has affected various genomes. For example, there are unique regions in the human genome known as human accelerated regions (HARs; for a creationary review see Tomkins 2016). These are higher in GC content than their orthologs in primates, so evolutionists have inferred they have arisen via gBGC (Galtier and Duret 2007). This led to the inference that “HARs, far from contributing to human adaptation, would represent weak points of our genome, whose function needed to be preserved, in spite of the ‘undesired’ fixation of numerous deleterious mutations.” (Galtier and Duret 2007, p. 276) This prediction isn’t holding up where HARs have been investigated in detail (Tomkins 2016). Based on the evolutionary assumption that biased gene conversion is random with respect to fitness, metanalyses and population genetic modeling have suggested that it is likely to fix deleterious alleles and thus it has been termed the “Achilles heel” of the genome (Galtier and Duret 2007), and via this “curse of the converted” significant increase of the spread of alleles associated with hereditary diseases is envisioned (Lachance and Tishkoff 2014). Interestingly, one study of human single nucleotide polymorphisms (SNPs), which used chimp data to help estimate ancestral alleles and computer predictions to “identify” harmful mutations, estimated that nearly 60% of the time gBGC works to reduce the spread of putatively disease-causing alleles (Necşulea et al. 2011). This brings up two interesting points. First, where are the validated examples of human hereditary diseases that are segregating at higher frequencies because of biased gene conversion? One paper listed over 40 known genetic diseases attributable to gene conversion, but nearly all were non-allelic gene conversions, meaning that a portion of DNA was copied over onto DNA from a different, non-homologous region (Chen et al. 2007). If biased gene conversion is random with respect to fitness and as common as empirical studies suggest, there should be a wealth of examples where it is involved in spreading hereditary diseases, many of which do not even manifest until after childbearing years. The second point is how gBGC compares to mutation. While gBGC tends to increase the transmission of strong (GC) alleles, ordinary mutation tends to produce weak (AT) alleles. So, while biased gene conversion tends to work like natural selection in decreasing variability through the fixation of alleles, when it is combined with mutation gBGC may lead to increased diversity (Boman et al. 2021). This is consistent with the fact that biased gene conversion is common in areas of high recombination and recombination is positively correlated with diversity, suggesting a creationary lens may serve better for understanding biased gene conversion. There are multiple lines of evidence suggesting that biased gene conversion was designed by God for the benefit of his creatures. First, there are numerous enzymes that need to be expressed in a tightly controlled manner for this highly complex process to occur; this alone is a logical reason to suspect it has a purpose. Second, the significant spread of deleterious mutations, which is predicted based on the assumption that it is an undesigned, neutral process, lacks empirical support. Due to the Fall, the creation model would predict biased gene conversion can fall short of its intended good purpose, but this should be a less common outcome. This appears to be the case (Chen et al. 2007). A third reason to suspect purpose in biased gene conversion is that there are obvious potential purposes. Diversity is considered healthy and important in populations. When combined with mutation, gBGC appears to provide a good mechanism for generating diversity. Also, biased gene conversion can help increase the spread of adaptive alleles and/or reduce the spread of maladaptive alleles, a predicted need based on a creationary review of natural selection (Lightner 2015). Based on the above considerations, the eKINDS project now has a new hypothesis posted on Researchgate: Mechanisms that bias allele transmission, such as biased gene conversion and other forms of meiotic drive, will eventually be shown to contribute significantly to the propagation and fixation of adaptive alleles. OTHER FORMS OF TRANSMISSION DISTORTION There are many other types of meiotic drive as well as other non-Mendelian processes that can work before or after meiosis, so the term transmission ratio distortion (TRD) has been suggested to describe them in general (Camacho 2022). Recent reviews provide excellent summaries of the current state of our understanding (Arora and Dumont 2022; Clark and Akera 2021; Dawe 2022; Friocourt et al. 2023; Kruger and Mueller 2021; Pajpach et al. 2021). Again, emotive language is often used to describe the process. Describing genes as “cheating” meiosis shows a bias that assumes Mendelian segregation should be the norm. In an evolutionary view that attempts to eschew design, this may seem reasonable. In a creationary worldview where there is a Designer who cares for His creatures, this non-random segregation provides an inviting field of study to discover its purpose as a mechanism by which God provides for and sustains his creatures today (Genesis 1; Isaiah 43:20; 45:18; Colossians 1:16-17). TRD systems include drive elements that cause the distorted transmission in the heterozygote of a linked locus (from a small region to a whole chromosome, depending on the specifics), causing it to be transmitted in a non-Mendelian fashion. These drive elements are often found in structurally complex loci (copy number variable regions, inversions, and satellite-rich regions, including centromeres and telomers) and are enriched in regions of low recombination (Arora and Dumont 2022). Interestingly, TRD systems are also characterized by suppressors, that can restore allele transmission to its more expected ratio. Evolutionists imagine that suppressors can magically arise via “selection pressure” and this is the basis for claiming there is an “evolutionary arms race” occurring as new drive elements and suppressors appear (Arora and Dumont 2022). One wonders how an arms race can occur without an intelligent force behind it. More likely this is from design, and as with so many other biochemical pathways, there are mechanisms to turn things on or off as needed by the organism. One interesting TRD system is called centromere drive, which also occurs during meiosis (and, thus, can be considered meiotic drive). Centromeres connect chromosomes to spindle microtubules and enable proper segregation of chromosomes during cell division. Interestingly, centromeric DNA can be profoundly different between difLIGHTNER Review of CRS eKINDS 2023 ICC 247
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