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

the process of being compared by this author to the current hg38 version of the human genome, end-trimmed trace reads, and the previous panTro4 version of chimpanzee. While the new assembly is likely to be greatly improved, it’s veracity as an unbiased construction needs to be critically evaluated given the history of human evolutionary bias in previous versions. While all of this information is important to consider when examining the plausibility of the fusion model, the most compelling data refuting it came when the actual fusion signature was analyzed in 2013 showing that it’s DNA sequence when read in the minus strand orientation is a functional transcription factor binding domain inside the first intron of the DDX11L2 noncoding RNA helicase, where it acts as a second promoter (Tomkins 2013; Figure 2). This data was further verified in a follow-up research report which revealed that the alleged fusion site binds to 11 different transcription factors, including RNA polymerase II, the primary enzyme that transcribes genes (Tomkins 2017). See Figure 3 showing ENCODE-related data from the UCSC genome browser. Additional data presented in the Tomkins 2017 paper showed that along with RNA polymerase binding, is the fact that transcription initiates inside the fusion-like sequence in a classic promoter-like expression pattern (Figure 4). As expected, these data implicating promotor activity also intersect with transcriptionally active histone marks and active chromatin profiles that are key features of gene promoters. As a whole, these combinatorial results strongly indicate that the alleged fusion sequence is a gene promoter, not a random accident of chromosomal fusion. When the products of the DDX11L2 gene were analyzed, it was found that it encoded RNA transcripts expressed in at least 255 different cell and/or tissue types (Tomkins 2013). The gene produces RNAs of two different lengths—short variants (~1,700 bases long) and long variants (~2,200 bases long). The alleged fusion site functions as a promoter for the shorter variants (Figure 2). Annotation of the transcripts revealed that they contained the capacity for complex post-transcriptional regulation through a variety of microRNA binding sites (Tomkins 2013). A number of the microRNA binding sites were shared with DDX11 protein coding gene transcripts (Tomkins 2013). Both the DDX11L2 and DDX11 genes are significantly co-expressed together in the same tissues (Tomkins 2013). Shared microRNA binding sites and co- expression suggest co-regulation between a protein coding gene and its noncoding RNA pseudogene counterpart, as revealed in the well-documented example of the PTEN protein coding gene and it’s PTEN pseudogene counterpart (Johnsson et al. 2013). If two chromosomes actually fused, then there would be two centromeres present and one of them would have to be deactivated to maintain chromosome stability. Centromeres are specific regions of chromosomes that play an important role in the assembly of the kinetochore—a complex structure that plays a key function in the separation of chromosomes during cell division. Evolutionists propose that an inactivated centromere in a post-fusion scenario would degrade over time and become a cryptic genomic fossil, such as that which is alleged to be present on human chromosome 2. A recent research report was published seemingly bolstering the evidence of a cryptic centromere in human chromosome 2 (Miga 2016). The author argues this point based on gene synteny (gene order) between human and chimpanzee. Of course, the problem with this premise is based on the artificially contrived assembly of chimpanzee chromosomes 2A and B which are bloated with gaps and assembled based on the human genome. Using an argument based on synteny is fallacious because the conclusion is assumed in the premise. Actual synteny between human and chimpanzee remains to be resolved until an unbiased assembly of the chimpanzee genome is produced. A problem with the alleged cryptic centromere is that its human alphoid repeat DNA sequence does not closely match chimpanzee centromeres and chromosomes (Archidiacono et al. 1995; Haaf and Willard 1997; Tomkins 2017). In addition to the problem of discontinuity with ape sequence, the alleged cryptic centromere is exceptionally small compared to a real centromere. It is only 41,608 bases in length, but this length includes non-centromeric Tomkins ◀ Interstitial telomeres and chromosome 2 fusion ▶ 2018 ICC 223 Figure 2. Simplified illustration of the alleged fusion site inside the second intron of the DDX11L2 noncoding RNA gene. The graphic also shows two versions of short and long transcript variants produced along with areas of transcription factor binding. Arrow in first exon depicts direction of transcription.