One study (Harding et al. 2000) found this locus nearly invariant in the African populations they sampled, with just five alleles that differed at the third base pair position. This does not change the amino acid in the protein produced. These authors tried to attribute this to natural selection since darker skin is protective against melanoma. However, there are a host of reasons for rejecting this hypothesis. First, many of the known variants involving amino acid changes are recessive and/or not associated with an increased risk of cancer. So, these could not be effectively removed. Second, no variant causes cancer; it is known that other genes and environmental factors also influence whether a person develops the disease. Finally, melanoma doesn’t normally develop until the end or after childbearing years. Thus natural selection is not going to effectively remove most mutations that arise. This made me suspect that environmental factors influence the rate of mutation in this gene in a way that was potentially adaptive. Based on this previous work of looking at intrabaraminic diversity within the historical narrative presented in Genesis, I boldly posted the following hypothesis on Researchgate for our eKINDS project: 1) Many adaptive mutations are not the result of random genetic errors. Instead, much like mutations involved in antibody formation, there are enzymes and mechanisms (e.g., nucleotide sequence motifs) that guide the process. Within a few years, evidence came forth that confirmed my prediction that eukaryotes have mutations biased to be adaptive (Monroe et al. 2022). The research was done with Arabidopsis thaliana, a plant commonly used in genetic research. The authors took pains to exclude natural selection from biasing the results. They found that mutations occur much less frequently in places where they may do damage, and much more frequently in places where they may be beneficial. PROPAGATING ADAPTIVE ALLELES Once an adaptive allele exists, how does it spread to be more common in a population? Traditionally, natural selection has been appealed to as the primary mechanism for the increase of adaptive alleles and the elimination of less adaptive ones. While one can always make up a good story about how this could be, there are a variety of reasons for suspecting such stories are unrealistic (Lightner 2015). One of the best-known long-term field studies on natural selection involved the Galapagos finches (Grant and Grant 2014). They were affected by natural selection during droughts, and it removed helpful variation rather than helping the birds adapt. Thus, natural selection can work against the well-being of the population. Further, it was found that hybridization restored much of the useful variation lost from natural selection, and immigrants that remained to populate the island were not a random genetic sample of those that visited. Creationists need to be aware of the various behavioral and ecological factors that can affect allele prevalence in a potentially adaptive way. In addition to hybridization, migration and founder effects can play a role among organisms that can choose the environment they find most suitable; bottlenecks and expansions affect allele frequency as well (Ahlquist and Lightner 2018; Lightner 2015; Lightner and Ahlquist 2017). Yet for this discussion, we will focus on genetic mechanisms that bias allele frequency, which often go by the general name of meiotic drive. Meiotic drive can be defined as an alteration in the process of meiosis so that in a heterozygote (individual carrying two different alleles for a gene/region) one allele is preferentially transmitted over the other. It was first described in 1928, and many examples were uncovered in the years that followed. An overview was published by Sandler and Novitake (1957) and it has remained an important topic in genetics. Meiotic drive is sometimes referred to as a type of “intragenomic conflict” where “selfish genetic elements” bias their own transmission (Burt and Trivers 2006). Unfortunately, this emotive terminology obfuscates what is really going on. As creationists, we need to examine the data being generated in this area from a biblical viewpoint. As we do, we will have a powerful apologetic that shows the wisdom and care of our Creator in all aspects of life, including adaptation. BIASED GENE CONVERSION Biased gene conversion is a well-studied form of meiotic drive. During meiosis, DNA is cut by enzymes so that homologous recombination (crossing over and gene conversion) can occur. Astounding details of these highly complex, well-designed processes continue to be uncovered, and the December 2021 edition (volume 71) of Current Opinion in Genetics & Development was devoted to the topic of homologous recombination. For those interested in more molecular details, see the review by Sanchez et al. (2021) from that special edition. Unlike crossing over, which swaps portions of DNA between chromosomes (though some gene conversion can accompany this), non-crossover gene conversion resolves the induced double-stranded DNA breaks by copying the sequence of one homolog over onto the other. If the copying is equally likely in both directions, then Mendelian segregation would be preserved. However, it has been found that this process tends to be biased, leading to transmission distortion. For example, it appears that breaks can preferentially occur on one chromosome, and the sequence from the unbroken homolog will be copied over onto the broken segment (Cole et al. 2012; Sun et al. 2012). Further, because a portion of the broken chromosome invades the unbroken homolog, mismatches will tend to be preferentially converted to strong (GC, which bond with three hydrogen bonds, as opposed to AT, which bond with two) nucleotides. The latter is known as GC-biased gene conversion (gBGC) and is believed to be prevalent in eukaryotic genomes (Chen et al. 2007; Glémin et al. 2015; Hämälä and Tiffin 2020; Muyle 2011). Gene conversion can be difficult to detect directly because the tract of DNA involved is generally short. If there is no difference in sequence between the homologs in the affected region, then it cannot be detected. One study in mice looked for gene conversion in highly polymorphic hotspots. It was concluded that although the tracts are much shorter, non-crossover gene conversion was more common and widely dispersed than crossing over within the regions studied (Cole et al. 2012). It is thus predicted to have a significant influence on transmission distortion and allele fixation. This means that biased gene conversion mimics natural selection in its ability to fix alleles (Duret and Galtier 2009). When evaluating the literature, it becomes obvious that the assumption of common ancestry has influenced conclusions on how gBCG LIGHTNER Review of CRS eKINDS 2023 ICC 246
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