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Genetic variability

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Recombination during Meiosis (a form of cell division). Chromosomes condense and pair-up, then recombine information to produce genetically unique daughter cells.

Genetic variability is the measure of the differences in genetic makeup (variations of genes) between individuals in a population. Variability is different from genetic diversity, which is the amount of variation seen in a particular population.

There are two primary sources for genetic variability; random mutations and recombination events. Although evolutionists almost universally attribute changes to genes to mutation, it is becoming recognized that recombination events are making nonrandom alterations to chromosomes. The cell recombines DNA for various reasons including the purposeful generation of diversity. Mutations on the other hand are changes resulting from exposures to foreign mutagens, or the result of errors during biochemical reactions such as DNA replication. Although it is possible that random mutations may produce a beneficial change to the genome, finely tuned environmental adaptations are not likely accomplished by randomly altering genetic code. [1]

Variable genes

Not all genes are variable. The sequence of housekeeping genes tends to remain relatively constant, as does the neutral regions between genes. In contrast, some genes change at a higher rate, and interestingly the genes involved with interspecies contact seem hypervariable. It is also clear that the genes which change are not randomly variable. Only a particular region of the gene is effected. There is always a conserved and variable portion of the gene. Certain codons within the altered area remain unchanged, and nucleotide substitution show a clear preponderance for transversional changes (AT to TA) rather than transitional. Although these new alleles were originally thought to be the result of mutation, it is now understood that genetic recombination is involved. A process known as gene conversion is now recognized as being responsible for the changes that are found in many genes, such as those used to make antibodies. The genes are not changing randomly due to errors. There is a cellular machinery that is intentionally changing their sequence to produce adaptive fitness.[1]

The fact that not all genes are variable has important implications for creationist genetics. The majority of genes in the genome are commonly found unchanged even when comparing vastly different organisms. In contrast, variable genes change significantly from one generation to the next and show nonrandom patterns within any given gene.[2] The characterization of variable genes to date suggests overwhelmingly that this diversity is systematically produced through gene conversion while under tight cellular control. For example, variable genes have hot and cold spots of activity similar to those found among gene crossovers in meiosis.[3] They also frequently have greater diversity than the neutral regions between reading frames.[4] It has likewise become evident that variable genes retain codons at specific locations within the variable region. [5] A preponderance of non-synonymous substitutions over synonymous has provided even further evidence against randomness.[6] It is becoming increasingly questionable that variability is the result of random mutations as commonly claimed by evolutionists. In the scientific journal Cell David Metzgar admits the following.

Adaptive evolution has long been regarded as the result of postmutational sorting by the process of natural selection. Mutations have been postulated to occur at random, producing genetically different individuals that then compete for resources, the result being selection of better adapted genotypes. Molecular biology has demonstrated, however, that the rate and spectrum of mutations is in large part under the control of genetic factors. Because genetic factors are themselves the subject of adaptive evolution, this discovery has brought into question the random nature of mutagenesis. It would be highly adaptive for organisms inhabiting variable environments to modulate mutational dynamics in ways likely to produce necessary adaptive mutations in a timely fashion while limiting the generation of other, probably deleterious, mutations.[7]

Sources of variability

Genetic Recombination

Main Article: Genetic recombination

Genetic recombination is the name given to a large group of reactions during which cellular machinery uses a stretch of DNA to alter or recombine with a similar (homologous) sequence. Unlike mutation, recombination is a large-scale rearrangement of a DNA molecule. This process involves pairing between complementary strands of two parental duplex, or double-stranded DNAs, and results from a physical exchange of chromosome material. Genetic information is recombined by the cell for several reasons including the repair of damaged DNA, and the production of population variability during sexual reproduction.


Main Article: Mutation

A mutation is any spontaneous heritable change in DNA sequence. They results from either cellular accidents during processes like replication or recombination, or due to exposures to foreign mutagens, such as chemicals or ultra violet rays. If even one nucleotide in a gene is changed, 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.


Main Article: Transposon


Main Article: Polyploidy


  1. 1.0 1.1 Genetic Variability by Design by Chris Ashcraft. Journal of Creation 18(2) 2004.
  2. Creation of immunoglobulin diversity by intrachromosomal gene conversion. Thompson, C. B. Trends in Genetics 8:416-422 (1992)
  3. The targeting of somatic hypermutation Jolly, C.J. et al. Seminars in Immunology 8:159-168 (1996)
  4. Gene conversion generates hypervariability at the variable regions of kallikreins and their inhibitors. Ohta, T. and C. J. Basten. Molecular Phylogenetics and Evolution 1:87-90 (1992)
  5. Position-specific codon conservation in hypervariable gene families Conticello, S. G., Y. Pilpel, G. Glusman, and M. Fainzilber.Trends Genet. 16:57­59 (2000)
  6. Mechanisms for Evolving Hypervariability: The Case of Conopeptides Conticello, S. G., Gilad, Y., Avidan, N., Ben-Asher, E., Levy, Z., Fainzilber, M. Mol Biol Evol 18:120-131 (2001)
  7. Evidence for the Adaptive Evolution of Mutation Rates. Minireview by David Metzgar, Christopher Wills (2000) Cell 101, p581.

Additional information