DID TWO CHIMP CHROMOSOMES FUSED TOGETHER TO MAKE CHROMOSOME 2?

Evolutionists believe that all humans and apes are related to each other through common decent. They also believe that chimps, a type of great ape, are our closest living relative. However, problems occur upon researching our genetics. Humans have 46 chromosomes while all great apes, including chimps, have 48 chromosomes. So what evolutionists have done to try and rectify this apparent inconsistency is come up with a rescue device by assuming that two of the great apes' chromosomes must've fused together in the past to form chromosome 2, which is one of the largest chromosomes in the human genome.

Unfortunately, their arguments fail for a number of reasons discussed below. On my YouTube channel I had a video with Donny for Standing for Truth ministries on Chromosome 2's alleged fusion event believed by the evolutionary community. This video can be found here. I was contacted in the chat by one Glenn Williamson who decided to chat with me in a series of emails to ask for further clarification of what I was arguing for and to be clear on my position regarding my position and arguments. After a few email exchanges it became clear that he was not understanding, did not want to understand, or just was looking for a debate. Finally, I laid my argument out into a formal argument. The argument which I laid out for Glenn Williamson will be laid out below, and discussed more in detail.

MY ARGUMENT AGAINST CHROMOSOME 2 FUSION

My argument will be set up below in the form of a formal argument complete with both premises and a conclusion. Further elaboration will be made for each premises as well. My argument is as follows:

P1: Telomere-telomere fusions are improbable, although not impossible.

Because of their rarity of use to the point where there is no known present observable examples of them happening outside of Cancer, indicates that these do not occur normally in nature and, thus, makes any specific examples of fusion unlikely. Because of this, any claims of specific examples of fusion must be extremely strong to be persuasive.

This isn't very controversial since the whole purpose of telomeres are to be used as caps on the ends of chromosomes to prevent fusion. If fusions were commonplace every chromosome in our bodies would be endanger of fusing together. The only time they're ever observed is Cancer patience whose cells and genetics are going hog-wild. However, this is an abnormal circumstance that isn't a natural occurance.

Also, the words nature mentioned in my premise is key. Williamson tried to point to some laboratory experiment with mice, but such conditions are not in nature. They are not under normal circumstances. The telomeres, in such instances, are being forced together, whether than seeing if it happens on their own. Evolutionists need the telomeres to fuse together normally. A laboratory condition is not a natural setting, thus my premise still stands.

Also, notice I am just arguing for the improbability of telomere-telomere fusions, not their impossibility. So, I'm not saying there's no way in the universe that this can be done, but just arguing since this is a rare occurrence, strong evidence needs to be applied to the counterargument. Bringing up the lab experiments would make more sense if I was arguing for their impossibility whether than their improbability, but as it were I am only arguing against their probability, as well as the need for strong evidence to persuade.

P2: The evidence against a specific fusion event occurring in chromosome 2 is strong.

Telomeres are generally 5,000 to 15,000 base pairs (bp) long. If a telomere-telomere fusion happened we'd expect the site to be 10,000 to 30,000 bp long (5,000 to 15,000bp long/chromosome), but it isn't. The alleged fusion site is only 798 bp long. In order to account for this you'd have to introduced an ad hoc rescue device, and they do. Evolutionists assumed that the area is degenerate (that the fusion event caused the base pairs to degrade, either from the event itself or with time). However, there is no evidence for this, but it get's worse. Evolutionists then turn around and use this degeneration as "proof" that this must be a fusion site, but they had argued in a circle. In addition to this, telomeres are never found in functioning genes, but the alleged fusion site is found right in the middle of the DDX11L2 gene. They try to get around this by claiming that it's a "pseudogene" (according to evolutionary view, pseudogenes are non-functional genes with no biological functions, or, at least, important ones) but, the DDX11L2 gene producing non-coding RNA and has over 250 biological functions. This is a huge problem for those who hold to this view. This evidence, combined with the rarity of this happening on its own in nature makes this event of a specific fusion highly improbable.

P3: The evidence in favor of a Chromosome 2 Fusion is weak.

To be clear, I'm not saying that the evolutionists don't have any evidence for Chromosome 2 Fusion happening, only that the evidence they do have is extremely weak. For example, you claim that there is evidence of a second centromere. Chromosomes typically only have one centromere, so at first gloss you'd assume this would be really strong evidence, until you learn the "evidence" for this second centromere is weak. This alleged "second centromere" is supposed to be evidence of a deactivated centromere accept it is found in a highly functional protein-coding (and non-coding) gene which means the area that it is in is not "deactivated" at all! This means this cannot be a deactivated centromere. Me and Donny discuss this in our interview. Tomkins had also written about it in a peer-reviewed paper in Answers Research Journal (https://answersresearchjournal.org/debunking-the-debunkers/). The strongest evidence you guys have on this, relevantly speaking, is the site's high density, which, as Donny mentioned in our interview, is the most dense area in the human genome. However, the density argument can only be stretched so far, and the argument appears circular. You assumed that the area had a fusion event, but then we ask why are there only 798 bp at the site, you say because it's degenerated, then I ask how do you know its degenerated, and then you say because its highly dense, then I ask how do you know that a fusion would lead to an increase in density, so you'd answered because the area is degenerate, and then this get's used as "proof" that it must've been a fusion site. This is a circular argument and the claim, as Donny had put it in our interview, is also arbitrary since that "degeneration" would have to account for the loss of a lot of bp at the fusion site numbering in the multitude of thousands, not to mention the whole argument being ad hoc to boot. The evidence you have is just not very strong. It is very weak evidence, and, thus, it stands non-persuasive.

P4: If a fusion event occurred in the past then the Biblical model could explain and account for it better than the evolutionary model.

Keep in mind, I am not claiming that it happened, I am only saying that if it happened such an event would have a hard time being explained within the evolutionary model. Now, for all intent and purpose, I think it is highly unlikely that a fusion event had occurred given the evidence, but if I am wrong, and a fusion event occurred, then it is better explained within the Biblical model.

The reason for to get the entire human race today to only have 46 chromosomes instead of 48, so an extinction-level event that would wipe all those who carried 48 chromosomes on the alleged evolutionary path so only the one or ones carrying 46 chromosomes would've had to survive to continue on and pass the 46 chromosomes to every human being living today. They would've been the the genetic parent of all modern humans, all of which have 46 chromosomes.

Again, I'm not arguing that it happened, only that if it happened, the evolutionary model would not explain or account for it very well. Noah's Flood, within the YEC paradigm, would account for it. Thus, even if stronger evidence was found for a fusion event, this would not prove common descent since both paradigm's claims to account for it, but the Biblical model accounts for it better. In order for the evolutionary model to defeat this premise it would have to offer a better explanation within the evolutionary model and paradigm than the one offered by the Biblical-Creation model, outstripping it, and explaining why all humans today have 46 chromosomes.

This is a tall order for the evolutionary model, since they think humans and the great apes broke off from their common ancestor in two different directions, and this event happening sometime after the humans broken off from this ancestor. Something had to happen to all of the humans that had 48 chromosomes. Within the Biblical-Creation model the event of Noah's Flood happened, and, so, if a fusion event occurred, such an event would've explained why no other humans possess 48 chromosomes.

C: Chromosome 2 Fusion happening in the past is improbable, but if it did happen, it would still not prove relationship between chimps and humans, nor common descent.

This type of argument is called a deductive argument, which means, if valid (the conclusion following logically from its premises) and all four of my premises are true, then the conclusion must be true. The only way to disprove my argument would then be to attack my four premises. My conclusion is valid because it follows logically from all four premises, so you'd need to attack 1 or more of the 4 premises that I have presented.

ANTICIPATING OBJECTIONS

I anticipate critical objections to my arguments. These premises flow logically to my conclusion, and, thus, the critic must attack my four premises. With that, I predict some criticisms will be made. Since all four of my premises are challenges to the evolutionary view, I predict that all four premises will be challenged. Since this is a deductive argument, I do not think my conclusion will be challenged as much. The only way to challenge my conclusion is if my conclusion was invalid, which its not. Once you take into account all four premises, if true, would, logically, lead to that conclusion. Thus, the critic is forced to deal with my four premises. These will be discussed below.

Premise One: Telomere-telomere fusions are improbable, although not impossible.

The evolutionary model claims that a telomere-telomere fusion had happened in the past. There is a spot on chromosome 2 where evolutionists think this fusion had happened. This premise argues to the rarity of this event occurring in nature and under normal circumstances. Although you wouldn't think there would be any disagreements on this, the critic have a number of arguments on it.

1. Fusion events have been known to occur in the past.

It is very common for evolutionists to claim this. However, it doesn't make a whole lot of since to claim that it was probable in the past but we don't observe it today. Suppose my argument for miracles is that it may not be probable today, but in the past it was probable. Would that make sense? Now, that's not my argument for miracles, I think they still happen today, but it doesn't make a whole lot of since to assume that something was probable in the past that we don't observe today.

Why can't these evolutionists find a peer-reviewed paper of such telomere-telomere fusions happening today? Why do they only seem to find these examples of studies done in the past of some some sort of organism (usually pigs and horses are brought up)? Even then, as Donny discussed in our interview, they can only point to a few examples. This speaks loudly of the rarity of such an event and sets this premise even more in concrete.

Again, this premise is arguing against the improbability of telomere-telomere fusions not their impossibility. So, bringing up a few examples of alleged telomere-telomere fusions won't do since that will only help solidify this premise even further. Also, bringing up lab results of a telomere-telomere fusions in mice won't do either. For one, you'd need this to have plentiful examples than what they will likely give us. Secondly, you'd need such occurrences to happen in nature and thus a situation under laboratory controlled experiments will not work since these conditions are not normally found in nature. The evolutionary view on alleged chromosome 2 fusion needs to happen naturally. Bringing up these kinds of examples would commit strawman fallacies since I am arguing for the improbability of telomere-telomere fusions happening, not their impossibility.

However, I do feel the need to examine these papers further. How do they "know" that an alleged telomere-telomere fusion happened within pigs or horses? The reason is because they see the kind of "evidence" of a telomere-telomere fusion happening within what they believe to be the actual fusion site, and then they look for it in other animals to see if they can find similar signatures. Ultimately, then, the evolutionists gets ahold of the paper and then use these examples of a possible telomere-telomere fusion. This is known as a circular argument. Because the argument is viciously circular, this renders its conclusion arbitrary.

The chromosomes of the babirusa, a species considered to have diverged from an ancestor of the pig during the Miocene epoch, about 12–26 million years ago, were studied to determine the sites of recent rearrangements during evolution of the domestic pig. It is shown that there is a pericentric inversion of the entire short arm on pig chromosome 1, compared to its counterpart in the babirusa (chromosome 15). We also present evidence suggesting that pig chromosome 3 was derived by a telomere-centromere fusion of two ancestral chromosomes homoeologous to babirusa chromosomes 12 and 17. Likewise, we conclude that pig chromosome 6 was most likely derived by a telomere-telomere fusion of ancestral chromosomes homoeologous to babirusa chromosomes 6 and 14. The detection of interstitial hybridization signals from presumptive subtelomeric repeats in the same chromosome region as the evolutionary fusion points on pig chromosomes 3 and 6 indicates that the fusion sites may still contain elements that are otherwise restricted to the telomere regions of pig chromosomes (https://karger.com/cgr/article-abstract/73/3/203/339558/Recent-fusion-events-during-evolution-of-pig?redirectedFrom=fulltext, bold and italics added for emphasis).

I do not find these papers convincing. They seem to be operating under their own assumption to what a "fusion site" should look like based upon these subtelomeric repeats found in the alleged fusion site. This argument appears circular and arbitrary. However, even if these papers were right, these are very few examples, and so they show that this is, if it happens, a rare phenomenon at best. This would also mean that this first premise is still intact. With such a claim being so rare, the evidence must be really strong to get away from the high improbability of this event happening at all.

Another paper that was brought up to me was a paper on alleged telomere-telomere fusions happening in ants. This was delivered to me by Glenn Williamson also (a.k.a., ruhiff). This paper can be found here. However, within the paper itself, they assumed a telomere-telomere fusion happened within ants due to the inconsistent nature of some of their chromosomes discovered through a chemical tests. However, I'm not sure that their conclusions was definitive since they had admitted to this being based upon an assumption where they felt that assumption was justified. It is really hard to say if an actual telomere-telomere fusion actually happened, or did they assume this on the basis of chromosomes that were inconsistent from other ants?

Even if telomere-telomere fusions happened within a colony of ants, this wouldn't be enough to substantiate it. So far, we have three alleged reported examples of a telomere-telomere fusion, none conclusive, and no examples of this observationally occurring in the present in nature. Also since I'm not arguing against the possibility of telomere-telomere fusions, only their improbability, then this first premise remained in tact.

2. Fusion events can be reproduced in a laboratory with mice.

This one was brought up to me by Glenn Williamson in my email exchange. He brought up a paper where such telomere-telomere fusions were induced in a lab in mice (https://www.sciencedirect.com/science/article/pii/S0092867401800064). A lab example is not a natural occurrence so it wouldn't count because it is a controlled environment by which the telomere-telomere fusions are induced. I could understand if I, or any YEC, was arguing for the impossibility of telomere-telomere fusions happening, but neither me, nor any YEC I know is arguing that. Whether the argument is over its rarity of use and under natural circumstances. Lab tests is hardly natural circumstances.

In addition to that, the paper explains how they conducted the experiment. They said:

To generate a mouse deficient for telomerase activity, we deleted the germline copy of the mouse telomerase RNA gene (mTR) (Thomas and Cappechi 1987). Genomic Southern blots probed with the transcribed region of the mouse telomerase RNA gene identified a single band, suggesting that mTR is a single copy gene (data not shown). To delete the mTR gene from the mouse germline, we constructed the plasmid pPNT-mTRΔ, which allows replacement of the entire mTR gene with the neomycin resistance gene (Figure 1A; see Experimental Procedures). Using standard protocols, WW6 mouse embryonic stem (ES) cells (Ioffe et al. 1995) heterozygous for the mTR gene replacement were identified. The mTR+/− ES cells were used to generate chimeric progeny that transmitted the neomycin resistance gene through the germline (Ramirez-Solis et al. 1993). The chimeric mice were backcrossed to C57BL/6J mice before intercrossing them to generate the first generation (G1) mTR-deficient mice. Intercrosses between mTR+/− heterozygous mice generated viable mTR−/− offspring (https://www.sciencedirect.com/science/article/pii/S0092867401800064).

There is nothing about this experiment that would scream a natural occurrance. For Glenn Williamson to bring this up was a strawman argument. I must've told him several times and he even repeated Tomkins "in nature" so the lab experiment was an attempt to show me that it could be done, when I was denying that. However, there is another problem associated with the lab results:

Telomerase activity is thought to be required for telomere length maintenance in mammals, as it is in yeast. In human primary fibroblasts that lack detectable telomerase activity, telomeres shorten by about 100 bp per cell division (22, 13). The terminal restriction fragment (TRF) containing the telomeric repeats in human cells is typically between 10 and 15 kb in length. Some mouse species such as Mus spretus have a similar TRF length and rate of telomere shortening in primary fibroblasts (Prowse and Greider 1995). The laboratory mouse species Mus musculus used to generate the mTR−/− strain has TRFs that have been estimated on pulsed-field gels to range from 40 to 150 kb (30, 48). However, recent experiments using fluorescence in situ hybridization (FISH) suggest that the TTAGGG repeats on mouse chromosomes range from only 10 to 60 kb (Zijlmans et al. 1997). The difference between the estimates of telomere length determined using FISH and that determined by Southern blot is likely due to the scarcity of restriction sites in the subtelomeric repetitive DNA on the mouse chromosomes. Thus, the very long TRFs may consist mostly of subtelomeric repetitive DNA and only a relatively short terminal portion of telomeric repeats (31, 53) (https://www.sciencedirect.com/science/article/pii/S0092867401800064).

In the mouse example, the telomere-telomere fusions were only shortened by 100 bp per cell division. This is a serious problem. Since telomeres are thousands and thousands bp long, and the alleged fusion site is only 798 bp long, these fusion event in mice would've required thousands of base pairs of degeneration, as would the alleged fusion site. This is a big problem for one who claims a telomere-telomere fusion event had occurred in humans.

I have no reason at this time to not trust the results of this experiment. However, this does not eradicate Premise 1 since my first premise is not arguing against the possibility of telomere-telomere fusion, only its improbability, or its rarity of use. Also, given the controlled nature of this experiment, this is not it happening in nature, and thus, such telomere-telomere fusions are induced rather than it happening on its own, but the evolutionists needs it to happen normally for their arguments to stick. Finally, given the results of this experiment, even the paper that Williamson submitted to me admitted that these fusions was only showing a shortening of their telomeres by a 100 bp per cell division, far too less to be a true comparison with the alleged human chromosome 2 fusion which showed, if it occurred, a shortening of thousands of base pairs.

3. The claim of needing plenty of telomere-telomere fusions happening in nature is arbitrary and subjective.

This is one that I anticipate the skeptic leveling at me. How much examples would be required to make this probable? One? Fifty? A hundred maybe? How much is needed to make this no longer a "rare" occurrence? I agree that words like "rare" may be like using words like "some", "few", or "many" whereby the amount is unspecific. However, I would reject the idea that it is a subjective criterion. "Some" is not subjective, for example, since the word has a solid definition to the word. Same is true with few. When I say it is a rare occurrence I mean it is something that does not happened normally or under normal conditions. When I say many examples, although unspecific, I mean many examples. It would have to be enough to make this event a probable event.

For example, it is probable, that after working nights, I will go to sleep in a few. Why is that probable? Because my body is tired after work, I work nights, I also have to work tonight, and that is my normal routine. However, if I had just got up, and it is not normal for me to sleep once I had been well-rested, then it is improbable that I would go back to sleep right after I wake up. However, such occurrences are not improbable for my wife. She is known to go to bed shortly after waking up. Of course, her sleep patterns are different than mine.

The less natural something is the more improbable that it will be. Once again, this does not overthrow my first premise. The accusation of my premise being subjective is false since these terms are clearly defined within our language, and does not depend on my personal opinions on the matter. However, regardless how rare something is, such improbability can be overturn with strong enough evidence. However, the evidence will need to be strong enough to convince, and, thus, it's Premise #2 that we turn our attention to next.

Premise Two: The evidence against a specific fusion event occurring in chromosome 2 is strong.

We have quite a bit of evidence against chromosome 2 fusing in the past. For example, the alleged fusion site is only 798 bp long where telomeres are general 5,000 to 15,000 bp long. Thus, if a fusion occurred we'd expect that the fusion site be anywhere between 10,000 and 30,000 bp long. As mentioned with the mouse paper earlier, when telomere-telomere fusions were induced in mice the fusion sight had only degenerated by 100 bp. Given that thousands of bp would have to degenerate, this is a massive blow to the idea that telomere-telomere fusion had occurred sometime in humanity's distant past.

In addition to that, telomeres are never positioned within a highly functional gene, and the alleged fusion site sits right in the middle of the DDX11L2 gene which has about 255 expressed functions and a number of co-expressed functions (other genes require the DDX11L2 gene to function). It is also a non-coding RNA gene. Yet, this fusion site sits right within this gene, making it less likely that this has occurred in the distant past. Given this strong evidence, coupled with such an event's improbability of occurring, it is highly improbable that this event occurred in the past. The only way to try and get around this evidence is to try and use ad hoc rescue device. We will deal with some of these below.

1. The DDX11L2 gene is a "pseudogene."

Within the evolutionary paradigm they believe that certain "leftover" genetics was left over from our alleged evolutionary development. They usually label this "junk DNA" and they also think, in accordance to that development, that certain genes are also left over from it that serves no biological function. They usually label the latter as "pseudogenes" which is what the evolutionists would label the DDX11L2 gene, accept it has about 2,000 functions and it producing noncoding RNA. It has 255 expressed functions, and a number of non-expressed functions within the gene. This would make this a highly functional gene.

Within the YEC paradigm there is no real term called "junk DNA" or "pseudogenes" either. These terms are assigned by the evolutionary community every time a particular function is unknown, but as we are delving more and more into human anatomy, biology, and genetics we are learning more and more that these things do have biological functions and are essential to the organisms survival.

Because of this, this "pseudogene" claim is false. The DDX11L2 gene is a highly functional gene. It is also ad hoc, meaning it is a non-evidenced assumption intended to get out of a spot, in this case, the fact that this region of the alleged fusion site is located in a highly functional gene. Again, combined with the improbability of such an event occurring, this is strong evidence against this view.

2. The Site is Degenerate.

This is another ad hoc explanation to get around the evidence. Remember, the alleged fusion site is only 798 bp long and telomeres are anywhere from 5,000 to 15,000 bp long. So, if a fusion event took place between two telomeres, then we would expect the fusion site to be around 10,000 to 30,000 bp long. Why is this site only less than a thousand bp long? To get out of this issue evolutionists say that either when this event occurred, or over time, the sites base pairs degenerated (It significantly reduced in size as it lost information). However, even if such an event occurred, as Donny mentioned in our interview on my YouTube channel, it would still be thousands of bp long.

Remember the mice experiment. When they forced the telomeres to fuse they only degenerated by a 100 bp. That's not enough. Because telomeres' base pairs are in the thousands we would expect, regardless of any supposed degeneration, that these numbers of base pairs would still be in the thousands. However, they are not. There's actually no evidence that such a massive degeneration had occurred, but it does seem to be improbable. However, the other side does think it happened because the site is far more dense than most, if not all, of the genome. However, since density is one of the arguments used by the other side to favor the alleged fusion event, we will be dealing with the site's high density when we discuss possible objections to the next premise.

Premise Three: The evidence in favor of a Chromosome 2 Fusion is weak.

Again, to be clear, I am not saying that the other side doesn't have evidence to present in favor of their position. They do, but the evidence is weak, appears to have logical fallacies in them so this invalidates their arguments, or make such evidence arbitrary. As such, this significantly weakens the evidence that they do possess. Below, we'll deal with the evidence that they claim to have to present.

1. Head-to-Head Subtelomeric Repeats

DNA is made up four chemical bases: Adenine, cytosine, guanine, and thymine. These chemical bases are identified by their respected letters: A, C, G, and T. Since DNA is double stranded, these always appear in pairs called base pairs. They had discovered that these bases are repeated in forwards and reverse in the alleged fusion site, in a head-to-head fashion. Since the claim is an end-to-end fusion they claims that this proves that a fusion must've occurred in this spot.

However, the problem occurs when you realize that there are other areas of the genome that is also in this "head-to-head" fashion but no one thinks a fusion event had occurred. Chromosome 9, for example, has this head-to-head repeats, but no fusion event is believed to have happened in chromosome 9. The fact that you find this head-to-head arrangement, although odd, does not necessarily follow logically that a fusion event must've occurred because DNA is double stranded and there is always the possibility of repeats happening in reverse computation within the genome. This appears to be a non sequitur. This is where the conclusion doesn't follow from the premise, so the conclusion is rendered invalid.

However, the other side retaliates with the claim that it is also the most densest region in the genome. They claim that this is part of the argument. However, I don't see why the density would matter accept as its own argument, but they use it as a way to argue that because of both the high density and the head-to-head subtelomeric repeats and the fact that such an area is the highest and most dense region in the genome. It is to this next piece of "evidence" that we now turn our attention to.

2. The Supposed Fusion Site is in High Density.

Admittedly, this is the "strongest" evidence they have, relevantly speaking that is. This area is claimed to be the densest area within the human genome, and it is. Chromosome 2 is one of the smallest chromosomes in the human genome. This would also mean it would likely be the most densest when it comes to these head-to-head repeats.

However, density wouldn't guarantee a fusion happening. This is a fallacy in logic called affirming the consequent. In logic there is a type of argument called a conditional propositions or just conditionals. These are the "if/then" statements. Example: "if I was wide awake in the morning then it is because I had plenty of coffee. What follows after the "if" in this statement is called the antecedent, because it precedes the "then" in this statement. What follows after the "then" in this statement is what is called the "consequent" since it follows after the antecedent. Some people make a fallacy with conditionals called affirming the consequent and denying the antecedent, both of which renders the argument invalid (denying the consequent and affirming the antecedent, however, are valid forms of this conditional statement). We won't be dealing with denying the antecedent since it is irrelevant to our point here.

This argument commits the fallacy of affirming the consequent. This is where you affirm the "then" part of a conditional statement. In my example above, for instance, my conditional commits the fallacy of affirming the consequent. Could there be other reasons why I am wide awake in the morning? Yes, there could be. Maybe I had plenty of sleep, or perhaps an emergency had my hearty racing in the morning, or perhaps a nightmare scared me awake. Any of these possibilities are on the table. Could there be other reasons for this site being so dense? Yes, there could be. Perhaps the reason is that this is one of the largest of the chromosomes and there is a higher chance of more repeats and head-to-head arangement like this. Perhaps it's just chance. Either way, there are other reasons whether known or unknown that could've resulted from this region being so dense. However, the point is that just because this site is so dense does not automatically follow logically that a fusion must've occurred since there could be other reasons for such a high density. Although, this argument is stronger than the others, it is not conclusive since other reasons could exist that also accounts for this high density.

3. They had Discovered a Deactivated Cryptic Second Centromere

These are the regions of the chromosomes that the microtubules of the spindle attach during cell division. Every chromosome has at least one centromere, and they usually only have one centromere. However, if two different chromosomes fuse they expected to find a deactivated second centromere within the chromosome. They claimed that they found such a signal.

At first gloss this seems like a strong argument until you realize that their evidence for a cryptic deactivated second centromere is weak. Dr. Jeffrey Tomkins, a geneticist, gives several problems for this alleged cryptic second centromere (Tomkins, "Chimps and Humans", pp. 59-60):

First, centromeres have what is called alphoid sequences or alphoid repeats. Although this site has repeats they don't have the ones that match the ones associated to actual centromeres. If this was once an active centromere then we would expect repeats that would be similar to the kinds of sequences that we see in functional centromeres, but we don't see the kinds of sequences that are associated with them. Also, the ones that are associated to centromeres in the human genome are unique to the human genome. There is no chimp counterpart.

Second, it is much smaller than the length of actual centromeres. Because of this, it shares the same problem as the alleged fusion site of being too small. Human centromeres are huge, spanning out between 250,000 to 5,000,000 base pairs long! However, this alleged second centromere is only 41,608 bp long! This means that it is too small to be a centromere. However, it get's worse. Three of the different regions are not even alphoid repeats at all. Two of them are referred to as retroelements, and one of them are LPA3/LINE repeat of 5,957 bp long and the other of the two are SVA-E element of 2,571 bp long. These come to 33,080 bp long (minus the insertions).

Thirdly, and finally, the most serious problem with this is that it is being located in a highly functional gene, which means it shares, again, one of the same problems with the alleged fusion site. This alleged cryptic centromere, which is suppose to be deactivated, is located in a gene called ANK-RD30BL or the Ankyrin Repeat Domain 30B Like gene. As Tomkins puts it:

Interesting, the alleged centromere sequence covers both intron exon regions of the gene. In fact, the part of the alleged fossil centromere sequence that lands inside an exon actually codes for amino acids in the resulting gene's protein...This type of ankyrin repeat protein is associated with the cell's membrane and is believed to be involved in the interaction of the structural network of proteins inside the cell called the cytoskeleton in connection with receptor proteins imbedded in the cell membrane. The fact that the so-called fossil or cryptic centromere is a functional region inside an important protein-coding gene completely refutes the idea that it is a defunct centromere (Tomkins, "Chimps and Humans", p. 60).

It seems the evidence against this being a deactivated and second centromere is strong. It doesn't seem very probable that such a second centromere exist within chromosome 2. However this is a problem for the claim that there was a telomere-telomere in the supposed evolutionary distant past. It would also seem that my third premises is still well-intact. The evidence claimed for a fusion event appears really weak.

Premise Four: If a fusion event occurred in the past then the Biblical model could explain and account for it better than the evolutionary model.

Essentially, this premise considers the chance, no matter how small it might be, that there could've been a fusion event. Although it seems at this point to be highly improbable, what if there was one? What if, somewhere in the distant past, two chromosomes fused making one chromosome, namely chromosome 2? Would this prove that we're related to the chimp? Would this prove human evolution? The answer to those questions is no, it wouldn't. However, we have to ask, which model would better explain this event? The biblical model or the evolutionary one?

If two chromosomes fused in the past within the human genome, then this would've had to have something happening to solidify this situation. All humans have 46 chromosomes and all great apes, including chimps, have 48 chromosomes. If this event happened in the past, then the one whose chromosomes fused together to form 46 chromosomes would be the ancestor of all modern humans. This would mean that something must've happened to all other human being that had 48 chromosomes, for only the one or ones with 46 chromosomes to survive. An extinction-level event, as it were. Since the Biblical model has one in the form of the global Flood then this would explain the survival of a few humans that now carried 46 chromosomes instead of 48. Below I have anticipated some possible objections.

1. The Pigs Did Not Experience an Extinction-Level Event.

This objection was brought up to me by Glenn Williamson (a.k.a., "ruhiff") in my email exchange with him. The claim was since telomere-telomere fusions are assumed then would it be required for an "extinction-level" event to have occurred since he thought it didn't happen for the pig and others that he assumed such fusions taken place. As he put it:

Did the pigs face an extinction level event? Did the zebra face an extinction level event? Did the jack jumper ant face an extinction level event? All these species seem to have survived just fine (Glenn Williamson, personal email exchange)

I think he's confused about the nature of an extinction-level event. First, the evidence that is claimed for telomere-telomere fusions for these other animals is weak and possibly circular. Second, if telomere-telomere fusions had happen in the past, why would it be more common in the past than it is today? Why wouldn't someone observe telomere-telomere fusions happening in the present? If it can't be observed commonly in the present, it is even more doubtful that it happened in the past.

Thirdly, even if the pigs, the ants, and the zebras all experienced fusion events, this doesn't take away from the argument. At some given point, assuming these alleged fusion events, that one pig, that one ant, that one zebra must've gotten two telomers at the end of two of their chromosomes and that one became the precursor for all others after. However, for the ants and the pig, at least, I know have different number of chromosomes, so this argument wouldn't apply to them, accept with that specific kind of pig or specific kind of ant that has that number of chromosomes. This is not the same as what we're arguing here. Since all human beings have 46 chromosomes without exception then that one that the fusion event happened in will be the precursor of all modern humans with 46 chromosomes, thus something extra would be needed to explain how the remaining humans with 48 chromosomes perished. The Biblical model has that explanation with the global Flood, but the evolutionary model lacks it. The point of this premise is that the Biblical model has that explanation, and better explains it, while the evolutionary model lacks it. I just think Williamson misunderstood the argument, and, thus, unintentionally, straw-manned me.

2. Maybe Multiple Fusion Events Happened Simultaneously?

This is both improbable and implausible. The idea that multiple telomere-telomere fusions happening simultaneously of each other and in the same area and in the same way would really stretch the boundaries of credulity. As high as the odds are of even one telomere-telomere fusions happening, they are even larger for multiple telomere-telomere fusions happening at the same time, between the same two chromosomes, in the same place, in the same way, with the same number of base pairs, and with the same organism. This doesn't seem at all likely, and, so far, I have never seen any of them suggesting this possibility. I asked Donny about it in our interview, but he didn't find the concept very plausible either. I honestly don't think any of them will suggest this, but, at the same time, I wouldn't put it passed them either.

3. There is a Wide Variation in Chromosomes in Both Genus and Species.

Again, this objection comes from Glenn Williamson in my email exchange with him. He writes to me:

There is huge variation in chromosome number at the family and genus levels … are you suggesting that one type of fusion (one involving centromeres rather than telomere-telomere) is more “survivable” than another? (email exchange with Glenn Williamson).

Once again, Williamson had failed to understand the argument. All modern humans have 46 chromosomes, without exception. There isn't a different number of chromosomes with and between humans the way it is with other organisms on the planet. Because of this we would need an explanation to account for why it is that all modern humans possess the same number of chromosomes. The fact that many animals had survived with different number of chromosomes just backs this point up even more: why didn't the humans who had 48 chromosomes survive into the present? I just don't think ruhiff understands this argument very well, and certainly not the point of it.

I think premise four is also well-established. If this event happened, then the Biblical can explain this conundrum, but the evolutionary model would lack any satisfactory explanation. This is problematic.

Conclusion: Chromosome 2 Fusion happening in the past is improbable, but if it did happen, it would still not prove relationship between chimps and humans, nor common descent.

This is a deductive argument, so one would have to disprove the four premises to disprove a valid deductive argument. The only objection they can try to level at the conclusion is by accusing it of being invalid. However, my conclusion follows logically from all four premises. Since the four premises appear to be true, and since the conclusion is valid, this makes this argument a sound argument.