either beneficial, negative or neutral are rare instances. They happen on average about once in every 10 million duplications of the DNA molecule (107, a one followed by 7 zeroes). For evolution to progress, organisms require a series of related mutations to occur. The odds of getting two mutations that are related to one another is the product of their separate probabilities. If every 107 duplications of DNA a mutation occurs the equation would start to look like this; 107 x 107 or 1014. a one followed by 14 zeroes, a hundred trillion. Mutations which are related or not would barely change finch beak sizes due to drought, or change the shape of a fly wing.

What are the odds of getting three related mutations? That is, again taking into account the mutation rate of duplicated DNA, one in a billion trillion or 1021. Suddenly the ocean isn't big enough to hold enough bacteria to make that chance very likely. You can quickly tell that at just three related mutations, evolution via related, dependent mutational change through natural selection as its mechanism to produce truly novel information or molecule-to-man change is woefully inadequate.

Mutation load
Although beneficial mutations are theoretically possible, natural selection does not act at the molecular level, but rather it operates only at the level of the organism. It selects only those mutations that produce a physiological change, which alters the survival or reproductive rate of the organism. As such, for every rare beneficial mutation that might occur, countless numbers of harmful mutations are accumulating within the genome of the organism - producing what is known as a "mutation load".

April of 2007 paper by the Proceedings of the National Academy of Sciences (PNAS) states that: Our theoretical findings indicate that mutator hitchhiking can set in motion a self-reinforcing loss of replication fidelity, but the question of how a process as robust as natural selection could allow this to happen remains. The key fact is that natural selection, although eminently robust, is a short-sighted process that favors traits with immediate fitness benefits. The fitness cost of mutator hitchhiking is generally not anticipated because of the slow accumulation of deleterious load. When a mutator hitchhikes with a new beneficial mutation, a simple model shows that the increased deleterious load due to the mutator is in fact suppressed during the spread of the beneficial mutation. Indeed, the full fitness cost of the mutator is only realized well after the beneficial mutation has stopped spreading (SI Text). A mutator may therefore enjoy the immediate benefit of producing a new beneficial mutation without anticipating the eventual increase in deleterious load. Because of this delay in the accumulation of deleterious load, natural selection can drive mutation rate up to the point of no return, where fMmMu2 becomes the dominant term (Fig. 4A); even if the increase in deleterious load is lethal, it is not anticipated (Fig. 4B). At the population level, this failure to anticipate the establishment of a lethal deleterious load is partly due to the sharpness of the threshold separating lethal from viable mutation rates (22, 24), such that there is no slow fitness decrease to "warn" of impending extinction.

Regarding the inevitable continuous degredation of the human genome by the high rate of accruing mutation, Alexey S. Kondrashov, a leading researcher in the field of evolutionary genetics, has stated,

Despite all of the elaborate mechanisms that a cell employs to handle its DNA with the utmost care, a newborn human carries about 100 new mutations, originated in their parents, about 10 of which are deleterious. A mutation replacing just one of the more than three billion nucleotides in the human genome may lead to synthesis of a dysfunctional protein, and this can be inconsistent with life or cause a tragic disease. Several percent of even young people suffer from diseases that are caused, exclusively or primarily, by preexisting and new mutations in their genomes, including both a wide variety of genetically simple Mendelian diseases and diverse complex diseases such as birth anomalies, diabetes, and schizophrenia. Milder, but still substantial, negative effects of mutations are even more pervasive. As of now, we possess no means of reducing the rate at which mutations appear spontaneously. However, the recent flood of genomic data made possible by next-generation methods of DNA sequencing, enabled scientists to explore the impacts of deleterious mutations on humans with previously unattainable precision and begin to develop approaches to managing them.