The Proceedings of the Eighth International Conference on Creationism (2018)

deleterious mutations, long before the simulation is complete. 7. Details of simulations of short-term populations with designed alleles For our designed allele simulations, each initial contrasting allele pair represents two alternative nucleotides at the same genetic locus. The sum of their allele frequencies must add up to 1.0, and both alleles will always remain in the same linkage block. We normally make all designed alleles co-dominant. We typically assign fitness effects according to a Weibull distribution, and specify the upper limit of total fitness benefit (i.e., the hypothetical fitness increase if every “beneficial” allele went to fixation). Lastly, we specify the fraction of individuals in the population who are initially heterozygous. If the fraction is 1.0, then both Adam and Eve are equally heterozygous and all designed alleles begin with frequency of 50%. Alternatively, if the initial heterozygous fraction is set to 0.5, then either Adam or Eve would be heterozygous for all alleles, while the other would be homozygous. In this case, all designed alleles start at a frequency of either 25% or 75%. RESULTS 1. Actual Allele Frequency Distributions The allele frequency distributions within the 1000 Genomes Project data for chr22, chrY, and chrM are shown in Figures 1a–c. Summary allele data for each of the three chromosomes are reported in Table 1. Figure 1a is the allele frequency distribution benchmark for this paper. At the time of submission, our analysis only included chr22 data. However, we have since calculated the allele frequency distribution for all human autosomal chromosomes included in the 1000 Genomes database and have observed a distribution essentially identical to chr22. Thus, in this case, chr22 is a suitable proxy for the rest of the genome. 2. Illustrating the Evolutionary Model – simulations without designed alleles In our evolutionary simulations, we have observed that mutational allele frequency distributions are determined by the rate of genetic drift, which is dependent on the parameter settings for population size, mutation rate, and time. For any biologically realistic population, the number of accumulated mutations increases linearly with time. Mutational alleles continuously enter the population at very low initial frequencies and those that are not lost to drift will very slowly drift toward the right (i.e., away from zero). The rate of drift in any population with 1,000 or more individuals is exceedingly slow. Only after deep time can a large population reach mutation/drift equilibrium, where older alleles are drifting to fixation as fast as new alleles are drifting into the population. When mutation/drift equilibrium is reached, the allele frequency distribution stabilizes. At the same time, the total number of polymorphisms in the population stops increasing. An example of an allele frequency distribution of an evolutionary population in mutation/drift equilibrium is shown in Figure 2a. In this run the population size was 1000, the mutation rate was 100 mutations per individual per generation, and it ran for 10,000 generations. Figure 2a shows the full range of allele frequencies (1–100%). As can be seen, a large number of alleles have drifted to fixation (100%). Figure 2b follows the convention of only plotting the minor allele frequencies (1–50%). Figure 2b is our benchmark for a stable Chromosome n All SNPs Common SNPs 22 2,504 918,038 215,313 Y 1,233 60,446 7,491 MT 1,074 2,618 424 Sanford et al. ◀ Designed genetic diversity in Adam and Eve ▶ 2018 ICC 204 Figure 1a. The minor allele frequency distribution for human chromosome 22, based upon 2,504 individuals from the 1000 Genomes Project. The vast majority of SNPs in the first bin (702,725) are not shown. Figure 1b. The allele frequency distribution for the human chromosome Y, based upon 1,209 individuals from the 1000 Genomes Project. The vast majority of SNPs in the first bin (52,955) are not shown. The extreme scarcity of high-frequency alleles suggests that chromosome Y is young. Figure 1c. The allele frequency distribution for the human mitochondrial chromosome, based upon 1,074 individuals from the 1000 Genomes Project. The vast majority of SNPs in the first bin (2,194) are not shown. The extreme scarcity of high-frequency alleles suggests the mitochondrial chromosome is young. Table 1. Three chromosomes, the number of sequenced individuals (n), the total number SNPs for each chromosome, and number of common SNPs for each chromosome, based on 1000 Genomes Project data.