1. Evolution or Design? Duons

Have you ever tried writing palindromes? How about writing phrases that can be read the same way in either direction? Here are some examples:
A man, a plan, a canal: Panama
Live not on evil
Was it a car or a cat I saw
These sentences were no doubt designed…
Can you imagine writing a book that can be read forwards and backwards containing 2 different stories that made sense? Not an easy task…

Watch the video and pay special attention to the following examples:

  1. Alternative splicing of RNA that produces multiple proteins from one gene
  2. Duons – Overlapping sequences that code for both protein expression and transcription factor binding sites simultaneously
  3. Dual coding genes in which one sequence is read in multiple frames to produce completely different protein

The magnitude of the dual coding problem in DNA would be the equivalent of writing a novel that could be read in either forward over reverse directions making two different stories both of which made sense…

And don’t forget that according to Darwinists the dual coding in DNA simply evolved, right?

403 thoughts on “1. Evolution or Design? Duons

  1. Corneel,

    I haven’t heard of it, but I could look it up. It is a membrane-bound tyrosine kinase, not a transcription factor for “cellular control”. Could you explain what exactly that cellular mechanism is that screams DESIGN at you?

    Its transcription is controlled by the HIF transcription factor protein. The non hypoxia condition (adequate cellular oxygen) is controlled by a degradation mechanism. The same strategy is used to control the cell cycle with a degradation mechanism targeting the beta catenin protein which is a cyclin (cell cycle) transcription factor. Consistency in mechanisms for cellular control is strong evidence of design in my opinion.

  2. Entropy,

    Sure, but the question remains: do you agree that, with time, the population might look different to the original population due to the increment in such more-suited-for-the-environment genetics (plus whatever those more-suited-genetics might carry with them by happenstance association)?

    Sure. I think Darwin’s finches are evidence of this i.e. beak shapes that help reach the food supply.

  3. John Harshman,

    Ah, I see. You just sprinkle vaguely relevant words at random to compose sentences. Yes, that’s exactly what word salad is. A better program would be to design your sentences carefully to communicate a clear meaning. A stable genius like you ought to be capable of that, right?

    I will try.

  4. colewd:

    As I said to John you can test if random change and selection can change “me thinks it is a weasel” into another coherent sentence by random change and so far it fails every time.

    DNA_Jock:

    I also laughed at your weasel assertion; are you trying to tell me that your random change and selection program never found

    “he thinks it is a weasel”

    ?
    It’s a bleeding neighbour!

    You didn’t even try, did you, Bill? How embarrassing.

  5. colewd,

    The non hypoxia condition (adequate cellular oxygen) is controlled by a degradation mechanism.

    Just to help you focus, I would like to point out that this is another example of sprinkling words to make nonsense. The non hypoxia condition is controlled by having adequate oxygen. It could be that down-regulation (or is it up-regulation?) of some protein is controlled by a degradation mechanism, but that isn’t what you said.

  6. Corneel,

    Here a description of the hif destruction complex:Von Hippel–

    syndrome (VHL) is a dominantly inherited hereditary cancer syndrome predisposing to a variety of malignant and benign tumors of the eye, brain, spinal cord, kidney, pancreas, and adrenal glands. A germline mutation of this gene is the basis of familial inheritance of VHL syndrome. Individuals with VHL syndrome inherit one mutation in the VHL protein that causes the protein’s normal function to be lost or altered. Over time, sporadic mutation in the second copy of the VHL protein can lead to carcinomas, in particular hemangioblastomas affecting the liver and kidneys, renal (and vaginal) clear cell adenocarcinomas.

    The protein encoded by this gene is a component of the protein complex that includes elongin B, elongin C, and cullin-2, and possesses ubiquitin ligase E3 activity. This complex is involved in the ubiquitination and degradation of a hypoxia-inducible factor (HIF), which is a transcription factor that plays a central role in the regulation of gene expression by oxygen. RNA polymerase II subunit POLR2G/RPB7 is also reported to be a target of this protein. Alternatively spliced transcript variants encoding distinct isoforms have been observed.

    Here is the wiki description of the APC gene which is part of the beta catenin (cell cycle transcription factor)

    The (Adenomatous Polyposis Coli) APC protein normally builds a “destruction complex” with glycogen synthase kinase 3-alpha and or beta (GSK-3α/β) and axin via interactions with the 20 AA and SAMP repeats[citation needed]. This complex is then able to bind β-catenins in the cytoplasm, that have dissociated from adherens contacts between cells. With the help of casein kinase 1 (CK1), which carries out an initial phosphorylation of β-catenin, GSK-3β is able to phosphorylate β-catenin a second time. This targets β-catenin for ubiquitination and degradation by cellular proteasomes. This prevents it from translocating into the nucleus, where it acts as a transcription factor for proliferation genes. APC is also thought to be targeted to microtubules via the PDZ binding domain, stabilizing them[citation needed]. The deactivation of the APC protein can take place after certain chain reactions in the cytoplasm are started, e.g. through the Wnt signals that destroy the conformation of the complex[citation needed]. In the nucleus it complexes with legless/BCL9, TCF, and Pygo[citation needed].

    The ability of APC to bind β-catenin has been classically considered to be an integral part of the protein’s mechanistic function in the destruction complex, along with binding to Axin through the SAMP repeats.[10] These models have been substantiated by observations that common APC loss of function mutations in the mutation cluster region often remove several β-catenin binding sites and SAMP repeats. However, recent evidence from Yamulla and colleagues have directly tested those models and imply that APC’s core mechanistic functions may not require direct binding to β-catenin, but necessitate interactions with Axin.[11] The researchers hypothesized that APC’s many β-catenin binding site increase the protein’s efficiency at destroying β-catenin, yet are not absolutely necessary for the protein’s mechanistic function. Further research is clearly necessary to elucidate the precise mechanistic function of APC in the destruction complex.

  7. colewd:
    Corneel,

    .Consistency in mechanisms for cellular control is strong evidence of design in my opinion.

    “It’s complex and looks designed to layman me, therefore it must BE designed!!”

    That about cover it Bill?

  8. colewd:
    Corneel,

    Here a description of the hif destruction complex:Von Hippel–

    Here is the wiki description of the APC gene which is part of the beta catenin (cell cycle transcription factor)

    Squid ink to hide the fact you have no idea what you’re talking about.

    It isn’t working.

  9. OMagain,

    What about if after each of those random changes we tested the change to see if fitness increased or decreased? And what about if we only “kept” the changes that increased fitness?

    Do you see where I’m going? Why are you so blind with regard to selection?

    A coherent sentence is selected and yes you are more likely to find one only a few mutations away from the original coherent sentence. What is dramatic here is how fast the sequence breaks down after the first few mutations.

  10. Wait a sec. I pointed out that you were wrong about cyclins, and you responded, writing:

    I was not talking about cyclins but the cellular control of one of their mission critical transcription factors. The method of control is the same as for vascular growth in the cell.

    Now you are saying that you are talking about cyclins.

    colewd: Its transcription is controlled by the HIF transcription factor protein. The non hypoxia condition (adequate cellular oxygen) is controlled by a degradation mechanism. The same strategy is used to control the cell cycle with a degradation mechanism targeting the beta catenin protein which is a cyclin (cell cycle) transcription factor. Consistency in mechanisms for cellular control is strong evidence of design in my opinion.

    Make up your mind, kiddo.
    Soooo, more than one protein is controlled via degradation (via different mechanisms) and THAT’s your “strong evidence of design”, because you call them both “cellular control”.
    Color me underwhelmed.
    Definitely Sal-like clarity of language.

  11. colewd: A coherent sentence is selected and yes you are more likely to one only a few mutations away from the original coherent sentence. What is dramatic here is how fast the sequence breaks down after the first few mutations.

    Just to help: here’s another example of your word salad. Please start trying harder to make sense and (which is helpful in that quest) type grammatical sentences. Here you seem to have left a word out of the first sentence, but even with that word you wouldn’t be communicating anything.

  12. DNA_Jock,

    I was not talking about cyclins but the cellular control of one of their mission critical transcription factors. The method of control is the same as for vascular growth in the cell.

    Now you are saying that you are talking about cyclins.

    Please read carefully. The discussion is about beta catenin the transcription factor for cyclins. Beta catenin is degraded to down regulate the cell cycle. This is by the DKK protein activating this destruction mechanism through the WNT pathway. The reuse of the same mechanism for cellular control is evidence for design in my opinion.

  13. colewd:
    DNA_Jock,

    The reuse of the same mechanism for cellular control is evidence for design in my opinion.

    Why?

    Oxygen bonds with hydrogen to form water H2O, oxygen bonds with nitrogen to form nitrous oxide N2O.

    Is that evidence oxygen is designed?

  14. Adapa: Why?

    Oxygen bonds with hydrogen to form water H2O, oxygen bonds with nitrogen to form nitrous oxide N2O.

    Is that evidence oxygen is designed?

    To Bill, yes.

    It’s ID, it is about declaring things to be designed. It is not about finding causes for effects, it is about invoking The Cause for whatever effects shall be credited to God.

    Glen Davidson

  15. colewd: Please read carefully. The discussion is about beta catenin the transcription factor for cyclins. Beta catenin is degraded to down regulate the cell cycle. This is by the DKK protein activating this destruction mechanism through the WNT pathway. The reuse of the same mechanism for cellular control is evidence for design in my opinion.

    So your evidence for design is that you found two proteins that are targeted for degradation as part of their regulatory control? And why couldn’t this have evolved, for example by one of the proteins becoming a target for the already existing ubiquitination machinery during eukaryotic evolution?

  16. colewd:
    Sure.I think Darwin’s finches are evidence of this i.e. beak shapes that help reach the food supply.

    OK! So far you seem to agree that Darwinian evolution makes sense. So, all that’s needed now it to understand why Darwin thought it was ok to extrapolate those phenomena and propose that, as the process goes on, the divergence between populations would increase. One of the line of evidence for this was that he found that more similar species tend to be geographically closer to each other (the extreme example being marsupials in Australia). That fossils of some extinct animals (like the giant sloth), were found where similar species live today (like the common-sized sloths). Etc. That made Darwin confident that he could extrapolate and that species diverge from prior species.

    Given that, do you agree that such evidence could convince somebody that, as selection does on, as populations spread, as environments change, such populations diverge, and that such divergence might lead to the populations becoming distinct enough to be called different species? It doesn’t have to convince you. I’m asking if you agree that it would convince somebody who’s just studying the data, found a potential mechanism for divergence, and then checked to see if that mechanism might lead to further and further divergence.

    What do you say?

  17. Entropy,

    Given that, do you agree that such evidence could convince somebody that, as selection does on, as populations spread, as environments change, such populations diverge, and that such divergence might lead to the populations becoming distinct enough to be called different species? It doesn’t have to convince you. I’m asking if you agree that it would convince somebody who’s just studying the data, found a potential mechanism for divergence, and then checked to see if that mechanism might lead to further and further divergence.

    I agree on the surface this is plausible and I accepted this explanation for most of my life.

  18. Corneel,

    So your evidence for design is that you found two proteins that are targeted for degradation as part of their regulatory control? And why couldn’t this have evolved, for example by one of the proteins becoming a target for the already existing ubiquitination machinery during eukaryotic evolution?

    Anything is possible. Is the explanation reasonable? If the mechanism is driven by a random front end how would it come up with the same strategy? These destruction mechanisms are having to interface with different proteins which are regulated by other proteins. The first one controls cell division. How would a multicellular organism be possible without this type of regulation? A step by step process does not make sense.

  19. colewd:
    I agree on the surface this is plausible and I accepted this explanation for most of my life.

    I don’t see why this would only work “on the surface.” Anyway, seems like Darwinian evolution makes sense to you. Maybe you should have said that you won’t accept it even if it makes sense because, maybe, you’re thinking of a different level of explanation. But that would not be Darwin’s problem, right? Darwin saw variation, we see variation, selection from such variation makes sense. that populations can continue diverging makes sense.

    So, now, maybe we could say, ok, but how long that variation? Once variation is filtered, how come we still have variation? Well, that’s a question about the source of the variation. So, to get there, what about we check something. Let’s start with a question you already said yes to, and ask a few more questions around it:

    1. Do you agree that there’s variation among organisms of the same species?
    2. Do you therefore agree that a lot fo variation might be selectively neutral?
    3. Do you agree that the mere existence of such variation indicates that there’s plenty of room for mutations/variations that are selectively neutral, at least in the environment where some species might be thriving?

  20. Entropy,

    1. Do you agree that there’s variation among organisms of the same species?
    2. Do you therefore agree that a lot fo variation might be selectively neutral?
    3. Do you agree that the mere existence of such variation indicates that there’s plenty of room for mutations/variations that are selectively neutral, at least in the environment where some species might be thriving?

    I agree with 1 and 2.

    For number 3 I see issues. There appears to be a limit to variation among the same species.

  21. colewd: There appears to be a limit to variation among the same species.

    What is your evidence for this? What is that limit? And do you refer to standing variation or variation over time?

  22. OK. Nobody even attempted to write any palindromes, so let’s try to make some intelligent changes to the flowing sentences and pretend that random processes did it. My kids have been working on those for a week and couldn’t make any changes that would improve the palindromes… Maybe the followers of sheer dumb lack can try again… after all they are competing with zero intelligence that somehow managed to “designed duons” …

    So , it should be no problem, should it?

    A man, a plan, a canal: Panama
    Live not on evil
    Was it a car or a cat I saw

  23. J-Mac: so let’s try to make some intelligent changes to the flowing sentences

    Sentences that were created, i.e. did not evolve via the processes you are suggesting we use to create new ones with.

    Noted.

    It’s not us, J-Mac, It’s you.

  24. keiths,

    Hopefully you will get a life one day…after you have retired, you are hardly getting any sleep… Is retirement just waiting for death were you come from?
    I hope you have insight into your behavior that this blog is not really real… You don’t use your real name … neither do I…Why would you spend the majority of your retirement talking to no one?
    Your case is very sad…

  25. keiths:
    J-Mac logic:If the name isn’t real, then the person behind it isn’t real, either.

    You are waiting for death wasting your life away…. whatever is left of it… You have no hope, so why would you even do it?

  26. J-Mac,

    You are waiting for death wasting your life away….

    Speak for yourself. I’m in Florida, having just witnessed the spectacular Falcon Heavy launch.

    “Waiting for death”, my ass.

  27. J-Mac,

    The problem is that you’re thinking about it the wrong way.

    In most cases, palindromes with functions in DNA sequences don’t have to be perfect. They often have variation and are still functional. What’s often palindromic is not each instance of, say, a transcription factor binding site, but the consensus obtained from aligning several of those sequences and looking at the most frequent “letter” at each position.

    There’s also the tiny little detail that actual “palindromes” are pretty short. It’s not impossible to write several palindromes with DNA, say, six letters long. It’s not impossible for those to occur, just by chance, in quite large numbers in a genome.

    Check this out. Suppose that every base has equal probability in the human genome. The probability of any sequence six bases long, including any of the potential palindromes, would be:

    p = (1/4)**6 = 0.000244140625

    Now, that means that the sequence can be present in a six billion bases long genome (like the human genome):

    0.000244140625 * 3.3e9 = 805,664.0625

    805,664 times without taking into account the potential for variability!

    With those kinds of numbers, the real problem is, from an analysis perspective, to distinguish the functional ones from the noise.

    There was an article, some years ago, showing how easily binding sites can evolve.

  28. colewd:
    For number 3 I see issues.There appears to be a limit to variation among the same species.

    However, we continue seeing new mutations in newly born individuals, and they are all right. No newborn comes without mutations not found in their parents. That suggests that if there’s a limit, it won’t be easy to find what that limit might be.

    So, given that, would you agree that it’s reasonable to expect that variability will continue to exist among individuals of the same species, even after natural selection has pruned and increased the presence of particular gene versions in some loci (aka changes in allele frequency due to natural selection)?

  29. Entropy,

    However, we continue seeing new mutations in newly born individuals, and they are all right. No newborn comes without mutations not found in their parents. That suggests that if there’s a limit, it won’t be easy to find what that limit might be.

    This is a tricky area which I am skeptical how good the data is that we have. What are mutations, or instead changes due to genetic recombination. How well are our direct measurements? Since DNA repair is continuous, how do we know the measurements that identified mutations won’t go away the next time the repair mechanism is run.

    The expected variation from two randomly selected humans is under .2%. If the human genome is 75% junk then yes their can be lots of neutral mutations but as you know this is a very controversial discussion. If this was true and there are around 100 neutral mutations in every generation then how could the expected variation between humans be so small.

    The other issue is that given the enormous sequential space of the genome, mutations in functional areas are going to move that section of the genome away from function very rapidly. How does this process generate new function?

  30. colewd:
    Entropy,

    This is a tricky area which I am skeptical how good the data is that we have.What are mutations, or instead changes due to genetic recombination. How well are our direct measurements?Since DNA repair is continuous, how do we know the measurements that identified mutations won’t go away the next time the repair mechanism is run.

    You have no fucking idea what you’re talking about.

    The expected variation from two randomly selected humans is under .2%.If the human genome is 75% junk then yes their can be lots of neutral mutations but as you know this is a very controversial discussion.If this was true and there are around 100 neutral mutations in every generation then how could the expected variation between humans be so small.

    Not 100 neutral mutations. 100 NEW mutations that didn’t come from either the mother or father thru sexual recombination. That’s new information no matter how much the IDiots whine.

    The other issue is that given the enormous sequential space of the genome, mutations in functional areas are going to move that section of the genome away from function very rapidly.How does this process generate new function?

    That would be true if the environment never changed. But the environment does change. Than means a mutation which moves away from a highly efficient function in the old environment can move towards a more efficient (i.e. beneficial) function in the new environment.

  31. colewd,

    Since DNA repair is continuous, how do we know the measurements that identified mutations won’t go away the next time the repair mechanism is run.

    Damn, Bill. How many times have we already explained this to you?

  32. John Harshman: Careful. Bill thinks that oxygen is designed.

    If there were a cosmic reference table somewhere out there for the properties of oxygen, one could imagine a Designer changing those. But (last I heard) the properties of the elements are all described by solutions of the Schrödinger Wave Equation. And also the properties of the chemical compounds. When people like Michael Denton talk about how wonderfully water is designed (see here) they are simply being silly, because a world in which the SWE did not apply would look unimaginably different, and might not even have anything like water.

  33. Joe Felsenstein: When people like Michael Denton talk about how wonderfully water is designed (see here) they are simply being silly, because a world in which the SWE did not apply would look unimaginably different, and might not even have anything like water.

    This sentence is illogical. Water can’t be deigned, because if it was different it would not be anything like water?

    I would ask you to elaborate, but I don’t really think it can be made better. B doesn’t follow A.

  34. colewd:
    Entropy,

    This is a tricky area which I am skeptical how good the data is that we have.

    Yeah, and that (plus the word salad that follows) is why it’s impossible to take you seriously.

  35. colewd,

    The data are of varying quality. High-quality data painfully gathered before the advent of second-generation sequencing, varying quality at the beginning of second generation sequencing. Today, still mostly second-generation sequencing, but refined and much cheaper, with human-focused genome centres acquiring lots of high-quality data. It’s undeniable. Kids come with new mutations.

    DNA repair mechanisms don’t fix established mutations Bill. They can only find potential problems when there’s a mismatch between complementary strands. Once the mutation has gone through, it’s there to stay.

    A difference of 0.2% between humans (I suppose that’s an average, and I don’t have time to check if the number is right), would be 0.2/100 * 6.6e9 = 13,200,000.0 differences Bill (6.6e9 would be the length of a diploid human genome). 13 million differences! I don’t see any problem here.

    Also take into account what we were talking about before. That natural selection would tend to reduce the proportion of differences within a population. So we have at least two forces: selection, which reduces variation, and mutations, which produce variation. Would you agree that these two phenomena could do that?

    colewd: The other issue is that given the enormous sequential space of the genome, mutations in functional areas are going to move that section of the genome away from function very rapidly.

    You cannot know that. This is why we’re examining the foundations. So that you get to understand that there’s plenty of variation that has phenotypic effects, yet are for the most part, selectively neutral.

    colewd: How does this process generate new function?

    That’s where we’re going. But you have to understand the bases first. Do you agree that there’s plenty of variation, a lot of it with phenotypic effects, that is selectively neutral?

  36. colewd: The other issue is that given the enormous sequential space of the genome, mutations in functional areas are going to move that section of the genome away from function very rapidly.

    Unless there is natural selection. An excess of offspring is continously generated, and carriers of very harmful mutations usually die(at least this is how it is in the wild, though industrialization, agriculture and modern medicine has done a lot to reduce the mortality rates of humans). That way the necessary functional genes are retained by what is called “purifying selection”. Because selection is in that sense “cleaning” the important functional genes from deleterious mutations.

    How does this process generate new function?

    The mutations either change the functions of existing genes into new ones, or existing genes are duplicated which then mutate to new functions, and/or new functional combinations of genes emerge by recombination and shuffling of existing genes.

  37. Entropy,

    DNA repair mechanisms don’t fix established mutations Bill. They can only find potential problems when there’s a mismatch between complementary strands. Once the mutation has gone through, it’s there to stay.

    For the sake of argument I will agree here and I agree that mutations happen and can escape the repair mechanisms. What is not clear is what is being counted when mutation rates are calculated.

    A difference of 0.2% between humans (I suppose that’s an average, and I don’t have time to check if the number is right), would be 0.2/100 * 6.6e9 = 13,200,000.0 differences Bill (6.6e9 would be the length of a diploid human genome). 13 million differences! I don’t see any problem here.

    Again, I will agree here for the sake of argument.

    You cannot know that. This is why we’re examining the foundations. So that you get to understand that there’s plenty of variation that has phenotypic effects, yet are for the most part, selectively neutral.

    Putting together a male and female of the same species will create off spring with genetic variation as two different gene sets are being recombined.

    Random mutation to a functional sequence is going to move that sequence away from function. The only way away from this is if the functional space is almost equal the sequence space and the data does not support this especially in the nuclear protein area.

  38. colewd,

    Random mutation to a functional sequence is going to move that sequence away from function. The only way away from this is if the functional space is almost equal the sequence space and the data does not support this especially in the nuclear protein area.

    Completely wrong, but I can’t be arsed to explain it to you. You’re hopeless, Bill.

  39. colewd: What is not clear is what is being counted when mutation rates are calculated.

    No, that’s completely clear. You just refuse to acknowledge it. Most mutations (in the germ line) happen during gametogenesis, and that would be where DNA repair would happen. Detection of those mutations happens in the next generation, long after any DNA repair has happened. Give it up.

  40. John Harshman,

    No, that’s completely clear. You just refuse to acknowledge it. Most mutations (in the germ line) happen during gametogenesis, and that would be where DNA repair would happen.

    Your claim is you’re understanding of DNA repair mechanisms is completely clear. Why is their up to 4x spread in mutation rate estimates at 95% confidence levels i.e. .3 to 1.3 x10 -8 mutations per generation? Have you read current papers on this subject?

    Are you really claiming that DNA repair is restricted to pre embryo development? Can you support this claim?

    BTW: I have conceded this point to Entropy to not bog down this conversation.

  41. colewd:
    For the sake of argument I will agree here and I agree that mutations happen and can escape the repair mechanisms.

    Of course they can. Otherwise we would be all identical.

    colewd:
    What is not clear is what is being counted when mutation rates are calculated.

    Simple, changes present in the offspring with respect to the parents.

    colewd:
    Putting together a male and female of the same species will create off spring with genetic variation as two different gene sets are being recombined.

    Sure. That too. But we’re talking about what keeps variation despite selection. recombination will be useful for later explanations.

    colewd:
    Random mutation to a functional sequence is going to move that sequence away from function.

    Again, you cannot know that. You’re forgetting that there’s such a thing as purifying selection, neutral and semi-neutral mutations, leaving aside, for the time being, beneficial mutations.

    colewd:
    The only way away from this is if the functional space is almost equal the sequence space and the data does not support this especially in the nuclear protein area.

    Not really, it’s enough if there’s functional space to play around, and all the evidence points to this being the case.

    Let’s summarize then.

    1. You agree that individuals within a population vary.
    2. You agree that the particular characteristics of some of them might give them advantages to survive-and-reproduce.
    3. You therefore agree that there’s such a thing as natural selection.
    4. You disagree that variation can continue building up in a population, despite the fact of new mutations in offspring that survives and, later, reproduce all right.

    Is that where we are? You don’t think that variation can continue? If so we can go to the evidence about that.

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