accident (random mutation). When attempting to account for adaptation, there is often a distinction made between standing variation (alleles already present in the population) and de novo mutations. If the adaptive alleles are already present, genetic adaptation can be quite rapid. If not, then it must await the appearance of a fortuitous, adaptive mutation. Creationists recognize the need for a Creator to explain the complex genetic and biochemical structure of living things. There is plenty of room to argue for lots of created diversity. However, the Flood caused a bottleneck that would affect the diversity we see today. How can we tell the difference between created alleles and ones that have arisen via mutation (either random or biased)? The most definitive way to identify a mutation is by doing parent-offspring comparisons. If we correctly identified the parents and the offspring, and the tests are reliable, we can have good confidence that an allele in the offspring that is not present in either parent (assuming a sexually reproducing organism) is from de novo mutation. The mechanism (accidental damage vs the result of genomic programming to generate adaptive mutations) cannot be known without considerably more study. Therefore, in this discussion mutation is simply referring to a change in the DNA sequence. There are several other ways of inferring that mutation has occurred. For a species (or group of related species) descended from a kind preserved on the Ark, the current genetic variability can be compared to the maximum diversity that could have been present in their ancestors on the Ark. For example, dogs are unclean and some of their genes have more than four different alleles represented in the species. Thus, some of them must have arisen via mutation (Lightner 2009). Another way of inferring an allele arose from mutation is to see how it affects the complex, biochemical pathways it is involved in. If an allele codes for a protein that disrupts a biochemical pathway, it is likely from mutation. It should be noted that many adaptive alleles disrupt a pathway; it just happens that the resulting phenotype is adaptive in a particular environment. This is even more evidence of amazing design; not only did God create amazing biochemical pathways, but their design allows for changes that are adaptive. Finally, if a new trait arises that is known to be genetic (e.g., a white horse) with no evidence it existed in the animal’s ancestry, it is reasonable to suspect a mutation (Lightner 2010). Once mutations are identified, we can look at patterns and see if they fit the standard assumption that they are from copying errors or other sources of DNA damage. The biggest problem with trying to import the standard evolutionary idea that all mutations are random errors is the evidence for rapid adaptation when new mutations are involved. Spetner (1998) examined evidence of rapid adaptation in bacteria and concluded mutations must be non-random and biased to be adaptive. Others have added to this evidence (Shapiro 2002, 2022). Based on patterns of phenotypic and genetic diversity, I have been advocating that mutations are biased to be adaptive in mammals as well (Lightner 2006, 2008b). And this was the foundation of an important eKINDS prediction. PREDICTIVE SUCCESS In my examination of sheep and goats (which I referred to as tsoan based on an anglicized form of the Hebrew word for flock), I considered diversity found in karyotype, horns, and pelage. I saw adaptive diversity that didn’t fit well with the bottleneck of the Flood. I concluded the paper by stating: The variation present within the Tsoan monobaramin is from both the variety created in this baramin initially and changes that have been acquired throughout history. Some characteristics naturally change as a result of environmental changes, for example growth of a heavier winter coat and moulting. However, the variation within the monobaramin far exceeds this. Mutations, any acquired change within the genome, have historically been considered to be due to random copying errors. As such, they do not significantly add information and often result in disease. However, within the last several decades evidence has been found that some changes within bacterial genomes are directed. Such mutations can be initiated by environmental signals which allow changes in a part of the genome that is likely to help the organism adapt.31 Much of the variation in pelage could be attributable to similar changes.32 For example, growth in any tissue is controlled by multiple factors; some work to stimulate growth, others to inhibit growth. If directed changes occurred as a result of environmental changes from a postFlood ice age, mutations may have occurred that increased factors stimulating hair growth and density33,34 or decreased factors inhibiting it.34 This would easily explain how animals which had no need for heavy coats prior to the Fall were able to acquire them when the need arose. (Lightner 2006, p. 64) When I examined genetic diversity in the melanocortin 1 receptor (mc1r), a transmembrane protein involved in pigmentation in mammals, the evidence was even more astounding (Lightner 2008b). There were some SNPs that were clearly mutations that appeared in different baramins. More remarkable, there were deletions that removed nucleotides in multiples of three; this eliminated some amino acids in the middle of the protein and left the end unchanged. In most cases, it was associated with a melanistic (black) phenotype. This is because the receptor no longer responded normally to its signaling molecules. Instead, it was “stuck” in an “ON” position and always signaled for the darker (eumelanin) pigment to be produced. One might be able to explain this improbable pattern in indels if frameshift mutations, which are not in multiples of three and would affect the other amino acids that follow it, were deleterious. However, loss-of-function mutations in this gene yield interesting variety as well, without harm. So, it appears there is bias in mutations that occur within this gene. The pattern in humans is a little different than in other mammals. Over 60 alleles are known for the MC1R, which means most must have been the result of mutation because the sons of Noah and their wives could not have carried more than twelve alleles (two each). While most mutations involve some loss of function, the degree of loss varies widely. Mutations in this gene are the most common cause of red hair in humans. A few of these genes are dominant or semi-dominant and may be associated with an increased risk of melanoma. LIGHTNER Review of CRS eKINDS 2023 ICC 245
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