The fixation problem is not a problem for it being a fusion

Most creationists will disagree until the end of time.

How about we test the hypothesis by observing that humans can make things by using intelligence. That is completely irrelevant of course, but that has never stopped its utilization before. Seriously, by your own approach, the hypothesis has been tested in that fusion and drift have been observed.

There is no fixation problem to resolve.

Per the several posts above, the evidence for fusion is close to incontrovertible. If you are not convinced, that is your prerogative, but such phantasmic incredulities do not oblige scientists to reconsider.
Fusion can happen. Fixation can happen. It appears they did happen with respect to chromosome 2. If some powerball winner is sitting at his mansion pool side, what is the point in arguing with him that he is not actually rich, because what are the odds of winning the lottery? Throughout human history, there have been innumerable genetic events which did not become fixed, and others have. This one was.

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Thats not my argument. We know a fusion happens once out of 1000 births. The probability challenge is around fixation and what sequences are claimed to have been-fixed in the population. The way to solve this is a plausible model that reconciles the change required. This is what the papers you are citing are attempting to do.

The alternative is the creation scenario of original design.

We can make a ballpark estimate.

We have a few recorded cases of people with 44 chromosomes;

A 1984 report describes a family with 3 adult siblings who had 44 chromosomes, #s 13 and 14 combined.
• A 1988 report tells of 3 distantly-related families in Finland, also involving #s 13 and 14, whose Rob chromosome passed in carriers through at least 9 generations, appearing in at least one homozygote.
• A 1989 paper describes a Rob between #s 14 and 21 in a homozygote whose carrier parents were related.

Trickling into the headlines was a case report from 2013 of a 25-year-old healthy Chinese man who has 44 chromosomes because each 14 joins a 15 – a combo not seen before.

Let us say for estimate’s sake hat there are currently 7 people out of 7 billion recorded to have 44 chromosomes.

Let us be generous and say 1 in 1000 people have been karyotyped.

Then the frequency of 44 chromosome person is 1 in a million.

The probability of fixation of a neutral mutation is 1/2N.

For argument’s sake, let us say the typical human/protohuman population throughout history was 1 million humans, who have existed for 10 million years, with a generation time of 10 years; ie 1 million generations.

Then the probability of a fusion mutant fixing in a population of 1 million over 10 million years is 1/2000000 * 1000000 = 1/2.

The probability is of course much higher if the fusion event is beneficial rather than neutral.

Btw, @colewd, do you think zebras, horses and donkeys are one biblical kind?

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Chromosomal translocations occur randomly and can become fixed in a population. Its just like we losing the ability to make our vitamin C and that loss becoming genetically fixed in all extant human populations. Why making a big fuss over something quite trivial?

The fusion event is a tested hypothesis. The signature of the head-to-head fusion is clear in Chromosome 2 is clear.

This is irrelevant to whether there is a fusion there or not.

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The problem is that you aren’t saying getting three straight flushes in a row is so unlikely that the player must be cheating. You are saying that because getting a straight flush three times in a row is so unlikely, they actually have two pair even though we can see the cards! It would be a fact that they did get the cards they got, just as it is a fact that Hsa2 is a fusion.

This thread is about what Hsa2 is, not how it happened. If you want to talk about how it happened, start a new thread and stop hijacking this one.

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That’s irrelevant to whether or not it is a fusion site. It clearly is a fusion site, regardless of the probability of such a fusion fixing in a population.

@Witchdoc please refer to this comment earlier in the thread. Bill is evidently uninterested in the subject of this thread, and I’d ask you not humor him in his attempts to hijack it.

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If I randomly draw a King of Diamonds do I need a new hypothesis if I draw a 3 of Spades on the next draw?

You could do the same for any 5 card hand, and the probability of any specific 5 card hand would be the same. That’s the problem with your Texas Sharpshooter fallacy. You wait until the cards are drawn, and then stand amazed at the improbability of drawing those specific 5 cards.

But you aren’t doing that. You are waiting until the cards are drawn, and then declaring that those cards were the target all along. It would be much more impressive if you predicted the specific sequence of the human genome 5 million years ago.

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As soon as you have neutral mutations occurring the chances of neutral mutations reaching fixation is 100%. It is inevitable.

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Please read this more carefully. This is not a probability argument but an argument on the assigned cause using probability as a filter to judge if the assigned cause is the actual cause. Essentially assigning a P value to the hypothesized cause. If the P Value is lower than a threshold say ,05 the hypothesis is rejected. I know you understand this process well.

When you calculate a p value you are calculating a probability. In essence, a p value is the probability of getting a false positive. You are pushing a probability argument.

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I am pushing a method to determine cause. The method is the scientific method. Probability or more formally statistics is a tool used in that method. Just as correlation graphs paredo diagrams are a tools.

Imagine I draw a card from a custom deck. You don’t know anything about this deck, nothing about the values, suits, etc. The card I draw is a 28 of Tangerines.

Now here is the question: What information about the probability of drawing that particular card from the deck could possibly convince you that I didn’t draw it? Hopefully your answer is: ‘Obviously nothing!’

Because it would be silly to suggest that any possible information about the probability of an outcome would change what the outcome is, right? Now realize that what you are doing is even worse! You are saying that if we don’t know the probability of drawing a 28 of Tangerines, we can’t even say that is the card we got. It doesn’t matter if it says so right on the face of the card, until we know how many cards, values, suits, etc, are in the deck the card could really be anything!

Do you understand why this is an exceptionally silly thing to say?

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Bill, these are not equivalent. This is why students studying probability first learn about permutation and combinations (basic combinatorics).

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@colewd I happen to know a bit about Casual Inference in statistics. I can try to boil it down for you if you like. However, the methods you propose cannot show cause in the way you want.

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@Dan_Eastwood & @T_aquaticus,

Honestly, I feel Bill’s attempts at hijacking this thread have gone on far too long already. Since he refuses to stay on the actual topic, can we get him a new one so he stop vandalizing this one?

Feel free to delete this rather than post it.

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A split is warranted. On it …

I’m a bit short of time, so if I move posts that ought to stay please let me know and I can fix it later.

And thanks for suggesting the new title! :slight_smile:

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How do you think this is revenant to determining the cause of drawing the 28 of tangerines? What we see is indeed a fact. What caused that event is a different question. When you make a claim that there was a fusion event that caused the chromosome in question then probability becomes a tool to determine if your claim is likely true.

Again, the creationists will claim the chromosome was designed from scratch.

A post was merged into an existing topic: Chromosome Fusion in Humans - or Not?

Fusions occur randomly, but probably do so less frequently. When they happen, however, and become fixed in a population it makes no sense to calculate the probability of it happening because it has already happened.

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Congratulations on finally arriving at the point. I expect your next comment to include an affirmative statement that Hsa2 is actually a fusion. Anything else will mark you as too dishonest to engage with.

It isn’t about the cause, it is about the result. The result is the result no matter the probability.

And what we see is a fusion. The probability is a separate question, and irrelevant to the observation that it is a fusion. Just like the probability of drawing a 28 of Tangerines is a separate question, and irrelevant to the observation that it is the 28 of Tangerines. See how that works?

That’s odd. I don’t claim that a fusion event caused the chromosome, I infer it from the fact that the chromosome is a fusion product. I make the claim that the chromosome is a product of a fusion because it demonstrably is, you can see that from the data. Much like I infer that the unknown deck contains a 28 of Tangerines from the fact that I drew one. The mechanism by which a fusion could happen or reach fixation is irrelevant to the fact that it is a fusion, so must have fused and reached fixation by some mechanism.

Which would be relevant if my claim was about the mechanism and not the observation. Then again, none of the current models are problematic for fixation. At most, they might be a problem for fixation without selective pressure. Is there a reason to rule out the possibility of selective pressure for the fusion? If so, then an extremely low probability of fixation under neutrality might suggest some additional mechanism.

Which would be interesting, but still irrelevant to whether or not it is a fusion.

They claim that the chromosome was designed with a fusion? First, odd design choice. Second, what is the mechanism by which a chromosome could have been designed with a fusion? Essentially they would be invoking ‘design’ as the additional mechanism mentioned in the prior section, but this mechanism isn’t actually an explanation because it would itself be unexplained. And at the very worst, you’ve got an unlikely outcome of known mechanisms against an unknown processes that would require more explanation than the thing they are invoked to explain. And that’s not a great solution.

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