A Bogey Moment: The Human Chromosome Count

_{Cornelius Hunter

August 24, 2009

Intelligent Design}

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In the 1954 movie The Caine Mutiny, Humphrey Bogart plays the compulsive-paranoid Captain Queeg who is relieved of duty when unable to deal with a dangerous storm at sea. Upon return to port two officers face a court-martial for mutiny. The trial goes badly for them and they appear to be destined for prison until the final testimony of Captain Queeg where his underlying paranoia is suddenly revealed. In the courtroom sideways looks and wide eyes reveal a collective revelation: “Ohh, noooowwww I understand.”

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I think when you say “prediction”, what you mean to say is that it harmonizes with existing data?
No. Common descent predicts their existence before they are found. ID only harmonizes with it after it has been found. Common descent is a useful theory for making predictions about reality. ID, so far, is not.SingBlueSilver_{August 29, 2009
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SingBlueSilver, "Not true. Design theories would not have predicted fused chromosomes. Design theories would not have predicted shared ERVs. Design theories would not have predicted shared transposons. Design theories would not have predicted the exact same mutated vitamin C gene." ID "predicts" these things in the same fashion of "prediction" which you've been talking about. I think when you say "prediction", what you mean to say is that it harmonizes with existing data? Is this an awkward use of the word prediction?lamarck_{August 29, 2009
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Joseph,
How can we test the premise that common ancstry is the ONLY explanation for the fused chromosome?
Common ancestry is not the explanation for the fused chromosome. Rather, the fused chromosome is a puzzle piece predicted to exist by the hypothesis of common ancestry. Hypothesis tested, and validated. "If common descent is true, we should find..." And this is just one of thousands.
All I am saying is that when one looks at the “evidence” for common ancestry it is very apparent that the same “evidence” can be used to support common design and/ or convergence.
Not true. Design theories would not have predicted fused chromosomes. Design theories would not have predicted shared ERVs. Design theories would not have predicted shared transposons. Design theories would not have predicted the exact same mutated vitamin C gene. You can certainly say "well, that's just how the designer designed it" but you can ALWAYS say that, no matter what. No matter what evidence is presented, the design answer is always "the designer made it like that." It's useless as a predictive theory. There are examples of creationists from the 1980s using the differing numbers of chromosomes as evidence that we are NOT related to chimps. Because of their theory, they did not predict this piece of data. Common descent PREDICTED a fused chromosome. Common descent PREDICTED shared ERVs. Common descent predicted shared transposons. Common descent predicted the mutated vitamin C. It's really quite beautiful, if you actually look at it. All these genetic elements can ONLY be inherited, and we share them with chimps, our closest living relatives. We share less with orangutans, as predicted, less with gorillas, as predicted, still less with macaques and baboons, as predicted, and still less with lemurs, as predicted. The family tree emerges quite beautifully from the molecular evidence in the same way it does from the morphological evidence.SingBlueSilver_{August 29, 2009
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2- Until one centromere becomes inactivated the new chromosome will have two active centromeres (dicentric). 3- Does being dicentric always result in chromosome breakage? No: http://pandasthumb.org/archives/2009/02/the-rise-of-hum.htmlDave Wisker_{August 29, 2009
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1- With telomeric fusions do both telemeres need to be uncapped and vulnerable? 2- Until one centromere becomes inactivated the new chromosome will have two active centromeres (dicentric). 3- Does being dicentric always result in chromosome breakage?Joseph_{August 29, 2009
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Blue Lotus, How can we test the premise that common ancstry is the ONLY explanation for the fused chromosome? What would satisfy me pertaining to common ancestry? Some scientific evidence that would demonstrate that the transformations required are even possible. It would be a good start if we knew what was responsible for form. Thinking organisms is a sum of their genetic material has proven to be a bust. Also common design does NOT rule out evolution. All I am saying is that when one looks at the "evidence" for common ancestry it is very apparent that the same "evidence" can be used to support common design and/ or convergence. With the rice IDists would see if that mutation was random or not- ie directed by some internal programming. See Dr Spetner's "Not By Chance".Joseph_{August 29, 2009
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Dave Wisker re plants- I am not the one parading around genetic engineering as evidence for evolution. That dishonest tactic is exactly what Dave Wisker and Art Hunt have done.Joseph_{August 29, 2009
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Blue Lotus, Don't ask Joseph about plants when discussing evolution. Their genetics are 'different'. In other words, Mendel was working in the wrong kingdom when he came up with his laws of inheritance.Dave Wisker_{August 28, 2009
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Joseph
The molecular evidence for common ancestry can be explained by common design and/ or convergence.
Where can I read about the common design explanation for the molecular evidence for common ancestry please? For example
Glutinous rice is a major type of cultivated rice with long-standing cultural importance in Asia. A mutation in an intron 1 splice donor site of the Waxy gene is responsible for the change in endosperm starch leading to the glutinous phenotype. Here we examine an allele genealogy of the Waxy locus to trace the evolutionary and geographical origins of this phenotype. On the basis of 105 glutinous and nonglutinous landraces from across Asia, we find evidence that the splice donor mutation has a single evolutionary origin and that it probably arose in Southeast Asia. Nucleotide diversity measures indicate that the origin of glutinous rice is associated with reduced genetic variation characteristic of selection at the Waxy locus; comparison with an unlinked locus, RGRC2, confirms that this pattern is specific to Waxy.
http://www.genetics.org/cgi/content/abstract/162/2/941 What's the common design explanation for the phenotype examined in that study? Is this evidence for the designer being in Southeast Asia? I'm happy to look at whatever reference material you can supply on the topic of the common design explanation for the molecular evidence for common ancestry.Blue Lotus_{August 28, 2009
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Joseph
BTW it could also be the fusion event is real, but that it occurred in the human lineage.
You say "could be". Sounds like you are hedging your bets either way. Can you think of an experiment that could be performed that would remove the "could be" from your mind? If so, what would it be? What would prove to your satisfaction one way or the other that the fusion did or did not have anything to do with common ancestry with chimps or evolution? Is it possible in theory to provide a level of evidence that will satisfy you? If so, what form would that evidence take? How could it be obtained?Blue Lotus_{August 28, 2009
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BTW it could also be the fusion event is real, but that it occurred in the human lineage. That is the original humans had 48 chromosomes. And the fusion didn't have anything to do with common ancestry with chimps, nor evolution.Joseph_{August 28, 2009
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SingBlueSilver, Seeing that I cannot read the references I cannot tell if they support your claim or not. The molecular evidence for common ancestry can be explained by common design and/ or convergence. There isn't anything in genetics which demonstrates the transformations required are even possible. We have no idea where the information for form is. And there isn't any evidence that says we are the sum of our genes. BTW just because DNA tests are OK within the same population, doesn't mean they can be used to link other species. The fused chromosome was a post hoc explanation. We don't have any idea what it had to do with "evolution" other than it may have changed allele frequency over time. Shared mutations? Are you serious? How many options are there for any one position along the double-helix? ERVs? Again do you understand the type of bottle-necks your scenario requires? Perhaps the alleged ERVs aren't from infectious agents. Perhaps ERVs owe their very nature- their origin- to those sequences they resemble. And they, like prions, are just leftover, decaying pieces that were consumed and then took over the new host. There was a study by Yale(?) that showed that there are ERV-like sequences that actually prevent ERVs from splicing in. I will see if I can find it.Joseph_{August 28, 2009
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Joseph,
How do you know they were looking for it and just didn’t stumble across it?
"A direct cytological comparison between species suggests that human chromosome 2 emerged as a result of a fusion..." Molecular evolutionary genetics "The mechanism which leads to a reduction in the number of chromosomes without causing severed damage is that of centric fusion." Perspectives in primate biology "Comparative chromosome banding shows that chromosome 2 in man is best matched with its arm homologues in Pan Troglodytes, as if the two fused by their short-arm telomeres..." The phylogeny of human chromosomes
By conflating investigation of today with biased inferences of the past all you are doing ius exposing your agenda of conflation and deception.
A robbery investigation, or a murder investigation are all examples of proving past events with leftover evidence. Are you saying it's impossible to prove a past homicide using DNA, blood, hair, fingerprints, etc? So in a jury you'll vote with the murderer every time, because you can't reproduce the actual event of the murder in the lab?
My point is that if there isn’t any evidence that the transformations required are even possible then the allged fusion event had nothing to do with common ancestry.
Fine. Then look at the shared vitamin C mutation. Look at the shared number of transposons on our genomes, in the same order, in the same place. These are elements that can only be inherited. Look at the shared endogenous retroviruses. We share ten with chimps, on the same spot, in the same order, and ERVs can only be inherited. Look how the cytochrome C gene studies show the entire family tree, exactly the same as family trees created by morphology. The molecular evidence for common descent is overwhelming. You can deny it if you want, but you might as well be the dad on Jerry Springer having just heard DNA proof of paternity: "That's not my baby! That's not my baby!"
And to date there isn’t any scientific data that supports common ancestry.
Absolutely and completely wrong. The only way you can say this is if you are unaware of the huge pile of evidence for it. However, it's beyond the scope of this thread...
I say that because I have asked you more than once to tell us how we can test the premise that the fusion is part of a common ancestry and you have failed to provide such a test.
Because it's a whole other argument that would take a lot of time, trying to prove the entire case of common ancestry. My argument is not "common ancestry is true." My argument is "the fused chromosome is predicted by, and thus has a LOT to do with, evolution, unlike what Cornelius says in the original post."SingBlueSilver_{August 28, 2009
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Relevant to the Wired article, IC and people's misunderstandings were discussed previously here: Carl Zimmer on Irreducible ComplexityPatrick_{August 28, 2009
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IRQ, I saw that article yesterday. I just shook my head. The WIRED article starts off badly:
Intricate cellular components are often cited as evidence of intelligent design. They couldn’t have evolved, I.D. proponents say, because they can’t be broken down into smaller, simpler functional parts.
It isn't about "evolution" and the smaller simpler parts can still function and IC would still be present. But anyway...Joseph_{August 28, 2009
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Does anyone else think that measuring fitness by the number offspring is nonsensical? Talk about post hoc...Joseph_{August 28, 2009
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SignBlueSilver:
Question: how did biologists know to look for a fused chromosome?
How do you know they were looking for it and just didn't stumble across it? Also "evolution" is not being debated. If you walk into your house, see a broken window, your TV missing, and muddy footprints out the door, and then declare that you’ve been robbed, I’m going to answer “the premise of you being robbed cannot be objectively tested.” By conflating investigation of today with biased inferences of the past all you are doing ius exposing your agenda of conflation and deception. My point is that if there isn't any evidence that the transformations required are even possible then the allged fusion event had nothing to do with common ancestry. IOW using the fusion as evidence for common ancestry is putting the cart before the horse. BTW I don't have an aversion. I have been disciplined to accept only SCIENTIFIC data, And to date there isn't any scientific data that supports common ancestry. As I said the premise cannot even be objectively tested. YOU have proved that beyond a doubt. I say that because I have asked you more than once to tell us how we can test the premise that the fusion is part of a common ancestry and you have failed to provide such a test.Joseph_{August 28, 2009
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Dr. Hunter. Have you seen this yet? "More ‘Evidence’ of Intelligent Design Shot Down by Science" Here is the money quote, I think it revealing. Lots of 'Couldn't have been this or that's' in this article as well. "Intelligent design mavens once cited flagella as evidence of their theory. Scientific fact dispelled that illusion. The mitochondria study does the same for protein transport." I wonder what the chances are that this argument misrepresents ID's position on the matter? http://www.wired.com/wiredscience/2009/08/reduciblecomplexity/IRQ Conflict_{August 28, 2009
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Hi mad doc, So you think an 11% increase in mean fitness after 10 generations (the progeny measure), and 5% increase (survival to maturity) was too much for large population size, epistatic compensatory mutations and wild-type-level sexual reproduction? What do you think the limit should have been?Dave Wisker_{August 26, 2009
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Thanks Dave very much for your reply. 10 generations is a very rapid, too rapid I believe, recovery on the basis of beneficial mutations and I can't see how this can be the mechanism. I think there must be actual information coming from somewhere. A back up copy in the genome perhaps? Is some information in the cyto-architecture? Of course I can only speculate.mad doc_{August 26, 2009
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Joseph,
1- Fusion was not predicted by evolution
Question: how did biologists know to look for a fused chromosome? Answer: because we have an "incorrect" number of chromosomes according to common descent. It's a prediction, and a valid scientific theory makes predictions. Like putting together a puzzle. "There should be a piece with a tractor wheel on it somewhere."
Without the scientific data which demonstrates that the transformations required are even possible it isn’t evidence for anything.
Like with bornagain77, you are attempting to avoid the argument by spiraling willy-nilly into a general argument about evolution. I'm not arguing whether evolution happens or not. I'm simply responding to Cornelius' incorrect assertion that the fused chromosome has nothing to do with evolution, which it most assuredly does. Even if it isn't necessarily direct proof of common ancestry by itself.
Especially since the premise of common ancestry cannot be objectively tested.
If you walk into your house, see a broken window, your TV missing, and muddy footprints out the door, and then declare that you've been robbed, I'm going to answer "the premise of you being robbed cannot be objectively tested."
Correction- some people WANT to be related to the apes.
Off topic, but some who shall remain nameless have an almost Victorian aversion to the idea of being related to animals. Pinkies out! Begin your Thurston Howell III laugh! "I'm not related to those filthy apes!"SingBlueSilver_{August 26, 2009
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# bornagain I do not try to impress you, I asked two specific questions. the first one was why you called their sequence library 'semi'random when it was not? the second one was why you think that the 'reactivity' of ATP which is a well defined chemical concept does matter in their experiment. I also pointed out that they found four different families each including multiple members of atp-binding molecules meaning four different kinds of binding sites. they found only atp-binders (just one binding site as you call it)because the only looked for binders to atp and nothing else. Experimental evidence from other selection experiments suggests that one can find (very) different functionalities in the same pool of random (in this case RNA) sequences.rna_{August 26, 2009
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bornagain77,
Dave Whisker,,,I mean this as nice as possible,,,,You are an absolute idiot if you think random “non-designed” processes compensated the information,
I tried to warn you, now I'm going to moderate your comments. If you stop with this nonsense rudeness, I will take you out of moderation after a while. Clive Hayden_{August 26, 2009
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Dave Whisker you state: "could produce a flush of new epistatic mutation combinations, resulting in an initial surge in fitness recovery." What is the size of the genome? 4^100,000,000???? What is the probability of finding ANY useful sequence whatsoever in that search space? .000001% to be generous? So please tell me why in the world you would even entertain, for the slightest moment, the belief that the "just right" combination of mutations would occur by totally random processes, to drive the compensation mechanism in such a rapid fashion (to the supposed equilibrium status),,,even if the entire universe were populated with nothing but C elegans to begin with??? There is clearly an algorithm present,,,which brings us back to the main question evolutionists dare not ask: Where did the complex information come from? "No man-made program comes close to the technical brilliance of even Mycoplasmal genetic algorithms. Mycoplasmas are the simplest known organism with the smallest known genome, to date. How was its genome and other living organisms' genomes programmed?" - David L. Abel and Jack T. Trevors, “Three Subsets of Sequence Complexity and Their Relevance to Biopolymeric Information,” Theoretical Biology & Medical Modelling, Vol. 2, 11 August 2005, page 8 On top of the fact that we now know the genetic code of the simplest organism ever found on Earth is a highly advanced algorithmic code, which far surpasses man's ability to devise as such, we also know for a fact no operation of logic ever performed by a computer will ever increase the algorithmic code inherent in a computer's program, i.e. Bill Gates will never use random number generators and selection software to write highly advanced computer codes: "... no operation performed by a computer can create new information." Douglas G. Robertson, "Algorithmic Information Theory, Free Will and the Turing Test," Complexity, Vol.3, #3 Jan/Feb 1999, pp. 25-34. The Evolutionary Informatics Lab:bornagain77_{August 26, 2009
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Hi mad doc, Thanks for reposting this-- I remember seeing and thinking about it, but then lost track of where it was. The issue you brought up about the majority of fitness recovery occurring very early was a very interesting one. I have my own idea why that might be so, so please take it as an hypothesis by someone who isn't an expert on C. elegans. I think the explanation may involve the the nature of compensatory epistatic mutations, and the reproductive strategies employed by C. elegans. Firstly, C. elegans reproduces primarily by selfing and thius was used to the investigators advantage to produce lines of individuals that were almost identical genetically. However, as the authors note, C. elegans also reproduces sexually in the presence of males, and the authors noted that the number of males rose to wild-type levels ( a very low percentage ) in only a few generations. What this means is, recombination could bring together epistatic mutations occurring in different individuals. The early-on presence of males (and sexual reproduction), coupled with a large population size--which increases the probability of mutations appearing-- could produce a flush of new epistatic mutation combinations, resulting in an initial surge in fitness recovery. This at least would be consistent with an epistatic compensatory mutation scenario. I'm not sure I think your assertion Estes and Lynch were being illogical in coming to their conclusion is warranted. They clearly laid out what they saw as the options available and ruled out those--given our current state of knowledge--which did not fit. And, as I said, Estes has gone one to focus on exploring compensatory epistatic mutations and fitness (including whole genome analysis). So it remains to be seen if furtrher work will establish their hypothesis further. I understand that you are positing instead the existence of a completely heretofore unknown mechanism to explain the "recovery of information". The actual discovery of something like that would be fascinating. Do you have any further ideas on the nature of it? As for your 'about time' remark, Suzanne Estes was a grad student at Oregon State when the paper was published, and her postdoc fellowship work immediately after was on a different topic. She became an assistant professor at Portland State and runs a lab maintaining several research programs. So let's cut her some slack ;)Dave Wisker_{August 26, 2009
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Hmmm rna,,, methinks you are being far to forgiving of their methodology for finding only one binding site with the universal ATP energy molecule,,,tell you what rna,,,you want to impress me??? show where they have successfully synthesized the absolutely critical ATP molecule, that is used by all life, and even viruses, by totally random processes!!! Evolution vs ATP Synthase - Molecular Machine http://www.youtube.com/watch?v=qE3QJMI-ljc ATP: The Perfect Energy Currency for the Cell Jerry Bergman, Ph.D. http://www.trueorigin.org/atp.asp Excerpt: Without ATP, life as we understand it could not exist. It is a perfectly-designed, intricate molecule that serves a critical role in providing the proper size energy packet for scores of thousands of classes of reactions that occur in all forms of life. Even viruses rely on an ATP molecule identical to that used in humans. The ATP energy system is quick, highly efficient, produces a rapid turnover of ATP, and can rapidly respond to energy demand changes (Goodsell, 1996, p.79). Furthermore, the ATP molecule is so enormously intricate that we are just now beginning to understand how it works. Each ATP molecule is over 500 atomic mass units (500 AMUs). In manufacturing terms, the ATP molecule is a machine with a level of organization on the order of a research microscope or a standard television (Darnell, Lodish, and Baltimore, 1996). Among the questions evolutionists must answer include the following, 'How did life exist before ATP?' 'How could life survive without ATP since no form of life we know of today can do that?' and 'How could ATP evolve and where are the many transitional forms required to evolve the complex ATP molecule?' No feasible candidates exist and none can exist because only a perfect ATP molecule can properly carry out its role in the cell. In addition, a potential ATP candidate molecule would not be selected for by evolution until it was functional and life could not exist without ATP or a similar molecule that would have the same function. ATP is an example of a molecule that displays irreducible complexity which cannot be simplified and still function (Behe, 1996). ATP could have been created only as a unit to function immediately in life and the same is true of the other intricate energy molecules used in life such as GTP. Although other energy molecules can be used for certain cell functions, none can even come close to satisfactorily replacing all the many functions of ATP. Over 100,000 other detailed molecules like ATP have also been designed to enable humans to live, and all the same problems related to their origin exist for them all. Many macromolecules that have greater detail than ATP exist, as do a few that are less highly organized, and in order for life to exist all of them must work together as a unit.bornagain77_{August 26, 2009
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#43 bornagain What do you mean by 'semi'random sequences? Do you think, they cheated in their experiments? Actually the took extra precautions, to keep their starting library as random (highly complex in sequence space) as possible. why would it matter in this experiment, that atp is also the 'energy currency of the cell' or is highly 'reactive'? It does not chemically react in this experiment, it just stably binds by non-covalent interactions.rna_{August 26, 2009
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1- Fusion was not predicted by evolution 2- At best it was post hoc "explanation 3- Without the scientific data which demonstrates that the transformations required are even possible it isn't evidence for anything. Especially since the premise of common ancestry cannot be objectively tested.
We are supposed to be related to apes.
Correction- some people WANT to be related to the apes.Joseph_{August 26, 2009
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Dave Whisker @40. I posted this to you in this thread on this blog "3 August 2009 Stephen Meyer’s Book Ranked #1 in Science/Physics/Cosmology at Amazon" It was in regard to the Estes paper you refer to but I received no reply. I would still be interested in your comments. Dave Whisker: “Actually, mad doc, the authors speculated on the cause, but only in the discussion section” Mad doc: I am aware of that and what I was trying to draw attention to was the illogicalities in their speculations: “The authors point out that compensatory epistatic mutations are not the same as “beneficial mutations” (even though they obviously benefit the organism). They postulate these mutations benefit the worst performing organisms the most. (It appears If the organism is mutated then the mutations are good and if the organism is not mutated, mutations are bad).” From their results, this is all supposed to have happened within 10 generations in several strains. This is a remarkable achievement for a random process and it puts Dawkin’s “weasel” program to shame. Basically I think random mutations are unable to do this in 10 generations. Either their experiment is flawed or there is another explaination. In any event their explaination in the discussion makes no sense for the reasons I have outlined before. I am glad that they are doing further investigations. About time too, as that paper is 6 years old. I would be interested to find out the results. I expect the answer will only be found when full genetic mapping of the mutated and non mutated strains can be done and I think you will find a highly efficient data recovery mechanism has been activated in the organism to recover the “lost” information. Thank you.mad doc_{August 26, 2009
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rna,,, Methinks you are blinded by your materialism,,,, given to the "specialized" in vitro circumstances they used,,,,on top of the fact they used ATP, a very highly reactive molecule which is the "energy currency of life", just in order to derive 1 binding site in 1 in 10^12 tries for functional proteins from "semi" random sequences,,,would be strong support for the work of Behe and Axe which actually looked for what could happen IN A CELL,,,,basically to clearly differentiate this from Behe's and Axe's work they would have to try the same process with 2 binding sites, since proteins work in "cooperation" and see what results they get.....1 in 10^24??? 1 in 10^48????,,,,the numbers should quickly fall in line with what has already been established.bornagain77_{August 26, 2009
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