Toward a Consensus
In my previous articles (here and here) I reviewed Dennis Venema’s articles (here, here and here) which claimed that the genomes of different species are what we would expect if they evolved, and in particular the human genome is compelling evidence for evolution. The claim that the empirical evidence powerfully confirms evolution is an objective claim that can be evaluated in the common language of science. There is no excuse why people holding even opposing views on origins cannot at least agree on what the science has to say. Unfortunately, origins discussions often get ahead of themselves, rushing to judgment and casting aspersions before the empirical science is objectively evaluated and agreed upon. My goal in this series of articles is to work toward such a common understanding.In my previous article I responded to professor Venema’s claims that the human genome, as well as the genomes from the other primates, together are compelling evidence for evolution. We saw several serious problems with Venema’s claim. And as always, we forestall the rebuttal that those problems can be explained. The claim was that the evidences “strongly support the hypothesis that our species arose through an evolutionary process,” not that one can envision speculative and unlikely explanations for problematic data. And there are a great many problematic data. While fair-minded thinkers can argue about the finer details and specific implications, it seems abundantly clear that the typical evolutionary claim, as exemplified by Venema, that the data (genetic data in this case) make evolution compelling, is false.
How could we possibly make this claim in light of the empirical evidence? There seems to be a disconnect here.
The Human Chromosome Two
There is one piece of contradictory evidence I did not discuss in my previous article. I omitted it because Venema gives it special emphasis and so it merits its own article. This evidence is that while we humans have 23 pairs of chromosomes, for a total of 46, the chimpanzee, bonobo and gorilla each have 24 pairs of chromosomes, for a total of 48.
In my previous article I pointed out several differences in the primate genomes that contradict evolutionary theory. This difference in chromosome count is yet another fundamental problem for evolution. According to evolution, humans have 23 rather than 24 pairs of chromosomes because of a chromosome fusion event in our past history. Early in our evolutionary history we had 24 pairs of chromosomes, but the fusion event reduced this number to 23. In fact, evolutionists such as Venema present this evidence as yet another great confirmation of their theory. You can see other examples of this here and here.
But this claim made by evolutionists is at odds with the science. There are many problems with their claim, and they fall into two major categories.
First, the specific DNA sequence found in the human chromosome in question, defies any such fusion event. The repetitive telomere sequence is far too short and too dissimilar to indicate a fusion event. Furthermore the supposed fusion region is full of genes with the supposed fusion site lying within a highly expressed RNA gene. None of this makes sense on the fusion hypothesis. You can see this article for the details on why the evolutionary account is not feasible.
Second, even if, somehow, such a fusion event occurred (in spite of the DNA sequence data), it would not demonstrate evolution as evolutionists claim. For such a fusion event would have occurred in, and spread through, an early human population. There is no evolutionary relationship revealed. Even if evolution is true, this fusion event would give us no evidence for it. The fused chromosome did not arise from another species, it was not inherited from a human-chimp common ancestor, or any other purported common ancestor.
Disturbing pedagogy
As noted above, in spite of these contradictions presented by the empirical evidence, evolutionists claim this as a powerful confirmation. In fact, their presentation of this evidence is carefully crafted. The failures and contradictions are not included and the student is led to believe the false conclusion that the science makes evolution compelling.
Evolutionist Ken Miller made precisely this argument as an expert witness in federal court. And here is a typical lesson informing students that these chromosomes are “striking evidence of [human and ape] common ancestry.”
And professor Venema recounts his lecture strategy on this topic. It is a particularly disturbing account of how he sets students up for a faith-versus-science crisis that is straight out of the Warfare Thesis.
Venema explains that “only I really know what is coming,” as he carefully tailors the information that is presented to the unwitting students.
Venema takes his students through fruit fly genetics and then presents them with a graphic showing chimp and human chromosomes. But the slide is not labelled, and the students are unaware they are not looking at similar species, such as flies.
According to the class information presented, the students are led to conclude that the two unknown species in question share a common ancestor. Venema then reveals to them they are talking about the chimp and human species.
Having carefully set up the students with false science, Venema then casts their rebuttals in terms of the Warfare Thesis:
As one might expect, teaching this subject matter at times engenders controversy, crises of faith, anger and fear in students
The students, Venema explains, are “caught between their faith communities and the science.” The students have been set up. They have been manipulated with a false narrative, and any lack of acceptance is cast as a personal issue. It’s straight out of the Warfare Thesis.
Conclusion
It is crucial that we understand and teach the science without bias. As we have seen, common descent in general, and the particular case of chimp-human common descent, are astronomically unlikely. This is no mystery. These problems and contradictions are from the empirical evidence. Common descent makes no sense on the science. And the arguments and evidences given by evolutionists in support of common descent do nothing to change this. In fact, generally they do not even address the problems and contradictions. I hope that changes.
Funnily enough I've recently written two articles about chromosome fusion directly addressing some of Jeff Tomkins claims.
ReplyDeletehttp://roohif.wordpress.com/
Would love to hear your thoughts.
Well you are making my point. The gene expression is an aside (yes, it is a relative term). Genes shouldn't be there, regardless of expression level, and TFs shouldn't be binding there. You also didn't address the problem that the alleged telomere sequence is too dissimilar to make sense. (And again, the point is not that some sort of explanation is not possible--there are always alternate hypotheses. But the evidence is not compelling for evolution).
DeleteOkay.
DeleteSo are you still claiming that this pseudogene is "highly expressed"? Relative to what?
Happy to address the other points in more detail later, but a quick summary is that TF binding sites are ubiquitous, and secondly, these are _subtelomeric_ sequences - you should not expect pristine telomeres.
It's Sunday afternoon here, give me a few days.
So are you still claiming that this pseudogene is "highly expressed"? Relative to what?
DeleteThis is tedious. I said the expression level is an aside.
these are _subtelomeric_ sequences - you should not expect pristine telomeres.
Again, this isn't going to work if every comment is tedious. I said nothing about expecting "pristine" sequences--we're nowhere close to that.
Tedious? You've only made four claims (too short, too dissimilar, full of genes, highly expressed), so I don't think it's "tedious" to press you on a full quarter of your claim.
DeleteAs for too short and too dissimilar, you're making an implicit claim that it should be longer and more pristine. If the sequence was longer and more pristine you would have a functional telomere, in which case it would have prevented fusion in the first place. So no, if you are looking for a fusion signature, you would NOT be looking for longer and/or more pristine telomere motifs.
And keep in mind, that "Highly Expressed" managed to make it into the title of Tomkins' paper - it's not a trivial claim.
DeleteTedious? You've only made four claims (too short, too dissimilar, full of genes, highly expressed), so I don't think it's "tedious" to press you on a full quarter of your claim.
DeleteUnfortunately this is how these discussions tend to go. Now it's tedious upon tedious.
As for too short and too dissimilar, you're making an implicit claim that it should be longer and more pristine. If the sequence was longer and more pristine you would have a functional telomere, in which case it would have prevented fusion in the first place.
The problems you are avoiding is how the sequence gets so short and "degenerate," and with all the genes. Your argument that, "Well there was a fusion event, therefore you'd expect it to be short and degenerate" is circular.
"Now it's tedious upon tedious."
DeleteWell, how about you just say "it's not highly expressed" and we can move on.
"The problem you are carefully avoiding is how the sequence gets so short and degenerate."
There are many reasons why the telomeres become shortened or non-existent, one of the simplest explanations is that telomerase was dysfunctional for a time.
By the way, I don't claim that the fusion site is "degenerate", I say that it is "sub-telomeric". If you look at the DNA sequences at the end of our chromosomes you will see that there is no single point at which the internal DNA stops and telomeres begin - there is a blending of the two.
What you see at the fusion site is NOT the result of perfect 'TTAGGG's "degenerating" over the last 6 million years or so.
Your argument that, "Well there was a fusion event, therefore you'd expect it to be short and degenerate" is circular.
No, I'm telling you what I would and would not expect of telomere sequences if there was a fusion. Fusions can only occur when the sequences that prevent fusion - telomeres - are dysfunctional. If the telomeres were functional, I would expect them to have prevented fusion in the first place. This is not circular - it is a prediction of a model.
What you see at the fusion site is NOT the result of perfect 'TTAGGG's "degenerating" over the last 6 million years or so.
DeleteIndeed.
There are many reasons why the telomeres become shortened or non-existent, one of the simplest explanations is that telomerase was dysfunctional for a time.
Ah, good, an explanation. Not a very good one though. So somehow telomerase is repressed or inhibited. How did that happen, where did it come from, and why did it conveniently go away? Aside from the disaster that would ensue, you have the problem of why does the absence of telomerase activity only affect the one chromosome? You may be correct that this is one of the simplest explanations, but it isn't simple.
You may be correct that this is one of the simplest explanations, but it isn't simple.
DeleteI can't go back a couple of million years with a microscope and watch exactly what happened - that appears to be your expectation of me in order to conclude there was a fusion.
But I could list a dozen species where it is clear that fusions have occurred and you wouldn't blink an eye. Sure most of these fusions are telomere-to-centromere, but there have been other telomere-to-telomere fusions before (see the Four-horned Antelope).
So if a telomere-to-centromere fusion is no problem, why is it suddenly intractable for a telomere-to-telomere fusion?
Evolutionist Ken Miller made precisely this argument as an expert witness in federal court. And here is a typical lesson informing students that these chromosomes are “striking evidence of [human and ape] common ancestry.”
ReplyDeleteAnd here I was thinking that the chromosomes were striking evidence of common design. The designers were obviously repurposing already available, tried and tested genes and adding functionality through class inheritance. This is the sort of design reuse that software designers/engineers do all the time.
Venoma is a typical Darwinist jackass. Judging from his fallacious and stupidly dishonest propaganda, one can only wonder if he believes that a modern BMW inherited tires, wheels, windshield and bumpers from a Ford Model T via common descent.
What a bunch of idiots these people are. Are they trying to fool and indoctrinate little children or are they just born stupid?
Great points, Louis, as usual.
DeleteWouldn't there have to have been two fusion events to go from 48 to 46 chromosomes?
ReplyDeletewe are talking about chromosomes pairs. so if 2 pairs from 24 (48 chromosomes)get fused now we have 23 pairs. one of them actually have 4 individual chromosome.
Delete"Genes shouldn't be there, regardless of expression level, and TFs shouldn't be binding there"
ReplyDeleteAre you certain? Isn't the gene present precisely the gene you'd expect if the fusion represents subtelomeric DNA:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2705379
"During a project aimed to analyze genes located in the telomeric region of the long arm of the human X chromosome, we have identified a novel transcript family, DDX11L, members of which map to 1pter, 2q13/14.1, 2qter, 3qter, 6pter, 9pter/9qter, 11pter, 12pter, 15qter, 16pter, 17pter, 19pter, 20pter/20qter, Xpter/Xqter and Yqter."
2q13/14.1!
Robert:
Deleteif the fusion represents subtelomeric DNA ...
But if you've gone subtelomeric you're dead. And it would have happened in the other chromosomes as well. Also, you don’t have a homologue in the chimp homologous subtelomere regions. Also, there is no relationship, in general, between the human and chimp DDX11L homologues. The genomes are 99% similar, except when they aren’t. So we’re back to “duplicate and move.” By the way, I’m not saying the fusion didn’t happen. Maybe it did, but this is not indicated by science.
But if you've gone subtelomeric you're dead.
DeleteCitation please.
By the way, I’m not saying the fusion didn’t happen. Maybe it did, but this is not indicated by science.
Really? You've got a human chromosome that looks very similar to two chimpanzee chromosomes combined, complete with forward telomere motifs butted up against
reverse telomere motifs, yet fusion isn't the most obvious conclusion? Wow. I think it's in the realm of a "Deceptive God" if the fusion did not in fact occur.
Also, there is no relationship, in general, between the human and chimp DDX11L homologues.
DeletePlease read:
http://www.ncbi.nlm.nih.gov/pubmed/16136133
... and get back to me. Figure 6 is interesting isn't it?
Citation please.
Deletehttp://genesdev.cshlp.org/content/13/18/2388.long
Quote: Clones with short telomeres continued to divide, then exhibited an increase in abnormal mitoses followed by massive apoptosis leading to the loss of the entire population. This cell death was telomere-length dependent, as cells with long telomeres were viable but exhibited telomere shortening at a rate similar to that of mortal cells. It appears that telomerase inhibition in cells with short telomeres lead to chromosomal damage, which in turn trigger apoptotic cell death.
Quote: Clones with short telomeres continued to divide, then exhibited an increase in abnormal mitoses followed by massive apoptosis ...
DeleteSo I've read that paper a couple of times, trying to ascertain at what lengths the telomeres (a) prevent fusion, (b) allow fusion and (c) trigger apoptosis - and came away virtually empty handed. The A431 cells died too rapidly, and hence they were "unable to observe a change in telomere length"; while the 293 cells had more variable telomere lengths, but the population as a whole made a comeback when the average length was around 4kb.
The puzzling thing for me is that you seem to be casting doubt on whether telomere-to-telomere fusions can occur in the first place, but they occur in the paper you cite:
Evidence of chromosomal end joining was observed in these telomerase-inhibited cells, suggesting that telomerase normally functions to protect the chromosome ends from fusion events.
I found this paper:
Deletehttp://www.cell.com/cell/fulltext/S0092-8674(01)80006-4
Which, if you have a look at Table 2 (and Figure 6), you can see that these mice lasted (at least) 6 generations, and by then about 5% of chromosome ends had less than 200 base pairs of telomere repeats. They also encountered (on average) two chromosome fusions per metaphase "including dicentric chromosomes, telomere associations, and Robertsonian fusions."
The fusion site on human chromosome is only about 800 base pairs long - roughly 250 on one side, 550 on the other. The 4th generation mice had some telomeres shorter than that, but they managed to have fertile offspring.
So ... what are your objections again?
The puzzling thing for me is that you seem to be casting doubt on whether telomere-to-telomere fusions can occur in the first place, but they occur in the paper you cite:
DeleteI don’t know how you could have arrived at that since I specifically addressed “the specific DNA sequence found in the human chromosome in question.”
So ... what are your objections again?
1. Telomeric-like sequence is way too “degenerate.”
2. Your idea that it went subtelomeric, say due to loss of telomerase activity, would be lethal and would show up in the other chromosomes.
3. Genes are present in the fusion region.
4. Those genes are not present in the homologous chimp region.
5. Bonus: Human and chimp DDX11L genes do not have synteny (your link notwithstanding). Human has about 3 times more.
There are more detailed problems. To forestall any misreads, no, I’m not saying it is impossible. That’s not the point. There are always complex explanations that can be contrived. But such explanations are needed. The fusion model has significant problems, and is motivated by the theory, not the empirical evidence.
1. Telomeric-like sequence is way too “degenerate.”
DeleteThen what exactly would you expect at a putative fusion site? Pristine sequences? More telomere repeats? Don't make me put words in your mouth.
2. Your idea that it went subtelomeric, say due to loss of telomerase activity, would be lethal and would show up in the other chromosomes.
No, the mouse study shows empirically that it's not lethal and it doesn't show up in other chromosomes.
3. Genes are present in the fusion region.
No, there is only one (pseudo)gene that spans the fusion site. Have you read my blog post about it?
4. Those genes are not present in the homologous chimp region.
Did you not read the nature article I posted?
http://www.ncbi.nlm.nih.gov/pubmed/16136133
It shows (empirically!) that the ends of our chromosomes are incredibly polymorphic - there was even variability among the three humans they analysed.
5. Bonus: Human and chimp DDX11L genes do not have synteny (your link notwithstanding). Human has about 3 times more.
"notwithstanding" ...? Seriously? The entire point of the link is to explain why there is no DDX11L synteny with chimp.
The fusion model has significant problems, and is motivated by the theory, not the empirical evidence.
Completely disagree - we know empirically that fusions happen. So if it walks like a fusion and quacks like a fusion, I'm going to say it's a fusion. It's by far the most parsimonious explanation. How else do you explain forward telomere motifs butted up against reverse telomere motifs precisely where they would be if there was a fusion?
Then what exactly would you expect at a putative fusion site? Pristine sequences?
Delete70% sequence identity is too "degenerate" to be telomere sequences. Something happened there. Perhaps you went subtelomeric, as you suggested, but that is lethal.
No, the mouse study shows empirically that it's not lethal and it doesn't show up in other chromosomes.
No, telomerase inactivity affects all the chromosomes. And it is lethal. In that study the mice only lasted 6 generations.
No, there is only one (pseudo)gene that spans the fusion site.
Of course, you can’t have more than one gene spanning the site (unless you use other frameshifts). In any case, that is not what you would expect from the fusion event. You shouldn’t have a gene spanning the fusion site.
Did you not read the nature article I posted?
I said there are no homologous DDX11L genes.
"notwithstanding" ...? Seriously? The entire point of the link is to explain why there is no DDX11L synteny with chimp.
Of course. There are always explanations. The human and kangaroo genomes have synteny because it turned out that way. Similar species have significantly different genomes because it turned out that way. The argument was “the chimp-human high genome similarity implies evolution.” Here we have a significant difference. You can say that’s because humans have a much bigger variation in their chromosomal ends, but that still means there is a significant difference.
So if it walks like a fusion and quacks like a fusion, I'm going to say it's a fusion. It's by far the most parsimonious explanation. How else do you explain forward telomere motifs butted up against reverse telomere motifs precisely where they would be if there was a fusion?
I don’t know, I’ve never made a human before. Yes, for sure, there is evidence for a very rare telomere-telomere fusion event. But there is also problems with that model. You can’t cover over those problems by insisting there is no alternative when you don’t know what the possible alternatives are. From a scientific perspective, there is evidence for the event, but there is contrary evidence against it that you can’t just brush away. I have no problem with the event occurring. Perhaps it did. But the science does not indicate that. You can’t just present the science as unequivocally supporting that conclusion. The science does not support your hypothesis.
70% sequence identity is too "degenerate" to be telomere sequences. Something happened there. Perhaps you went subtelomeric, as you suggested, but that is lethal.
DeleteFirst of all, it's never a good idea to stand behind ANYTHING that Jeff Tomkins says - the fusion site is 86.03% identical to a pristine sequence over the 798bp sequence. See here for the alignment:
https://roohif.files.wordpress.com/2016/06/pristinealignment.pdf
Secondly, your tumour cell paper does not give any measurements of telomere length at which the cells died - in fact it says explicitly they they were unable to measure them. You have clearly overstated the results of the paper. The mouse study on the other hand, shows that the mice were viable with some telomeres shorter than an estimated 200bp. The fusion site in human chromosome 2 is equivalent to approximately 250bp of pristine repeats on the forward side, and around 530bp on the reverse side.
No, telomerase inactivity affects all the chromosomes. And it is lethal. In that study the mice only lasted 6 generations.
Of course it affects all chromosomes, but not all chromosomes will fuse because not all telomeres are the same length. Clearly the shorter ones are going to be the ones more likely to fuse, and the longer ones will be fine. How is that not obvious? As I said above, it's empirically not lethal for telomeres in the order of 200bp.
And no, the mice did not "only last 6 generations", you need to be more careful with your language. You accuse me of being tedious, but you're being incredibly sloppy both with this and the human tumour cell paper. "The mTR-/- mice are viable through at least six generations." "... more than 200 cell divisions without loss of viability ..." "... cells that have gone though an estimated 300 cell divisions or more are viable." There is nothing in the paper to say that the 6th generation was infertile.
You shouldn’t have a gene spanning the fusion site.
You shouldn't have a functional, important gene crossing the fusion site - sure. But just how important and/or functional is DDX11L2, and is it plausible that the longer transcript is just a genetic accident? On the first point, I would say DDX11L2 does jack all and that Tomkins is either grossly incompetent or lying when he concludes that it is "critical" based on the evidence he has put forward. On the second point, of course it's plausible - TFBS's are all over the genome ... but we'll get to that in my next blog post.
The science does not support your hypothesis.
You're off in philosophy land now, and that's fine because I know that's where you're more comfortable. We're all aware that science is inductive, and nothing can truly ever be "proven". But in the practical world the fusion is a fact "confirmed to such a degree that it would be perverse to withhold provisional assent".
It’s amazing you are maintaining this line of argument.
Deletethe fusion site is 86.03% identical to a pristine sequence over the 798bp sequence.
So what? That is still too dissimilar to be a telomere-telomere sequence. Unless, of course, if the mutation rate happened to increase right in that spot. There are always explanations.
The mouse study on the other hand, shows that the mice were viable with some telomeres shorter than an estimated 200bp. The fusion site in human chromosome 2 is equivalent to approximately 250bp of pristine repeats on the forward side, and around 530bp on the reverse side.
You are completely misrepresenting the science. Without telomerase bad things happen in only a few generations. Aging is accelerated, organs fail, you have decreased fecundity, tissues atrophy, diseases increase, and individuals quickly become decrepit. This paper indicates nothing different. To say that the mice were “viable” simply means that in a lab environment, with warm meals and free drinks, a few of them could still reproduce after 6 generations. And even that won’t last. Aneuploidy is rampant and growing rapidly as things go downhill fast. There is no comparison with primates in the wild.
Of course it affects all chromosomes, but not all chromosomes will fuse because not all telomeres are the same length. Clearly the shorter ones are going to be the ones more likely to fuse, and the longer ones will be fine. How is that not obvious? As I said above, it's empirically not lethal for telomeres in the order of 200bp.
Again, this is absurd. I didn’t say “all chromosomes will fuse.” My point was that you need only one to fuse, which is another unlikely, just-so, story. Even your paper shows more than half the cells with aneuploidy when only 5% of the telomeres have no detectable repeats. As the paper explains: “Quantitative FISH analysis showed that progressive loss of (TTAGGG)n telomere sequence repeats occurred with each generation and that chromosomal rearrangements were frequent in the later generations of mice. […] Aneuploidy and chromosomal end fusions were frequent in cultures from mTR−/− mice in G2 to G6 cultures”.
“Empirically not lethal”? That simply means that the population has not completely died off quite yet in the comfort of the lab. They are doing very poorly by the 6th generation.
And no, the mice did not "only last 6 generations", you need to be more careful with your language. You accuse me of being tedious, but you're being incredibly sloppy both with this and the human tumour cell paper. "The mTR-/- mice are viable through at least six generations." "... more than 200 cell divisions without loss of viability ..." "... cells that have gone though an estimated 300 cell divisions or more are viable." There is nothing in the paper to say that the 6th generation was infertile.
Yes, you got me, it was “at least six generations.” As if that’s going to make a difference. This is silly. You are straining at the details while misrepresenting the science.
Continued …
There is nothing in the paper to say that the 6th generation was infertile.
DeleteFertility is going to be way down by that point. More importantly true fitness, not in the cozy lab, is gone by that time.
"... more than 200 cell divisions without loss of viability ..." "... cells that have gone though an estimated 300 cell divisions or more are viable."
And your point is …? Ah, you have no point. This is just brute misrepresentation. Here’s the entire quote, for those interested in the science:
Our data indicate that telomerase null mouse cells can be established in culture and grow for more than 200 cell divisions without loss of viability and that mTR−/− G6 cells that have gone through an estimated 300 cell divisions or more are viable.
Now we’re not even talking about mice in a cozy lab, but mouse cells in a nice warm culture. By the way, human cells call it quits after about 40-80 divisions.
CH: You shouldn’t have a gene spanning the fusion site.
Glenn: You shouldn't have a functional, important gene crossing the fusion site - sure. But just how important and/or functional is DDX11L2, and is it plausible that the longer transcript is just a genetic accident?
No, there shouldn’t be a gene spanning the fusion site, period. That would require that you just happened to have two sequences, at the ends of randomly degraded telomeres which, when joined head to head gave you a gene!
But plausible? Well of course it is for evolutionists. There are always explanations. But evolutionists are their own judge, as they have insisted the gene does not span the fusion site, to avoid this falsification. This, over against the empirical evidence. Evidence be damned. Now, for evolutionists who realize the evidence won’t go away, it’s “Oh, yeah, a gene spanning the fusion site is actually no problem.”
CH: The science does not support your hypothesis.
Glenn: You're off in philosophy land now
Always a convenient fallback.
We're all aware that science is inductive, and nothing can truly ever be "proven".
Please, don’t fool yourself. We are a long way from anything remotely close to “proven.” The evolutionist’s failure to “prove” their case is not even close to what the problem is. And yet we hear this all the time. Evolutionists promote their scientifically failed, religious, ideas, and when criticized on the science they blame the other guys for being sticklers.
Me: the fusion site is 86.03% identical to a pristine sequence over the 798bp sequence.
DeleteCH: So what? That is still too dissimilar to be a telomere-telomere sequence.
So first you say that 70% is too dissimilar, then you say you're not expecting pristine sequences .. but then 86% is still too dissimilar. At what percentage similarity to pristine telomeres are you saying you will recognise a sequence as subtelomeric? Seriously, I'm asking you for a number. Begging for a number.
You are completely misrepresenting the science. Without telomerase bad things happen in only a few generations.
Misrepresenting how exactly? Was I misrepresenting the science when I said the mice lasted at least 6 generations? Was I misrepresenting the science when I said cells were still viable with less than 200bp of telomeric repeats?
You, on the other hand made a blanket claim - "you go subtelomeric and you're dead" that is not subsantiated by the paper you cited. Please show me in that paper any data that show how short the telomeres need to be before apoptosis is triggered.
My point was that you need only one to fuse, which is another unlikely, just-so, story. Even your paper shows more than half the cells with aneuploidy when only 5% of the telomeres have no detectable repeats.
I'm not following. What makes one (and only one) fusion so unlikely? These are cells at metaphase for a 2n=40 organism - why can't a figure of 5% equate to more than 50% of cells having fusions? You're going to need to spell this one out for me nice and slowly, sorry.
Yes, you got me, it was “at least six generations.” As if that’s going to make a difference.
There's quite a lot of difference between "you go subtelomeric and you're dead" and having a second generation mouse be viable for four more generations with some undetectable telomere repeats, wouldn't you say? Where is this magic point at which the cell dies? Clearly it's less than 200bp in mice. So why is it suddenly impossible for a human to survive a fusion event with 250bp of subtelomeric repeats? I'd really like an answer to that.
And your point is? Ah, you have no point.
DeleteMy point was that you were being sloppy, which you have acknowledged. Thank you. The other two quotes were to highlight that the paper was merely setting a minimum, not a maximum.
That would require that you just happened to have two sequences, at the ends of randomly degraded telomeres which, when joined head to head gave you a gene!
Wow, and here I was thinking I was discussing this with someone that wasn't completely ignorant of the facts. This is not a case of having two chromosomes come together to form a gene. The gene already exists on one side of the fusion site. If we split the chromosome into two parts at the fusion point, we would still have the DDX11L2 gene. All we would lose is this longer transcript that Jeff Tomkins tries to ascribe function to.
The fact that you would make such a mistake like this means you haven't bothered to read and/or comprehend my post on this topic. And that's saddening, because I thought I was discussing this with someone that had a PhD in a related field, not some random YEC on YouTube. Disappointing.
as they have insisted the gene does not span the fusion site
Ken Miller made that claim, and it turned out he was wrong: he was looking on Ensembl (whih does NOT have the longer transcript) while Tomkins was looking on NCBI.
Always a convenient fallback.
Oh the irony! :D
... they blame the other guys for being sticklers.
Yes. Apologies for "straining at the details" (Cornelius Hunter, 2nd June, 2016)
Your evolutionary explanation involves the removal of telomerase which is lethal. You are focusing on the details of lab studies while a population in the wild would have crashed. You ignored this. You cite quotes that have no relevance. You insist the gene does not span the fusion cite when it does. And then you make tedious comments. And unfortunately this discourse is better than usual.
DeleteThis is a good example of the point of this series of posts. If any progress is to be made in origins discussions there needs to an agreement on the basic scientific evidence. You are working from a commitment to evolution rather than allowing the evidence to speak from a theory-neutral perspective.
Are there fusion-based explanations for chromosome 2? Sure. You have an explanation -- great. But there are always explanations, and we need to evaluate the pluses and minuses without the commitment.
1. The telomerase sequences in the fusion region are too degraded for a telomere-telomere fusion.
2. The telomerase sequences in the fusion region are too short for a telomere-telomere fusion, without loss of most of the telomere.
3. Going subtelomere, to resolve these, introduces a wide range of serious disease and dysfunction that are lethal and will crash a population. Aging is accelerated, organs fail, decreased fecundity, tissues atrophy, diseases increase, and individuals quickly become decrepit. In order to solve a problem, you are introducing enormous problems. You are going from the frying pan to the fire. To save the day, you reinstate telomerase just in the nick of time.
4. A gene spans the alleged fusion site, with the fusion site in the first intron where there is an alternate operon. Your argument against this simply ignores the data.
5. There is no homologous gene in the corresponding chimp location.
These evidences are not expected on the fusion hypothesis. This is even evident in evolutionists attempts to deny these evidences. Therefore these evidences reduce the probability of that hypothesis. Does that make it impossible? No, that’s not the point.
There are two things that are needed: (i) Agreement on what the evidence is, and (ii) agreement on what the evidence indicates. We’re not even at (i) yet. You have ignored or denied most all of the above evidences.
You insist the gene does not span the fusion cite when it does.
DeleteYes, It's pretty hard to agree on what the evidence is when you blatantly misrepresent my comments:
Glenn: No, there is only one (pseudo)gene that spans the fusion site. Have you read my blog post about it?
Glenn: You shouldn't have a functional, important gene crossing the fusion site - sure. But just how important and/or functional is DDX11L2, and is it plausible that the longer transcript is just a genetic accident?
Glenn: This is not a case of having two chromosomes come together to form a gene. The gene already exists on one side of the fusion site. If we split the chromosome into two parts at the fusion point, we would still have the DDX11L2 gene. All we would lose is this longer transcript that Jeff Tomkins tries to ascribe function to.
Glenn: ... Ken Miller made that claim, and it turned out he was wrong: he was looking on Ensembl (whih does NOT have the longer transcript) while Tomkins was looking on NCBI.
Please confirm that I have never insisted that the gene does not span the fusion site.
OK, good, glad to confirm. Glenn concurs. (by the way, instead of "The gene already exists on one side of the fusion site," something along the lines of "Yes, agreed, a gene spans the fusion site" would do wonders).
DeleteNow, Step 2: The fact that a gene spans the fusion site further complicates and reduces the likelihood of the fusion model. Concur?
Cornelius: instead of "The gene already exists on one side of the fusion site," something along the lines of "Yes, agreed, a gene spans the fusion site" would do wonders).
DeleteI would say that "there is only one (pseudo)gene that spans the fusion site" is pretty unequivocal. And as someone who (allegedly) has a PhD in the field, I would hope that you can appreciate the nuance of having one transcript that does cross the fusion site and one that doesn't.
Now, Step 2: The fact that a gene spans the fusion site further complicates and reduces the likelihood of the fusion model. Concur?
In the absence of a plausible explanation, yes. Given a plausible explanation, no.
"Genes shouldn’t be there, regardless of expression level, and TFs shouldn’t be binding there."
DeleteMy belated response:
https://roohif.wordpress.com/2016/06/19/chromosome-2-fusion-its-a-binding-site-whoopty-frikkin-do/
So .. do you concede the point?
I'll take that as a yes.
DeleteAMEN to the whole series.
ReplyDeleteWe should be more different if we had common descent with chimps and company.
in fact we are very alike as it would be from common DESIGN.
Comparing or dNA with primates is still just a line of reasoning that it indicates common descent. its just a hunch by people who think its a reasonable hunch.
Any like or nonlike is still just a line of reasoning for biological relationship between us and apes.
Its not biological evidence and so its not scientific if the claim IS that dna is biological scientific evidence for evolution.
Its flawed reasoning.
Thanks Dr. Hunter. I'm very concerned about students being adversely influenced by this man and his cronies. I doubt too many students could stand up to him or be able to answer his arguments so I'm assuming he is quite effective in turning young people to his point of view. Very concerning!
ReplyDeleteThe first question darwinists should answer is If the fusion could happened with or without common ancestor how can it be evidence of common ancestor?
ReplyDeleteI don't claim that it is positive evidence for common descent, I merely claim that it is consistent with it. I've tried to stop several people making this claim - it is a formal logical fallacy:
DeleteP1. If evolution is true, then two chromosomes must have fused.
P2. Two chromosomes have fused.
C. Therefore evolution is true.
Bzzt.
Oh, the great art of the circular argument.
DeleteOne of your best posts, Cornelius. Also one of your best collections of responsive comments. Great work!
ReplyDeleteI'd forgotten about you, Cornelius!
ReplyDelete1. The telomerase sequences in the fusion region are too degraded for a telomere-telomere fusion.
2. The telomerase sequences in the fusion region are too short for a telomere-telomere fusion, without loss of most of the telomere.
https://roohif.wordpress.com/2016/07/09/chromosome-2-fusion-what-should-we-expect/