You ignored my statement about fused chromosome number 2.
Creationists have been refuted on this decades ago.
"You ignored my statement about fused chromosome number 2."
Because it is a MYTH, nd even IF it were true, Chromosome Count is
MEANINGLESS (wouldn't you agree?)
Here is more info that exposes the myth, but it might get pretty technical..
A major argument for human evolution from a shared common ancestor with the great apes, particularly chimpanzees, is the ‘chromosome 2 fusion model’. This molecular model involves the hypothetical fusion of two small acrocentric chimpanzee-like chromosomes (2A and 2B) at some ancient point in the human evolutionary lineage. Our analysis of the available genomic data shows that the sequence features encompassing the purported chromosome 2 fusion site are too ambiguous to accurately infer a fusion event. The data actually suggest that the core ~800 bp region containing the fusion site is not a unique cryptic and degenerate head-to-head fusion of telomeres, but a distinct motif that is represented throughout the human genome with no orthologous counterpart in the chimpanzee genome on either chromosome 2A or 2B. The DNA sequence evidence for a purported inactivated cryptic centromere site on chromosome 2, supposedly composed of centromeric alphoid repeats, is even more ambiguous and untenable than the case for a fusion site. The alphoid sequences in this region are quite variable and do not cluster with known functional human centromeric sequences. In addition, no ortholog for a cryptic centromere homologous to the alphoid sequence at human chromosome 2 exists on chimpanzee chromosomes 2A and 2B.
123rf.com/molekuul
One of the most cited DNA-based arguments for human evolution is the hypothetical head-to-head fusion of two small ape-like chromosomes to form human chromosome 2.Science
215:1525–1530, 1982." data-offset="-10" data-variation="small wide">1 The corresponding chromosomes supposedly represented in the great apes are 2A and 2B in the chimpanzee genome. A majority of the research that undergirds this model utilized indirect methods of DNA analysis. These data were derived from DNA probe hybridization, chromosomal banding (staining), and limited DNA sequencing techniques that were available prior to the advent of high-throughput DNA sequencing technology.1,et al., Origin of human chromosome 2: an ancestral telomere-telomere fusion,
Proc. Natl. Acad. Sci. 88:9051–9055, 1991." data-offset="-10" data-variation="small wide">2
Chromosome staining and hybridization techniques do not provide detailed DNA sequence information, but rather indicate putative areas of homology. Chromosome staining used to achieve visible banding markers yields information related to GC base content, repeat content, CpG island density, and degree of condensation over large areas rather than specific sequence homology.Human Mol. Genet.
12:1037–1044, 2003." data-offset="-10" data-variation="small wide">3,Proc. Natl. Acad. Sci.
99:797–802, 2002." data-offset="-10" data-variation="small wide">4 Probe (DNA) hybridization is a more direct and accurate method for detecting DNA homology, but is subject to lab protocol variability and does not provide actual DNA sequences. Early DNA sequencing projects were largely limited to small, isolated regions of eukaryote genomes, a scenario that changed with the introduction of large-insert DNA cloning (bacterial artificial chromosomes; BACs) and BAC contig-based physical mapping strategies.
The advent of high-throughput DNA sequencing and its accompanying technologies has largely replaced these earlier technologies for comparing both chromosomes and genomes. The first working draft of the human genome generated in both the public and private sectors was available in 2001 and a more complete draft of the public human genome sequence became available in 2003.Nature
409:861–920, 2001." data-offset="-10" data-variation="small wide">5–7 The chimpanzee genome project also received funding, and a 5-fold redundant shotgun sequence coverage was published in 2005.Nature
437:69–87, 2005." data-offset="-10" data-variation="small wide">8 Another 1.5-fold coverage was completed after this along with the construction of a BAC contig-based physical map for chimpanzee. Genome Res.
16:768–775, 2010." data-offset="-10" data-variation="small wide">9
While the chromosome 2 fusion model has been routinely discussed in reviews of human evolution, very little new supporting genomic data, although readily available for analysis, has been forthcoming. For the purpose of propagating the dogma surrounding human evolution, several science authors have recently published novice-level science books promoting the hypothetical chromosome 2 model.Relics of Eden, Prometheus Books, Amherst, NY, 2007." data-offset="-10" data-variation="small wide">10,Only a Theory: Evolution and the Battle for America’s Soul, Viking, New York, 2008." data-offset="-10" data-variation="small wide">11 This so-called factual data is routinely used as one of the leading arguments for human evolution from a shared common ancestor with apes.
Figure 1. Depiction of a hypothetical scenario where chimpanzee chromosomes 2A and 2B supposedly fuse to form human chromosome 2. The two sites showing where the fusion occurred and an inactivated cryptic centromere are depicted.
The general model involves the hypothetical fusion of two small, acrocentric,
Telomeres: implications for aging and evidence for intelligent design,
J. Creation 25(1):86–97, 2011.' data-offset="-10" data-variation="small wide">13 The second key region supposedly represents a cryptic non-functional centromere that was inactivated following the fusion event. For each chromosome, a single functional centromere is required for proper stability and function because a dual centromere situation created by such a fusion would cause cellular instability and destruction. Although there are no well-defined mechanisms for inactivating human centromeres, it is believed that one of the two resulting centromeres was somehow silenced as a result of fusion. The chromosome 2 fusion is thought to account for the fact that humans have only 46 (2N) chromosomes and the great apes, including chimpanzee have 48 (2N). Modern humans supposedly evolved from a shared common ancestor with a diploid genome of 48 chromosomes, requiring a fusion event.
Examining the genomic evidence for fusion
Of the two genomic regions that are claimed to support the fusion model, the primary evidence is the purported fusion site. This site is located in a region close to the present functional centromere on the long arm of human chromosome 2. This particular area containing the ‘fusion region’ is often called 2qfus or 2chr2fus and occupies the genomic area between 2q13 and 2q14.1.14 The two small chimpanzee chromosomes that supposedly contributed to the fusion event are currently identified as 2A and 2B.
The human 2qfus region has been sequenced and annotated for telomeric repeats, a variety of important functional genes, processed pseudogenes, and various open reading frames (ORFs). A fairly thorough and complete 614 kb (614,000 bases) annotated genomic landscape was constructed that encompasses the fusion site and was published by a lab in several related reports shortly after the initial first working draft of the human genome project.et al., Genomic structure and evolution of the ancestral chromosome fusion site in 2q13-2q14.1 and Paralogous Regions on Other Human Chromosomes,
Genome Res. 12:1651–1662, 2002." data-offset="-10" data-variation="small wide">15,et al., Gene content and function of the ancestral chromosome fusion site in human chromosome 2q13-2q14.1 and paralogous regions,
Genome Res. 12:1663–1672, 2002." data-offset="-10" data-variation="small wide">16 The primary substrate for the effort relied on the assembled sequence from five overlapping, large-insert DNA clones (bacterial artificial chromosomes; BACs). As a result of this effort, a 177 kb region of contiguous sequence directly surrounding the 2qfus site corresponding to BAC clone RP11-395L14 (accession number AL078621) is available for public access and download. For the purpose of clarifying claims related to the fusion site, we subjected the complete BAC sequence of RP11-395L14 to a variety of telomere motif analyses (see Materials and Methods).
The putative fusion site is ‘highly degenerate’ and a vague shadow of what should be present given the model proposed.
Fusion site DNA sequence analysis
Our DNA sequence analysis confirmed conclusions reached by Fan
et al. The putative fusion site is ‘highly degenerate’ and a vague shadow of what should be present given the model proposed.15 One of the major problems with the fusion model is that, within the 20- to 30-kb window of DNA sequence surrounding the hypothetical fusion site, there is a glaring paucity of telomeric repeats, and those that are present are mostly independent monomers, not tandem repeats. In fact, many of the motifs in the 30-kb region surrounding the putative 2qfus site are not only isolated monomers, but are separated by up to several thousand bases of DNA.
Even while completely disregarding a consensus 6-base reading frame when iterating through the repeats, for the left (plus strand) side of the fusion site, there are only 34 intact TTAGGG motifs (table 1). This analysis uses a generous allowance of 92,690 bases to the left of the fusion site where the first TTAGGG repeat is found on BAC RP11-395L14, well beyond the size of any normal human telomere. Based on the predicted model, thousands of intact TTAGGG motifs in tandem should exist. This is true even if allowing for an extremely high rate of degeneracy, which is an unreasonable expectation because meiotic recombination is suppressed in pericentric DNA due to its close proximity to the centromere. Recombination, the most likely theoretical source of sequence shuffling leading to the fusion site degeneration would therefore be less of consideration. Also, based on the predicted model, little, if any TTAGGG motifs should exist on the plus strand to the right of the fusion site. However, 18 intact TTAGGG motifs are found on the right of the fusion site; 35% of the total number of TTAGGG motifs located within a generous 156,911 base window surrounding the fusion site.
Table 1. Telomere DNA sequence data for the 177 Kb BAC containing the fusion site.
The reverse complement telomere sequence (CCCTAA) should be present in near-perfect tandem to the right of the fusion site. Like the TTAGGG motif, one would expect approximately 1667 to 2500 CCCTAA motifs if an end-to-end fusion occurred. However, only 136 intact motifs exist to the right of the fusion site, with the last CCCTAA on the BAC clone terminating at 64,221 bases to the right of the fusion (table 1). Again, this very generous stretch of sequence is much longer than a normal human telomere, and contains a paucity of motifs. In similar fashion to the TTAGGG forward motif, the CCCTAA motif was also located on both sides of the fusion site. Our analysis located a total of 18 occurrences of the CCCTAA motif (12% of the total) scattered throughout the opposite side of the fusion site, where it would not be expected to be found. In other words, both the forward and reverse complement of the telomere motif populate both sides of the fusion site. As a side note, the GC content of the 177 kb region encompassing the putative fusion site is significantly higher (45%) than the average (40%) for chromosome 2 (table 2).
Table 2. Telomere DNA sequence data for the for the assembled euchromatic sequence of human chromosome 2.
A complete scan of the 237+ million bases of the assembled euchromatic sequence of chromosome 2 using the Skittle Genome Viewer software package showed that the entire landscape, from end to end, is populated with TTAGGG and CCCTAA motifs. Small, isolated dense clusters of telomere motifs occurred in at least 5 internal locations (data not shown). A complete iteration of the entire plus strand sequence of chromosome 2 (Per script written by Tomkins) indicated a total number of ‘TTAGGG’ and ‘CCCTAA’ occurences at 45,450 and 45,770, respectively (table 2). These numbers are roughly equal, indicating that both the forward and reverse orientation of the telomere motif occurs quite frequently at internal sites across the length of chromosome 2. These numbers indicate that a total of at least 547,320 internal bases on chromosome 2 are composed of widely distributed intact telomere motifs.
An important attribute associated with these internal telomere motifs is that they are largely monomeric. Of the 52 intact TTAGGG motifs on both sides of the fusion site, only three tandem occurrences were found, with the rest existing as independent monomers. Of the 154 intact CCCTAA motifs on both sides of the fusion site, eighteen tandem motifs were found, with the rest appearing as independent monomers. Although the density of motifs and dimeric repeats increases somewhat within the immediate vicinity of the putative fusion region, their positions in the reading frame from one 6-bp telomeric repeat to the next are erratic (not in frame).
Because of the extreme paucity of telomeric repeats, their largely monomeric condition, and their ubiquitous presence on both sides of the supposed fusion site, there exists little data to indicate that they may have once formed 10- to 15-kb stretches of perfect, tandem 6-base repeats. The 2qfus sequence is clearly degenerate beyond the point of indicating that intact telomeres once existed. Given the location in a region of suppressed pericentric recombination, one would expect a considerably higher amount of telomere sequence preservation if the model was tenable.
In attempting to correlate rates of evolutionary change with the extreme degeneracy observed in the putative fusion region, one research group concluded that “the head-to-head repeat arrays at the RP11-395L14 fusion site have significantly degenerated from the near perfect (TTAGGG)n arrays found in telomeres.”15 This caused them to raise the question, “Why are the arrays at the fusion site so degenerate if the fusion occurred within the telomeric repeat arrays less than ~6 Mya?”15
