Common Design vs. Common Descent

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I promised John Harshman for several months that I would start a discussion about common design vs. common descent, and I’d like to keep my word to him as best as possible.

Strictly the speaking common design and common descent aren’t mutually exclusive, but if one invokes the possibility of recent special creation of all life, the two being mutually exclusive would be inevitable.

If one believes in a young fossil record (YFR) and thus likely believes life is young and therefore recently created, then one is a Young Life Creationist (YLC). YEC (young earth creationists) are automatically YLCs but there are a few YLCs who believe the Earth is old. So evidence in favor of YFR is evidence in favor of common design over common descent.

One can assume for the sake of argument the mainstream geological timelines of billions of years on planet Earth. If that is the case, special creation would have to happen likely in a progressive manner. I believe Stephen Meyer and many of the original ID proponents like Walter Bradley were progressive creationists.

Since I think there is promising evidence for YFR, I don’t think too much about common design vs. common descent. If the Earth is old, but the fossil record is young, as far as I’m concerned the nested hierarchical patterns of similarity are due to common design.

That said, for the sake of this discussion I will assume the fossil record is old. But even under that assumption, I don’t see how phylogenetics solves the problem of orphan features found distributed in the nested hierarchical patterns of similarity. I should point out, there is an important distinction between taxonomic nested hierarchies and phylogenetic nested hierarchies. The nested hierarchies I refer to are taxonomic, not phylogenetic. Phylogeneticsits insist the phylogenetic trees are good explanations for the taxonomic “trees”, but it doesn’t look that way to me at all. I find it revolting to think giraffes, apes, birds and turtles are under the Sarcopterygii clade (which looks more like a coelacanth).

Phylogeny is a nice superficial explanation for the pattern of taxonomic nested hierarchy in sets of proteins, DNA, whatever so long as a feature is actually shared among the creatures. That all breaks down however when we have orphan features that are not shared by sets of creatures.

The orphan features most evident to me are those associated with Eukaryotes. Phylogeny doesn’t do a good job of accounting for those. In fact, to assume common ancestry in that case, “poof” or some unknown mechanism is indicated. If the mechanism is unknown, then why claim universal common ancestry is a fact? Wouldn’t “we don’t know for sure, but we believe” be a more accurate statement of the state of affairs rather than saying “universal common ancestry is fact.”

So whenever orphan features sort of poof into existence, that suggests to me the patterns of nested hierarchy are explained better by common design. In fact there are lots of orphan features that define major groups of creatures. Off the top of my head, eukaryotes are divided into unicellular and multicellular creatures. There are vetebrates and a variety of invertebrates. Mammals have the orphan feature of mammary glands. The list could go on and on for orphan features and the groups they define. Now I use the phrase “orphan features” because I’m not comfortable using formal terms like autapomorphy or whatever. I actually don’t know what would be a good phrase.

So whenever I see an orphan feature that isn’t readily evolvable (like say a nervous system), I presume God did it, and therefore the similarities among creatures that have different orphan features is a the result of miraculous common design not ordinary common descent.

5,163 thoughts on “Common Design vs. Common Descent”

  1. stcordova:
    Rumraket,

    Do you remember how I intelligently designed sequences that created a phylogenetic tree?

    The fact a phylogenetic tree can be built from data that have similarity to each other is no proof of phylogeny, it’s proof of similarity.

    I understand this objection, but it doesn’t work as an objection when the ancestral states can be inferred using that phylogeny, and tested to be functional.

    There’s no reason why it would be possible to take a bunch of genes with somewhat similar sequences, use them to construct a phylogenetic tree, look at that tree and find the nodes, infer what the sequence at the nodes must have been, recreate those nodes in the laboratory, and test them to be functional molecules with the sorts of functions implied by theories about the past evolution of life.

    This is the part you’re not getting. They’re testing the phylogeny by inferring nodes on the tree and recreating them, and seeing if those nodes actually work and what they do. A bifurcating tree implies a node connecting two branches. Using enzyme sequences that exist in life today, a common ancestor molecule can be inferred. This common ancestor node in turn can be used with other common ancestor nodes, and an even older node can be inferred to connect those. And so on it goes back in time, until they infer the universal ancestor of all the aaRS genes in known life. This gene sequence is then reconstructed and tested in the laboratory. Does it work at all? What does it do?

    It turns out it does work. And it works in the way predicted by hypotheses about the earliest stages of life, before the universal common ancestor, before fully encoded protein synthesis.

    Why would that work? Sal?

    Are you saying functional molecules are hyperabundant in sequence space? Or extremely well interconnected so that one functional molecule can be incrementally changed into another functional molecule without going through a significant nonfunctional state?

  2. stcordova:
    I already point out how remarkable the ancestor must have been so that it’s genes could be read two ways.

    Yes, the ancestor. Why would there even be such a thing? You understand that these inferred ancestral molecules are from PRE-LUCA evolution?

    But since we’re talking about the paper, when we are talking anti-codons, my understanding is “TTT” is the anti codon of “AAA”,“CCC” is the anti codon of “GGG”.

    We could also say T is the complement of A, and C the complement of G.Is that right?

    Yes.

    So, these UR genes in question, if they are anti-parallel, are we reading one in the reverse complement direction or are we reading them in the forward complement direction? I presume reverse complement, but perhaps you can tell me what you think.

    I agree, they are complementary in the antiparallel sense. The N-terminal of the class I ancestor is encoded complementarily to the C-terminal of the class II ancestor.

    But if the UR-gene is readable simultaneously in the forward way, and then in the reverse complement way, the gene is dual coded by being able to be read one way and create a functional protein and then able to be read upside-down complemented and backward and still create another functional protein.

    when transcription takes place, double stranded DNA is “unzipped” by helicases, exposing both strands to the possibility of transcription. In so far as the one strand is being transcribed, so the other one can be also.

    You think random chance can may such POOFs of dual function like this?

    Isn’t it more likely than random chance having to create two genes de novo?

    What’s more unlikely? Having to create a DNA strand that encodes a 46-residue peptide once? Or twice?

    It seems to me the fact that you get two genes for one chance event is a fact in it’s favor.

    So your phylogenetic phantasies rest on the miraculous emergence of a dual coded ancestor gene essential for life

    How do you know it’s essential for life? How do you know an even simpler stage of life isn’t possible?

    actually about 10 such miracles simultaneously.

    As already explained this is false.

    Like so many of your phylogenetic phantasies, it needs a miracle here and there to make it actually feasible.

    How are these results even possible? Are you saying these molecules are functional by chance? Doesn’t that imply either a hyperabundance of function in sequence space, or an extreme interconnectedness that would render evolution and common descent highly plausible?

  4. stcordova: Thanks for all of you venturing a guess, but I was being coy earlier, and I’ll be more direct…..

    Good idea. Your attempts to be coy are annoying rather than illuminating. Unless that’s what you’re going for.

    We have living fossils do we not?

    Not in the way you seem to mean it. Some taxa have changed morphologically more than others, but there are no species much more than 10 million years old, younger for vertebrates.

    Let’s say hypothetically we had living fossil shark populations that were reproductively isolated from each other 300,000,000 million years ago, maybe even before the era of dinosaurs……

    So morphologically they are the same, more or less.A shark is a shark.What do you expect the gene differences to look like between individuals of the two populations.Will the shark genes diverge between other sharks about as much as shark genes from humans?I mean, all this insistence on branching pattern is driven by the assumption of inevitable divergence barring coalescence.

    I would expect about as much divergence within an order of magnitude or so. Molecular evolutionary rates can vary quite a bit. But there will be no molecular living fossils. Not sure how you suppose coalescence figures into it.

    Coalescence may limit the branching pattern to some extent within each population, but between populations what would you expect? Obviously this issue could be extended to the aaRS gene of bacteria that have been around for millions of years and are geographically isolated.

    I don’t know what data you’re talking about there. I don’t think you have a clear idea what coalescence is or what it does. This is you not being coy? Why can’t you come out and say what you mean?

  5. stcordova: Do you remember how I intelligently designed sequences that created a phylogenetic tree?

    Yes, and that’s because you designed them specifically so they would create a phylogenetic tree. We all agree that god could fake a phylogeny if he wanted to, but is that your explanation for the nested hierarchy of life? If so, say so.

    The fact a phylogenetic tree can be built from data that have similarity to each other is no proof of phylogeny, it’s proof of similarity.

    At this late date why are you still confusing nested hierarchy with similarity?

  6. John Harshman:

    Good idea. Your attempts to be coy are annoying rather than illuminating. Unless that’s what you’re going for.

    I was asking a basic question, you all just didn’t know where it was going. But the question was clear enough. This was the question:

    If we, for example have two isolated populations of sharks for 300 million years, the genes in the population should diverege between the two populations right? Should the morphology necessarily diverge.

    You answered:

    John Harshman:

    Yes, genes will necessarily diverge. Morphology probably will too, but perhaps not to a great extent. Depends.

    That looks like an admission that there is really no firm prediction of the rates of genetic vs. morphological change. Ergo, the claims that evolution predicts the branching morphological pattern are over inflated.

    Look at the difference in morphology of the coelacanth vs. a bird, yet the coelacanth is a smidgen more similar genetically to a bird than it is to a zebra fish (actinogypterii) on average (but not necessarily every gene as I’ve shown).

    John Harshman:

    I would expect about as much divergence within an order of magnitude or so. Molecular evolutionary rates can vary quite a bit. But there will be no molecular living fossils.

    Hypothetically speaking if we have two populations of sharks from 300 million years ago that split into reproductively isolated populations (allopatric speciation if you will), it is hypothetically possible the genes between individuals of the shark populations could be about as numerically different (whatever distance metric is used) between the two shark species as the sharks are to a human.

    But the shark DNAs aren’t that different from each other, therefore the mRCA of all EXTANT sharks might only go back a few million years if we did a clock analysis of the DNA.

    I would expect the mRCA of all extant groups of bacteria in the aaRS gene will show a similar mRCA pattern.

  7. This just in:

    https://www.nature.com/articles/d41586-017-08325-y

    A study of some of the world’s most obscure marine life suggests that the central nervous system evolved independently several times — not just once, as previously thought1.

    The invertebrates in question belong to families scattered throughout the animal evolutionary tree, and they display a diversity of central nerve cord architectures. The creatures also activate genes involved with nervous system development in other, well-studied animals — but they often do it in non-neural ways, report the authors of the paper, published on 13 December in Nature.

    “This puts a stake in the heart of the idea of an ancestor with a central nerve cord,” says Greg Wray, an evolutionary developmental biologist at Duke University in Durham, North Carolina. “That opens up a lot of questions we don’t have answers to — like, if central nerve cords evolved independently in different lineages, why do they have so many similarities?”

    So much for common descent explaining the branching pattern of similarities. The paper mentioned the BMP gene. I provided a phylogeny tree earlier in this discussion using the BMP gene.

  8. stcordova: But if the UR-gene is readable simultaneously in the forward way, and then in the reverse complement way, the gene is dual coded by being able to be read one way and create a functional protein and then able to be read upside-down complemented and backward and still create another functional protein!!!! You think random chance can make such POOFs of dual function like this?

    Sal,

    This is an example of dual coding I have asked you about a while back:

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

    Theses sentences can be read forward and backwards and according to our logically thinking friends from “Darwin’s church” dual coding genes just happened by random mutations and natural selection…

    These three sentences above were without a doubt designed by intelligent agents… So the magnitude of the dual coding problem would be the equivalent of writing a novel that could be read in either forward or reverse directions making two different stories both of which made sense…

    Do you really think that one needs more evidence for design in DNA?

  9. J-mac:

    This is an example of dual coding I have asked you about a while back:

    Yes, I remember, and in all honesty, I didn’t have a good answer at the time. Thank God for Rumraket! He came through an reported on God’s designs!

    But a couple notes. I pressed some of the researchers at NIH for an answer about dual coding genes. They said they are rare, but they do exist. Part of the problem now is a lot of gene prediction and annotation (as in “guess where the genes are in the DNA because we don’t have complete experimental data”) operate on the assumption that overlapping genes are rare or don’t exist!

    The UR-gene Rumraket describes is not as strong an example as I thought, it is not as exact as your sentence above because the forward-backward UR-gene is only a hypothetical ancestor, it is only a hypothetical ancestral construct required to make an evolutionary scenario work! However, this backward upside down motif is weakly reflected in genes today.

    Better examples do exist however in biology, particularly in viruses and phages and some bacterial.

    One of the best-documented examples of translational frameshifting occurs during translation of the mRNA for the overlapping gag and pol genes of the Rous sarcoma virus (see Fig. 26–34). The reading frame for pol is offset to the left by one base pair (–1 reading frame) relative to the reading frame for gag (Fig. 27–9).

    Nelson, David L.; Cox, Michael M.. Lehninger Principles of Biochemistry (Page 1111). W.H. Freeman. Kindle Edition.

    But that example too is weak as the over lap involves only 4 bases.

    But a survey was done that found a few dual coding genes in the upside down reverse direction (the complementary strand, reverse direction read).
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2335118/

    Increasing evidence suggests that overlapping genes are much more common in eukaryotic genomes than previously thought. In this study we identified and characterized the overlapping genes in a set of 13,484 pairs of human-mouse orthologous genes.

    Results

    About 10% of the genes under study are overlapping genes, the majority of which are different-strand overlaps. The majority of the same-strand overlaps are embedded forms, whereas most different-strand overlaps are not embedded and in the convergent transcription orientation. Most of the same-strand overlapping gene pairs show at least a tenfold difference in length, much larger than the length difference between non-overlapping neighboring gene pairs. The length difference between the two different-strand overlapping genes is less dramatic.

    You asked:

    Do you really think that one needs more evidence for design in DNA?

    I can’t speak for the Darwinists here as it seems that even if they saw a miracle with their own eyes, they would interpret that as meaning miracles happen naturally without God or that they are hallucinating. Whereas for me, I simply enjoy pondering God’s works.

    The LORD’s works are great, pondered by all those who delight in them.

    Pslam 111:2

    I delight in God’s great works, and I ponder them frequently.

  11. stcordova: I pressed some of the researchers at NIH for an answer about dual coding genes. They said they are rare, but they do exist. Part of the problem now is a lot of gene prediction and annotation (as in “guess where the genes are in the DNA because we don’t have complete experimental data”) operate on the assumption that overlapping genes are rare or don’t exist!

    Sal,

    Here is a quote from one of the papers on the theme:

    “Despite redundancy in the genetic code, the choice of codons used is highly biased in some proteins, suggesting that additional constraints operate in certain protein-coding regions of the genome. … The authors determined that ~14% of the codons within 86.9% of human genes are occupied by transcription factors. Such regions, called “duons,” therefore encode two types of information: one that is interpreted by the genetic code to make proteins and the other, by the transcription factor-binding regulatory code to influence gene expression. This requirement for transcription factors to bind within protein-coding regions of the genome has led to a considerable bias in codon usage and choice of amino acids, in a manner that is constrained by the binding motif of each transcription factor.”

    http://science.sciencemag.org/content/342/6164/1325

  12. J-mac

    Here is a quote from one of the papers on the theme:

    “Despite redundancy in the genetic code, the choice of codons used is highly biased in some proteins, suggesting that additional constraints operate in certain protein-coding regions of the genome. … The authors determined that ~14% of the codons within 86.9% of human genes are occupied by transcription factors. Such regions, called “duons,” therefore encode two types of information: one that is interpreted by the genetic code to make proteins and the other, by the transcription factor-binding regulatory code to influence gene expression. This requirement for transcription factors to bind within protein-coding regions of the genome has led to a considerable bias in codon usage and choice of amino acids, in a manner that is constrained by the binding motif of each transcription factor.”

    http://science.sciencemag.org/content/342/6164/1325

    I wasn’t familiar with that. I thought “duon” referred to something else. I learned something! Thanks a million!

  13. I forgot to respond to Alan Fox a while back about the idea that species evolve to occupy niches.

    The problem with that is, as Richard Lewontin points out, birds don’t eat leaves and snakes don’t eat grass. That is evidence right there niches don’t get occupied as evolutionary theory would predict.

  15. stcordova:
    I forgot to respond to Alan Fox a while back about the idea that species evolve to occupy niches.

    The problem with that is, as Richard Lewontin points out, birds don’t eat leaves and snakes don’t eat grass.That is evidence right there niches don’t get occupied as evolutionary theory would predict.

    Yea, and Filipinos don’t eat shit…often.

    Oh come on its Christmas, we are just having fun!

    Feliz Navidad Sal! No mames!

  16. It’s worth pointing out an exchange I had with Rumraket, which echoes an exchange I had with John Harsman (which John lost) a couple years back over the Random Access Memory in proteins:

    Phylogenetic Systematics

    Rumraket:

    By the way Sal, your whole argument from “RAM” here is completely nonsensical. RAM can only function as RAM if it is editable and rewritable. It has to be possible to change it basically on the fly, as memories are stored, deleted, rewritten and so on.

    Well, well, well…..
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3415845/

    Phosphorylation sites are formed by protein kinases (‘writers’), frequently exert their effects following recognition by phospho-binding proteins (‘readers’) and are removed by protein phosphatases (‘erasers’). This writer–reader–eraser toolkit allows phosphorylation events to control a broad range of regulatory processes, and has been pivotal in the evolution of new functions required for the development of multi-cellular animals. The proteins that comprise this system of protein kinases, phospho-binding targets and phosphatases are typically modular in organization, in the sense that they are composed of multiple globular domains and smaller peptide motifs with binding or catalytic properties. The linkage of these binding and catalytic modules in new ways through genetic recombination, and the selection of particular domain combinations, has promoted the evolution of novel, biologically useful processes. Conversely, the joining of domains in aberrant combinations can subvert cell signalling and be causative in diseases such as cancer. Major inventions such as phosphotyrosine (pTyr)-mediated signalling that flourished in the first multi-cellular animals and their immediate predecessors resulted from stepwise evolutionary progression. This involved changes in the binding properties of interaction domains such as SH2 and their linkage to new domain types, and alterations in the catalytic specificities of kinases and phosphatases. This review will focus on the modular aspects of signalling networks and the mechanism by which they may have evolved.

    Someone got crushed in that exchange. It wasn’t me. 🙂 So much for the endless litany that I don’t understand. 🙂

    This supports colewd’s point about the variety of computers creating a nested hierarchy. In the case of living creatures, each creature implements the Random Access Memory on proteins, and thus the creatures overall computer/information processing system, a little differently.

    As I said, it is naïve to think the changes are random copying errors as Rumraket is modelling them to be. The look like sophisticated gene-wide changes.

    To further this point, consider the discussion here:

    Chargaff Parity Rule 2, Biased/Non-Random Mutations

    THE ratio of guanine plus cytosine to adenine plus thymine (GC/AT) in the deoxyribonucleic acid (DNA) of a given species of a micro-organism is constant, but the GC/AT ratio of different kinds of microorganisms can vary by a factor of as much as five times

    So the “fix” claimed by evolutionists is some sort of biased copying mechanism that changes the distribution so that the distributions are still random.

    But note:

    Actinobacteria : some have 75% GC some have 37%

    Streptomyces: an Actinobacteria, has high GC

    Why is that??? That doesn’t agree with the random copying error model of phylogenies does it? Maybe like a biased-random distribution at best, but that would be just speculation. If we found functional significance for this, the copying error explanation starts to fall apart.

    FWIW, that “Chargaff Parity Rule 2, Biased/Non-Random Mutations” thread had a rather comical exchange with RobC as I pointed out to him that ovaries don’t get a lot of UV radiation — overturning his errant speculations as to the reasons for the strange biases in DNA.

  18. Here is what got my exchange with Rumraket started (note the links to the TopoIsomerase II phosphorylations):

    Phylogenetic Systematics

    colewd to Glen Davidson:

    Nonsense. The Mac air uses a silicon mass storage system. The Mac Book uses disc mass storage. Their can be variation in other components as well.

    Well said. Merry Christmas.

    The gene can be thought of as a basic mother board or chassis for miniaturized RAM. The RAM patterns of phosphorylations of amino acids are different between species.

    Depicted below are 3 species with segments of the TopoIsomerase IIA homologs. I sent this recently at the request of a professional biochemist researching TopoIsomerases in connection with chemotherapy research. Since I’m a bit of a data clerk, it was a natural task for me.

    A publication in the mid 1990’s showed that we can insert human TopoIsomerase II into a yeast, and as far as chromosome segregation, it works fine for the yeast. Would anyone dare think of doing the reverse considering the importance of phosphorylation in the process of memory and cognition?

    Phosphorylation in the brain can change rapidly by factors of 2 in the process of learning based on a study where they trained rats in a maze and then examined the phosyphorylation degree in their brains compared to a control group that weren’t trained. The phosphorylation acts like a miniature RAM.

    See:
    https://www.sciencedirect.com/science/article/pii/S0166432814000618

    But back to the diagram of this amazing Random Access Memory machine that is species specific on the TopoIsomerase IIA protein:

    Row 1: yeast
    Row 2: chicken
    Row 3: human

    The Red triangles are the phosyphorylation marks on the human, the green on the yeast. I omitted the chicken because UNIPROT has no reports on the chicken. The purple stars are the lysine acetylation positions. I omitted the huge amount of ubiquitination positions effected by SUMO (that’s a whole nother story).

    http://theskepticalzone.com/wp/wp-content/uploads/2017/12/human_1295_1377_yeast_1252_1272_mhy.png

    http://theskepticalzone.com/wp/wp-content/uploads/2017/12/human_1387_1449_yeast_1353_1356_mhy.png

    http://theskepticalzone.com/wp/wp-content/uploads/2017/12/human_1469_1525_yeast_1408_1423_mhy.png

    In human Topoisomerase IIA, 11 of the 25 positions involving S (Serine) are followed by a D (Aspartic acid). So we have the “SD” motif over represented. A rough calculation using the binomial distribution indicates the odds of that happening by chance are 1 in 80 million. That difference is not consistent with random mutation changing genes in the evolution of higher eukaryotes, it suggests the differences have functional significance for the molecular Random Access Memory specific to the architecture of the species.

    The list of phosphorylations could well be incomplete. I see a lot of “SD” sites that haven’t yet been identified as phosphorylation targets. I have to check it out, but I think the “SD” motif in human topoisomerase IIA is way outside ordinary expectation. My first estimate was 1 out of 80 million, it could be beyond that if all “SD” motifs are considered. That doesn’t look random to me!

  19. stcordova: Biased/Non-Random Mutations”

    Good one Sal!
    There is enough evidence to support the notion that many neutral or beneficial mutations are non-random… It all reaches all the way down to quantum coherence level…

    I had been researching it for a while on and off… There are quantum restrictions on most mutations: 50/50 , 1 out of 2 spots where mutation can happen etc…

  20. Thanks to Rumraket citing Rodin and Ohno, I found this gem of non-random/biased mutations:

    http://www.pnas.org/content/90/10/4723.full.pdf

    One of the fundamental rules of construction obeyed by all
    modem DNA sequences is that two dinucleotides, CG and
    TA, are consistently underrepresented and that these deficiencies
    are compensated by overrepresentation of three
    dinucleotides, TG, CA, and CT, when their observed frequencies
    were compared with what are theoretically expected
    from a given base composition (1-4).

    Inasmuch as both underrepresented dimers, CG and TA,
    are palindromes, and two of the three excessive dimers, TG
    and CA, are complementary to each other, the above rule
    imposes symmetry on two complementary strands.

    NOTE: my understanding tis that the reverse complement of “CG” is “CG”, and “TA” is “TA” thus in view of opposite strands they are “palindromes”.

    One can explore this at:
    http://www.bioinformatics.org/sms/rev_comp.html

  22. Reminds of this:

    Mung: dazz: MDNARMNS

    Actual proof that the DNA arose by Random Mutation and Natural Selection. Wow!

  23. J-mac,

    Regarding CTFC binding sequences, get a load of this, the CTFC binding sites have to be paired, sometimes even thousands of bases away. They have to be paired based on “mirror” images of each other. 🙂

    But what you taught me was something I was not really aware of since I thought duon referred to something else. This is non-random design x100.

    This also suggests, that since species would have different CTFC biding sites, duons, and extrusion loops, the differences in DNA between species is non-random, unlike the way John Harshman and Rumraket model the supposed phylogenetic changes.

  24. stcordova:
    I forgot to respond to Alan Fox a while back about the idea that species evolve to occupy niches.

    Not my view. Populations are shaped by the niche they find themselves in. Species appear when a part of a population stops sharing genes with the main population; i. e. it becomes genetically isolated from the main population.

    The problem with that is, as Richard Lewontin points out, birds don’t eat leaves…

    Some do. Geese graze. The hoatzin is herbivorous,

    …and snakes don’t eat grass.

    There are no known herbivorous snakes, that’s true.

    That is evidence right there niches don’t get occupied as evolutionary theory would predict

    This is a non sequitur. So snakes are, apparently, all carnivorous. Why is that a problem for evolution?

  26. Alan Fox: So snakes are, apparently, all carnivorous. Why is that a problem for evolution?

    Nothing is a problem for a theory where, “well, that just didn’t happen,” is an acceptable explanation. #meh

    ETA: Why didn’t other mammals migrate to Australia? Well, by chance, it just didn’t happen, that’s all. Meh.

  27. stcordova,

    Thanks Sal!
    I’m glad I could be of help… 🙂

    I have to digest what you just wrote and get back to you… There is lot’s more to it…

  28. stcordova: So much for common descent explaining the branching pattern of similarities. The paper mentioned the BMP gene. I provided a phylogeny tree earlier in this discussion using the BMP gene.

    So what? You provided a phylogeny… and? As usual your post amounts to regurgitating some irrelevant factoid but supplying zero reasoning to show how this leads to any of your desired conclusions. You do that a lot.

  29. stcordova:
    The UR-gene Rumraket describes is not as strong an example as I thought, it is not as exact as your sentence above because the forward-backward UR-gene is only a hypothetical ancestor, it is only a hypothetical ancestral construct required to make an evolutionary scenario work!

    Which nevertheless works as predicted. For reasons you can’t explain if common descent didn’t take place.

    The view of protein evolution and of the merits of phylogenetic inferences that you hold, if correct pretty much rules out that an inference based on phylogenetics, as they did in these experiments, should yield a functional gene.

    Remember, you believe the nodes implied by the trees do not correspond to ancestral states that ever existed. Your claim is they are fantasies.

    Also, you believe new proteins can’t evolve, and that functional sequences are either so rare or so isolated in sequence space that evolution can’t “create” them through the blind sampling of mutations in sequence neighborhoods, or by de novo evolution of proteins ala frameshift mutations.

    The views you must hold in order to deny evolution are contradicted by experiments such as these. If the views you hold were really true, these results should be impossible.

  30. Rumraket,

    The views you must hold in order to deny evolution are contradicted by experiments such as these. If the views you hold were really true, these results should be impossible.

    Can you elaborate why you think the results prove unguided evolution is real?

  31. stcordova:
    It’s worth pointing out an exchange I had with Rumraket, which echoes an exchange I had with John Harsman (which John lost) a couple years back over the Random Access Memory in proteins:

    This supports colewd’s point about the variety of computers creating a nested hierarchy.

    You people keep claiming this, but you never get around to actually demonstrating the truth of your claim. All you do is assert. You make claims about facts that you never back up.

    In the case of living creatures, each creature implements the Random Access Memory on proteins, and thus the creatures overall computer/information processing system, a little differently.
    Even if they do, so what?

    As usual there is no arguments. There is no reasoning going on. It’s all empty stating of fancy-sounding factoids with no supporting reasoning. You never actually support any conclusion. You just state “it looks complicated”. Or “there are multiple levels of contraint”.

    … and?.

    As I said, it is naïve to think the changes are random copying errors as Rumraket is modelling them to be.

    What changes? Are you talking about the differences in sequence of orthologous loci in different species?

    The look like sophisticated gene-wide changes.

    Oh, the argument from “it looks sophisticated”. Which isn’t even an argument, there is no conclusion and no premises. There is no reasoning going on. No entailments or implications of various hypotheses are evaluated in light of any facts.

    You are nothing but vacuous bluster.

    To further this point, consider the discussion here:
    http://theskepticalzone.com/wp/chargaff-parity-rule-2-biasednon-random-mutations/

    So the “fix” claimed by evolutionists is some sort of biased copying mechanism that changes the distribution so that the distributions are still random.

    As above, there is no content to actually deal with. You just state some irrelevant factoid and act as if you’ve said something meaningful from which anything follows.

    But note:

    Why is that??? That doesn’t agree with the random copying error model of phylogenies does it?

    What is the random copying error model of phylogenies?

    Where do I find it? What dies it say? In what way is it relevant to anything here?

    Please, try to actually make an argument. Spell out the reasoning.

    Maybe like a biased-random distribution at best, but that would be just speculation.If we found functional significance for this, the copying error explanation starts to fall apart.

    Wait a minute, so you think the random in random mutations means the frequency of bases in genomes should be equiprobable, and if it is not equiprobable, that means mutations can’t be random in that sense and therefore changes between species in the frequencies of bases can’t be explained as accumulated mutations?

    Is that what you’re saing? If that’s what you’re saying, then please confirm that this is what you’re saying and proceed to also supply the reasoning that entails that conclusion.

    Why do I have to even try to guess what you’re trying to say here? It’s almost like, if you stay deliberately vague and handwavy while using technical jargon and making an occasional obscure reference to some biological factoid, you can better keep up the pretense that you’re saying something profound or meaningful.

    Wait. No, it isn’t almost like that. It is actually what you do.

    FWIW, that “Chargaff Parity Rule 2, Biased/Non-Random Mutations” thread had a rather comical exchange with RobC as I pointed out to him that ovaries don’t get a lot of UV radiation — overturning his errant speculations as to the reasons for the strange biases in DNA.

    That’s some selective memory right there. Here’s what he said:

    RobC:Sal, Really? You have a bunch of people asking what point you’re even trying to make, and you come at me with what, this:

    “So how do you propose UV light gets into someone’s ovaries to form T-dimers in the gametes. How about the testicles, does he walk around in the sunlight trying to get UV deep into his testicles. Hahaha! And you present yourself to criticize me? Hahaha!”

    Your original post mentions the differing GC content of Actinobacteria, Streptomyces, Saccharomyces, Arabidopsis. Do they have testes, Sal? Are they exposed to light? Your stupid statement makes my point: different organisms have different environments, different mechanisms acting on their DNA and different DNA repair activities in their germlines. We’ll find different, but phylogenetically related GC and AT content.

    If you think there’s a point to be made about these differences, please state it.”

    I can only mirror his call for you to try to make a coherent point. Not just mindlessly state some factoid and then act like it means something profound. Spell out the logic. Show with correct logical reasoning what the implications are so that we can at least discuss whatever your point is.

    It is hilarious and sad at the same time to see you flail around post after post unable to understand RobC’s entirely logical point, that the high GC content of some particular species of single celled organisms can be explained as the result of a long-term adaptive response to UV radiation in their environment. They have evolved high GC content because the G and C bases are less prone to mutate under exposure to UV light, in contrast to A and T bases which are more prone to mutation under UV.

    Thanks for bringing up that thread Sal. Another one among your uncountably endless failures.

  32. stcordova:
    Here is what got my exchange with Rumraket started (note the links to the TopoIsomerase II phosphorylations):

    What about them? “Note them”. Why? What is the implication? Try to spell it out.

    The gene can be thought of as a basic mother board or chassis for miniaturized RAM. The RAM patterns of phosphorylations of amino acids are different between species.

    Doesn’t that imply, that if these RAM patterns can’t evolve, then the Ark would have to have carried all species that currently exist on Earth?

    Doesn’t it imply, that the Ark would have to carry at least ten million pairs of organisms?

    You just said they are different between species. This contradicts your view that the extant biodiversity evolved from a much smaller number of original, independently created common ancestors of the various biblical “baramins” or “kinds”.

    In human Topoisomerase IIA, 11 of the 25 positions involving S (Serine) are followed by a D (Aspartic acid). So we have the “SD” motif over represented. A rough calculation using the binomial distribution indicates the odds of that happening by chance are 1 in 80 million. That difference is not consistent with random mutation changing genes in the evolution of higher eukaryotes

    Why not?

    Explain why not. You assert it isn’t, but you don’t explain why.

    it suggests the differences have functional significance for the molecular Random Access Memory specific to the architecture of the species.

    And why can’t that evolve?

    The list of phosphorylations could well be incomplete.I see a lot of “SD” sites that haven’t yet been identified as phosphorylation targets.I have to check it out, but I think the “SD” motif in human topoisomerase IIA is way outside ordinary expectation.

    Really? What is the ordinary expectation and why is that the ordinary expectation? And what are the implications of it being outside of the ordinary expectation?

    My first estimate was 1 out of 80 million, it could be beyond that if all “SD” motifs are considered. That doesn’t look random to me!

    What does it mean to say that it looks random? What are the implications of it being non-random? Are you saying you expects an equiprobable distribution? Why would you expect that? Could natural selection explain a non-equiprobable distribution? Why not?

  33. stcordova: Thanks to Rumraket citing Rodin and Ohno, I found this gem of non-random/biased mutations:

    Sal, did you really believe that both mutations that happen, mutations that get fixed, and the frequencies of the bases AGCT were supposed to be equiprobable, according to evolution?

    If you really believed that, why? Who told you it was so?

    http://www.pnas.org/content/90/10/4723.full.pdf

    One of the fundamental rules of construction obeyed by all
    modem DNA sequences is that two dinucleotides, CG and
    TA, are consistently underrepresented and that these deficiencies
    are compensated by overrepresentation of three
    dinucleotides, TG, CA, and CT, when their observed frequencies
    were compared with what are theoretically expected
    from a given base composition (1-4).

    Inasmuch as both underrepresented dimers, CG and TA,
    are palindromes, and two of the three excessive dimers, TG
    and CA, are complementary to each other, the above rule
    imposes symmetry on two complementary strands.

    NOTE: my understanding tis that the reverse complement of “CG” is “CG”, and “TA” is “TA” thus in view of opposite strands they are “palindromes”.

    One can explore this at:
    http://www.bioinformatics.org/sms/rev_comp.html

    And? What’s your point with this?

  34. stcordova:
    J-mac,

    Regarding CTFC binding sequences, get a load of this, the CTFC binding sites have to be paired, sometimes even thousands of bases away.They have to be paired based on “mirror” images of each other.

    https://youtu.be/Tn5qgEqWgW8

    But what you taught me was something I was not really aware of since I thought duon referred to something else.This is non-random design x100.

    Why?

    This also suggests, that since species would have different CTFC biding sites, duons, and extrusion loops, the differences in DNA between species is non-random, unlike the way John Harshman and Rumraket model the supposed phylogenetic changes.

    And by non-random you mean they don’t follow an equiprobable distribution, and since you have been led to believe that the random in “random mutation” means “has an equiprobable distribution”, any deviation from such a distribution means it can’t be evolution, right? That’s how you think here, right?

  35. Mung: Nothing is a problem for a theory where, “well, that just didn’t happen,” is an acceptable explanation. #meh

    ETA: Why didn’t other mammals migrate to Australia? Well, by chance, it just didn’t happen, that’s all. Meh.

    What’s the design explanation again?

  36. colewd:
    Rumraket,

    Can you elaborate why you think the results prove unguided evolution is real?

    I wouldn’t claim the results of the experiments I referenced proves that evolution is unguided. As usual you’ve confabulated some strange idea nobody holds.

  37. stcordova: This supports colewd’s point about the variety of computers creating a nested hierarchy.

    No, you and colewd constantly and conveniently forget that the nested hierarchy of life depends entirely on derivation (morphology doesn’t have orphans, even if some genes are said to), that morphology must be related even if it ends up being quite different. Apple computers, conveniently, are not restricted to related systems, rather some Apples have flash storage while others have magnetic storage. The two storage systems are not related, one is not derived from the other, there is no decent evolutionary scenario in which one could turn into the other, even if computers reproduced.

    There may be a kind of nested hierarchy in Apple computers, I really don’t know or care (for one thing, to mimic evolution they’d need to nest into another nested hierarchy, which sensibly they do not). What there isn’t is the kind of necessarily derivative nested hierarchy that evolutionary processes produce, the kind in which unrelated structures (as in morphology) do not appear.

    Glen Davidson

  38. Rumraket,

    Isn’t it fucking hilarious that creationists will go out of their way to deny the biasing effect of natural selection, to then proclaim evolution is all random, “sheer dumb luck” and stuff like that… and the next thing you know another biasing factor all of a sudden makes mutations… wait for it! COMPLETELY NON-RANDOM.

    Praise sweet baby jeebus!

  39. stcordova: Me: Yes, genes will necessarily diverge. Morphology probably will too, but perhaps not to a great extent. Depends.

    Sal: That looks like an admission that there is really no firm prediction of the rates of genetic vs. morphological change. Ergo, the claims that evolution predicts the branching morphological pattern are over inflated.

    You are still confused about what a nested hierarchy means. It doesn’t involve sorting species in order of similarity. You persist in equating a nested hierarchy with an ordering of similarity. You do it again just below:

    Look at the difference in morphology of the coelacanth vs. a bird, yet the coelacanth is a smidgen more similar genetically to a bird than it is to a zebra fish (actinogypterii) on average (but not necessarily every gene as I’ve shown).

    That may be true, but it’s irrelevant. What’s relevant is that we see the same nested hierarchy in morphology and molecules, even though the branch lengths are not the same, or even in the same relative order. How nested hierarchy works is something you need to learn if you want to discuss any of this. Give up the ordering by distance.

    Me: I would expect about as much divergence within an order of magnitude or so. Molecular evolutionary rates can vary quite a bit. But there will be no molecular living fossils.

    Sal: Hypothetically speaking if we have two populations of sharks from 300 million years ago that split into reproductively isolated populations (allopatric speciation if you will), it is hypothetically possible the genes between individuals of the shark populations could be about as numerically different (whatever distance metric is used) between the two shark species as the sharks are to a human.

    Sure it could.

    But the shark DNAs aren’t that different from each other, therefore the mRCA of all EXTANT sharks might only go back a few million years if we did a clock analysis of the DNA.

    That also may be true. Species extinctions prune the tree, in a process analogous to coalescence within species. Now, I don’t know the age of the MRCA of extant sharks, but I doubt there’s any reason to believe it’s as old as 300 million years.

    I would expect the mRCA of all extant groups of bacteria in the aaRS gene will show a similar mRCA pattern.

    Here I’m even less familiar with the data, nor does your expectation seem to be anything more than word salad. What bacteria? What similar mRCA pattern? What would you expect, and why?

  40. stcordova: The problem with that is, as Richard Lewontin points out, birds don’t eat leaves and snakes don’t eat grass.

    I don’t know of any grass-eating snakes, but there certainly are leaf-eating birds. Lewontin was apparently misinformed. Anyway, why should there be an open niche for a legless grass-eater?

  41. Mung: Nothing is a problem for a theory where, “well, that just didn’t happen,” is an acceptable explanation. #meh

    ETA: Why didn’t other mammals migrate to Australia? Well, by chance, it just didn’t happen, that’s all. Meh.

    Actually in large part such “why didn’t X happen instead of Y?”- questions can be answered in no other way. This is not some uniquely vague feature of evolutionary theory, that isn’t also difficult to answer on basically all other scientific theories. Even on design you can’t really answer that. Why didn’t the designer make grass-eating snakes? Well he just didn’t, that’s all.

    Why didn’t the himalayas form in south America, or Africa form 3000 kilometers further north? Why isn’t the sun 9000 light-years closer to the galactic center? Why is there the particular distribution of tree-species in the local forest, and a slight different different distribution in another forest further away? Why isn’t there 0.073% more meteoric matter in the asteroid belt?

    Well, the conditions just weren’t right for that. Whether you believe chance played a role in determining why the world is the way it is, or whether you believe an invisible designer had a hand in orchestrating such affairs, there’s no qualitative difference in the answer you can give to “why isn’t things different?”-type questions. Well, for reasons that are obscure to us this is just how things are. The designer made it so has no greater explanatory content.

  42. Mung: Nothing is a problem for a theory where, “well, that just didn’t happen,” is an acceptable explanation. #meh

    There are biological explanations for why snakes are exclusively carnivorous. Simply, you need a big gut to store the microbes and mass of vegetation required and there ain’t no room in a snake’s body.

    ETA: Why didn’t other mammals migrate to Australia? Well, by chance, it just didn’t happen, that’s all. Meh.

    It didn’t happen because variation in sea level blocked placentals from following the route the marsupials took. Are you interested enough about the Wallace Line to warrant a separate thread?

  43. Alan Fox: There are biological explanations for why snakes are exclusively carnivorous. Simply, you need a big gut to store the microbes and mass of vegetation required and there ain’t no room in a snake’s body.

    Alan please, you know full well the outstanding number of cases in evolution where something that is “needed” just so happens to come along. If a snake need a bigger stomach to digest vegetables, well then it would just get a bigger stomach (pythons can’t have large stomachs?). We can never use the excuse in evolution that something was needed, to make life possible, and it couldn’t, whilst at the same time arguing that eyes were needed so they got them, kneecaps were needed so they got them, ears that can balance a body were needed so we got them…

    The notion that things that were needed came to be is ubiquitous in evolutionary theory, so how can you turn around and then say, the need is also a barrier. The just so stories of evolution are impossible to refute.

  44. phoodoo: The just so stories of evolution are impossible to refute.

    In stark contrast to the just so stories of design. Oh wait…

  45. Rumraket: In stark contrast to the just so stories of design. Oh wait…

    If you want to say that evolution uses the same assumptions as design, ok then.

  46. phoodoo: Alan please, you know full well the outstanding number of cases in evolution where something that is “needed” just so happens to come along.

    The number is zero, as far as I can tell.

  47. phoodoo: We can never use the excuse in evolution that something was needed, to make life possible, and it couldn’t, whilst at the same time arguing that eyes were needed so they got them, kneecaps were needed so they got them, ears that can balance a body were needed so we got them…

    Explain extinction then.

  48. J-Mac: There is enough evidence to support the notion that many neutral or beneficial mutations are non-random

    When you say “non-random” you really mean “the designer intended that to happen specifically” presumably. Then why don’t you just say that?

    Here, let me help:
    There is enough evidence to support the notion that many neutral or beneficial mutations are designed.

    Not so difficult is it?

    Now, a question: Were the non-random mutations that caused organisms present in the fall to become injurious (i.e. they became parasites) to human health designed?

  49. J-Mac: This is an example of dual coding I have asked you about a while back:

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

    Theses sentences can be read forward and backwards and according to our logically thinking friends from “Darwin’s church” dual coding genes just happened by random mutations and natural selection…

    These three sentences above were without a doubt designed by intelligent agents… So the magnitude of the dual coding problem would be the equivalent of writing a novel that could be read in either forward or reverse directions making two different stories both of which made sense…

    Do you really think that one needs more evidence for design in DNA?

    J-Mac,
    I can tell you don’t design or create anything. I’ve written this several times now but nobody seems to want to engage with me on this particular topic (I don’t wonder why, no, it’s clear why).
    I’ll probably make an OP to demonstrate your fear of this but here goes anyway:

    Every designer I know strives for simplicity and elegance. You IDcreationists make a big deal about how the design we observe in life can be determined to be design by virtue of the fact it’s so similar to the design we observe all around us.

    The domain of design I am most familiar with is programming. In that domain we strive to avoid all of the “signals” of design you’ve just noted. Writing a program where changing one part affects multiple other parts in unpredictable ways is what we observe in biology and in badly designed code. As you and BornAgain77 note, it’s all overlapping multi level codes in biology.

    https://en.wikipedia.org/wiki/Law_of_Demeter

    Each unit should have only limited knowledge about other units: only units “closely” related to the current unit.
    Each unit should only talk to its friends; don’t talk to strangers.
    Only talk to your immediate friends.

    So the simple fact is that your “evidence for design” in DNA is actually the opposite when considered by people who do actual design for an actual living. If you don’t believe me why don’t you ask Mung, who claims to be a programmer.

    SImply put, the “design” of life’s “program” is utterly unlike the designs humans create.

    However it is indeed possible to generate “computer code” that is similar in complexity to “biological code”. How, I hear you ask! It’s quite simple. You evolve it!

    http://web.mit.edu/remy/

    The researchers have put up a lengthy FAQ and source code where they admit they don’t know why the system works, only that it goes faster than normal TCP.

    So we evolve some code without human design principles and we look at it and we fail to understand why or how it works. It’s too complex to follow. Does that remind you of anything J-Mac or does your capability to make inferences only work one way?

  50. John Harshman:

    You are still confused about what a nested hierarchy means. It doesn’t involve sorting species in order of similarity

    So what are you going to build it on, the order of evolution which assumes common descent? In that case you’re defining nested hierarchy based on your evolutionary assumptions, not direct structural evaluation. The problem is your circular reasoning and circularly reasoned definitions. Structural comparison minimizes assumptions about evolution.

    You’re trying to force your definition of nested hierarchy (phylogenetic) on me and argue there is one and only one way to build a nested hierarchy. That’s false. A conceptual nested hierarchy can be built based on structure with no assumption of common descent. If it disagrees with your phylogenetic nested hierarchy, then all the better for the claim of common design.

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