The probability of something happening E in the past that actually happened is 1.
The question, however, is how likely is something like E happening in a model with X and Y processes. Or course, any number we compute needs to be compared to the results of others models, with A and B processes, to understand the relative likelihood. That relative number can give insight into whether or not E is best explained by X and Y or rather better explained by A and B.
Of course, this is not how the anti-evolution argument goes.
Because Bill doesnât take any stands on practically any idea put forth by a creationist or ID supporter, except that any idea might be feasible. There literally is no filtering being attempted. You may recall a few years ago when I asked Bill if there were any ideas, past or present, coming out of the Discovery Institute that no longer seemed viable. He did not venture an opinion. Out rather the opinion was that none were currently out of the running.
Thatâs quite deliberate fence sitting. There are any number of completely incompatible hypotheses that have been put forth by the ID and Creationist communities. Some within those communities have had tremendous debates about the relative viability of the opposing ideas. Those few at least know that robust science is based on a winnowing of ideas, separating the good from there bad. Not so with Bill. He may learn more but never progress a step further at resolving answers.
IMHO, of course. But thatâs why I wonât engage him anymore on science. Cheerleading is not science. Dithering around is not science. Perfectionists tend to make terrible progress.
Do you see any difference between taking a stand on historical science like human and chimps sharing a common ancestor and a laboratory experiment which yielded a p value of .01?
What is the p value of humans and chimps sharing a common ancestor? We donât have one and thats why I sit on the fence. The evidence has gone back and forth over the few years I have looked at this hypothesis. Historical biology is really hard.
Now that Nathaniel Jeanson has shown that the molecular clocks may be several orders of magnitude shorter than this hypothesis requires I think the creationists have nosed in front. I also think the evidence of the second âcentromere being crypticâ is very troubling for the fusion hypothesis. This would depend on the detail of how cryptic.
Why? Itâs obviously going to be cryptic, because if it wasnât then it would still be functional, and a fused chromosome canât persist with 2 functioning centromeres, as it would get torn in half.
They werenât in the race to begin with, but Jeanson has shown nothing of the sort. His methods are ridiculously wrong, and donât come close to overturning decades of conventional research in this area.
What makes you think the changes would be neutral? Often the way the centromeres get inactivated in the first place is by deletions of significant fractions of the sequence.
By the way, I seem to recall Old Earth Creationist Fuz Rana presenting a similar argument on a podcast, perhaps a decade ago. (Sorry, I donât have a citation. I was listening to him while driving.)
POSTSCRIPT: I just now found this article by Dr. Rana from June 1, 2010. Iâve only skimmed it for now but Rana concludes:
To summarize, in order for human chromosome 2 to arise from the fusion of two chromosomes, a succession of several highly improbable events would have had to have taken place. Thus, the evolutionary account of the history of human beings seems untenable.
So perhaps Ranaâs view of human chromosome 2 has âevolvedâ over time.
We may be approaching from different directions. Iâm thinking of likelihood analyses in phylogenetics. Iâd say that the data are 2N=48 for whatever primates you put into a tree and 2N=46 for humans. All the data are in the tips of the tree. The probability of observing those data given the tree is quite low, just as the probability of the observed distribution of any characters is low on any tree. Again, I donât see this as different from the likelihood you get out of any phylogenetic analysis, the probability of observing the sequence data you have given a particular tree and model of evolution, P(D|T). That probabililty isnât 1, and it isnât high. However, if you compare it to the probability of observing the data in the absence of a tree, itâs a much larger tiny probability. But all that increase, in the current case, arises not from the probability of the change happening on the branch but from the lack of a need for independent explanations of the states in different taxa. We donât have to explain 2N=48 separately, in that case. The change from 2N=48 to 2N=46 happens in the same way and has the same likelihood in either case.
I donât think so, and I canât think why recombination would be inhibited given homologous pairing. Do you have a citation for it? And even if they accumulated mutations independently, it would take a long time, on average, for this to result in genetic incompatibility. Now, Iâm thinking there might be reduced fertility because if there were multiple centrosomes, the spindle wouldnât always pull the paired bits in the right direction, so if you had chromosome AB paired with a and b, a and b might be pulled toward opposite poles and AB could be pulled to both poles. Still, there are a number of examples of living populations with fusion polymorphism in which there are few if any problems for heterozygotes.
Alas, no. But Iâll go digging in some archived threads where I think the original account might be and if I find anything Iâll let you know. I suspect that this may be a case of my having incorrectly understood what was being said in the originalâŚ
Biologists already knew there was a fusion somewhere in the human genome once it was determined that we have only 46 chromosomes, compared to 48 in the other great apes.
And, as you have acknowledged, the likelihood of such a fusion existing in a genome is very low.
Yet, when the technology eventually arose to see if the fusion was there, there it was.
IOW, evolutionary theory was able to predict something so unlikely that, if it was just a lucky guess, would be the equivalent of picking a winning lottery ticket number just by chance.
Of course, it was not a lucky guess, but a demonstration of the predictive power of the theory of evolution (more specifically, common ancestry).
Could you cite the successful predictions made by ID theorists based on the same observation? Iâd love to hear them.
It might be worthwhile quoting Ken Millerâs comprehensive debunking of Tomkinsâs attempt to deny the chromosome fusion, which was posted on Sandwalk:
I exchanged a couple of emails with Tomkins last year, pointing out the errors in his papers (in creationist journals) on the Chromosome 2 fusion site. As you all know, heâs very excited that heâs found a âhighly-expressedâ gene that âspansâ the fusion site. This means, he claims, that the fusion site couldnât possibly be what it seems.
Heâs wrong, and many of the reasons why have already been pointed out in this discussion. First and foremost, the gene in question (actually a pseudogene with no known function) is a member of a transcript family known as DDX11L. Tomkins pointedly ignores the Costa (2009) paper, which identified 18 members of this gene family. Each of them is next to a sequence known as âWASH,â which is transcribed in the opposite direction of the DDX11L pseudogene. And, more to the point, each and every one of them is located right next to a telomere â except for one. Thatâs the DDX11L2 sequence, which is parked right next to the fusion site. That alone is very strong evidence that site is exactly what it seems to be â the remnant of a telomere-to-telomere fusion.
Most of the genome databases show the DDX11L2 sequence as off to one side of the fusion site, so it really doesnât span it. However, in some of the databases there are transcript variants that include the head-to-head telomere sequence motifs as one of the introns in the primary transcript. That is basis on which Tomkins claims that the gene spans the site. But the very same data are easily explained by variability in the termination of transcription so that occasionally a somewhat longer RNA is produced. This is exactly what I pointed out to TomkinsâŚ. So that any claim that I âadmittedâ he was right about his interpretation is bogus.
And, if Larry permits me to rant on a bit:
⢠Tomkins said that âsomeâ chromosome banding patterns were similar between humans and other great apes. Some? The matches were so extensive that Yunis & Prakash (1982) were able to align each and every chromosome from four different species!
⢠He said there were too few telomere repeats in the fusion site. A âpristineâ site would have 20,000 â 30,000 bases. But the fact is that âpristineâ telomeres would prevent fusion, and treatments that dramatically shorten telomeres actually cause fusion, which is why there are so few repeats in chromosome 2. The small number of telomere repeats is exactly what should be expected at a fusion site.
⢠Tomkins said that the DDX11L2 gene was unique to humans. Wrong. As Costa (2009) showed, there are members of this family in chimpanzees and gorillas. And, as you might expect, they are located right next to telomeres.
⢠Finally, Tomkins lays great emphasis on the observation that transcription factor binding has been found throughout this region. But simple binding says nothing about the specificity of binding or its biological importance.
⢠Tomkins has constructed a straw man in which an authentic fusion site would have to be an exact replica of the ends of two present day chimpanzee chromosomes to be valid. What he does not seem to realize is that the fusion occurred millions of years after our lineage separated from chimpanzees, and that both lines have continued to evolve along separate pathways. That accounts for the differences he regards as so significant.
The evidence for a chromosomal fusion in the ancestry of our species is on very solid ground, and has been greatly strengthened by the very research he wishes to use against this idea.
I donât know how easily an exact probability could be calculated. Suffice it to say it is probably very low.
Which gets us back to my point above: Evolutionists were able to predict that there would be a fusion in our genome based on three pieces of knowledge:
Our closest relatives are the other Great Apes.
Those relatives have 48 chromosomes in their genome.
We have only 46.
Then, a few decades later, Bingo! The fusion was in fact there.
You are missing the mark here for I am not negating evidences for the fusion event, not at all. What I am interested in is whether we can get an idea of the likelihood of such an event. Donât you think it is a scientific question? And in that case, donât you think that a way to answer this question is to see how many such events have been documented in other lineages?
Then why do so many professions ID-Creationists (Dembski, Behe, Axe, etc.) push the âitâs too improbable so it must be DESIGNED!â false argument?
A straw man again, for design theorists donât infer design from mere improbability alone. Something else is required. Specificity for Dembski; Irreducible complexity for Behe; Fonction for Axe.