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: Much (not all) the heterozygosity and alleles were created and thus differences were strategically positioned and most of the mutations thereafter are rare variants and slightly damaging.

    I don’ t understand how this interfaces with your view of molecular constraints. Did the original created kind have multiple molecular networks co-existing in a single species which segregated into different extant species?

  2. Joe Felsenstein: it is quite clear that shifts in frequencies of already-existing signals do change the information content of the message.

    What’s the mechanism by which changes in frequency change the information content of the message?

  3. I don’ t understand how this interfaces with your view of molecular constraints.

    Not every position is functionally constrained, many are. There is a lot we don’t know.

    Did the original created kind have multiple molecular networks co-existing in a single species which segregated into different extant species?

    We don’t have enough data to answer what positions don’t have regulatory effect. We only recently confirmed, synonymous mutations have regulatory effect for some of the reasons I described earlier. Along those lines:

    https://www.ncbi.nlm.nih.gov/pubmed/17508390

    While it has often been assumed that, in humans, synonymous mutations would have no effect on fitness, let alone cause disease, this position has been questioned over the last decade. There is now considerable evidence that such mutations can, for example, disrupt splicing and interfere with miRNA binding. Two recent publications suggest involvement of additional mechanisms: modification of protein abundance most probably mediated by alteration in mRNA stability and modification of protein structure and activity, probably mediated by induction of translational pausing. These case histories put a further nail into the coffin of the assumption that synonymous mutations must be neutral.

    So created alleles with non-synonymous differences might not have damaging effects on function if the difference is in the right spot, it will just be a different function.

  4. Regarding my views of selection which are related to fitness, Richard Lewontin articulates many of the problems I see with Darwinian ideas. You’ll have to scroll down to find his essay in the link below:

    https://sfi-edu.s3.amazonaws.com/sfi-edu/production/uploads/publication/2016/10/31/winter2003v18n1.pdf

    FINALLY, WE MUST CONSIDER the way in which differential fitness constrains the occupancy of the taxonomic space. Unfortunately the determination of fitness
    is a great deal more complicated than is usually supposed. It is easy to say that fitness of a type is its “relative probability of survival and reproduction” but
    turning that phrase into a coherent measure that can do work in evolutionary explanation is not so easy.
    …
    the relative fitnesses of genotypes may depend both on the population density of the organisms and on the relative frequency and identity of the competing types.
    ….
    The difficulties of the concept of fitness are,
    unfortunately, much deeper than the problem of frequency and density dependence. The problem is that it is not entirely clear what fitness is. Darwin took the metaphorical sense of fitness literally. The natural properties of different types resulted in their differential “fit” into the environment in which they lived.

    The better the fit to the environment the more likely they were to survive and the greater their rate of reproduction. This differential rate of reproduction would then result in a change of abundance of the different types.

    In modern evolutionary theory, however, “fitness”
    is no longer a characterization of the relation of the organism to the environment that leads to reproductive consequences, but is meant to be a quantitative expression of the differential reproductive schedules themselves. Darwin’s sense of fit has been completely bypassed.
    …
    Yet this complete reproductive information is insufficient to predict whether a type will increase or decrease in frequency in the population! It is also necessary to know whether the population as a whole is growing larger, is stable in numbers, or is decreasing in numbers. The same type that may be favored in a growing population may be disfavored in a shrinking population. Suppose the only difference between two types is not in their total reproduction but in their age schedule of progeny production. A type that produces offspring at an early age will increase in relative frequency in a growing population because it has reproduced while the total population is still small. If the population is shrinking, however, it pays to postpone reproduction…

    If a type increases in a population then it is, by definition, more fit. But this suffers from two difficulties. First, it does not distinguish random changes in
    frequencies in finite populations from changes that are a consequence of different biological properties. Finally, it destroys any use of differential fitness as an explanation of change. It simply affirms that types change in frequency. But we already knew that.

    So for all of John Harshman’s complaints about coherency, one of the central concepts of Evolutionary theory, “fitness”, isn’t quite as clear cut as to its meaning.

    Some other thoughts as it relates to Hierarchical Patterns:

    The real problem for the evolutionist is not to explain the kinds of organisms that have actually ever existed. The real problem for the evolutionist is how
    it is that most kinds of potential and seemingly reasonable organisms have never existed. The problem is to explain the location of the empty spaces in the
    clustered assemblage of occupied points. It is easy to describe organisms that have never existed. There are snakes that live in the grass, but there are no grasseating snakes. Birds perch in trees, yet , aside from a few exceptions, they do not eat all that greenery around them, but rather spend a great deal of energy
    searching for food. So why are there virtually no leafeating birds? The fact that the measure of the unoccupied space is so big compared to the measure of the
    occupied space, means that explanations of that lack of occupancy are not so easy to come by.

    Lewontin has essentially restated the problem that bother Darwin about the Peacock’s tail and Rube Goldberg machines of biology.

    He also has some interesting thoughts:

    THE STRUCTURE OF THE OCCUPANCY is another matter. Organisms are underdispersed in taxonomic space and we need to understand the causes of the hierarchical clumping. One reason for hierarchical clumping in taxonomic
    space is simply that organisms arise one from another. If an organism is someplace in taxonomic space it is likely that its immediate descendants will
    be someplace close by in the space rather than someplace far away. It may not be that a particular region in the space is impossible to fill or that you can’t get
    there from here, but that there has not been enough time for evolution to fill that space.
    On the other hand, the structure of accessibility may make it impossible to get there from here without retracing the steps to a remote branch point that led
    from a distant ancestral state. One remarkable evolutionary example of not being able to get there from here is that no vertebrate has ever succeeded in evolving wings without giving up something. There are no hexapod vertebrates. Bats and birds have had to give up their forelimbs to produce wings. We will never evolve into a race of angels because we do not have the genotype that will allow for the possession of arms, legs, and wings.

  5. Here is powerful evidence of immutability of basic form. After N-generations and 80 million years, we should reasonably expect a fish will give rise to a fish, not a Kangaroo or a Parrot, that is my theory. My theory is consistent with observation.

    http://www.newsweek.com/dinosaur-era-frilled-shark-insane-teeth-found-portugal-708764

    Prehistoric, Dinosaur-Era Shark With Insane Teeth Found Swimming Off Coast of Portugal

    The rare frilled shark is considered a “living fossil,” because evidence of its existence dates back to at least 80 million years ago. This summer, researchers found one alive and thriving off the coast of Portugal, adding yet more clues about the resilience of this ancient sea creature.

    The shark was discovered off the Algarve coast by researchers who were working on a European Union project in the area, the BBC reported. The aim of the project was to “minimize unwanted catches in commercial fishing,” the researchers told SIC Noticisas TV, as the BBC noted. but the team unknowingly unearthed one of the rarest and most ancient animals on the planet.

    Scientists believe the frilled shark has remained the same, both inside and out, since the Cretaceous Period,

  7. phoodoo: What’s the mechanism by which changes in frequency change the information content of the message?

    If someone offered you two collections of 100 discount coupons for a product, which would be more valuable to you, one in which 80% of them had expired, or one in which only 30% had expired?

  8. stcordova: After N-generations and 80 million years

    Huh? Are those the 80 million years that you believe did not happen?

    stcordova: My theory is consistent with observation.

    In your theory how old is the earth?

  9. stcordova: So created alleles with non-synonymous differences might not have damaging effects on function if the difference is in the right spot, it will just be a different function.

    Only created alleles are tolerated? What distinguishes a created non-synonymous substitution from a spontaneous non-synonymous substitution?

  11. colewd: Why would the re use of parts not show a pattern like this? In the case of cars new designs do not abandon older parts where those parts still do the job.

    Yes Bill, but even if you do that, it doesn’t explain why the trees you get are so similar.
    This is what you are supposed to explain, and which common descent does explain. Let’s try to cut it into tiny little bits so the logic becomes more obvious.

    First of all, what is it you’re supposed to explain? The similarity of the trees.

    Okay, what does that mean? It means the trees show similar branching orders. As in, some things are systematically grouped closer together (share more recent descent), than other things, no matter what attribute of the organism is used to construct the tree from.
    Let’s dig into that even more. Suppose we want to use a particular gene to construct the tree from. We take the gene sequence of the gene from (say) 10 different organisms and compare them (make an alignment). Then we use a phylogenetic algorithm to make one or more trees from that alignment. We don’t tell the algorithm what species is what, or from what species the sequences come from. The only thing the algorithm knows is the sequence alignment we feed it.
    An often used algorithm works like this: What evolutionary explanation (i.e. what tree) that invokes the least number of character state changes, explains this set of sequences?
    Another way of saying the same thing is, how little evolution does it take to “make” all these sequences from a common ancestor, using only copying with mutations?
    The algorithm then does this basically by comparing lots and lots of trees with the sequences at different branches, then counting how many total mutations it takes to make all the sequences given a certain tree, and gives it’s result(s) by showing the “best” tree(s). Some times there’s more than one “best” tree, as some of them have close or equal scores. A score here is, again, really just a reflection of how many “mutations” the tree implies. Lower is better with this sort of algorithm.

    Okay? So we now have a gene sequence from several different species, and this set of gene sequences was used to built a tree with this method.

    The question now is, suppose we take a different gene entirely, from the same 10 species, and submit it to the same algorithm, what kind of tree will the algorithm make? Well it turns out that, when we do this, we get a tree that is highly similar to the first one.
    Some times they’re basically identical. Other times they’re not identical, but still very much similar to each other. So similar, in fact, that it demands an explanation why they are so consistently pretty much the same tree. Mammals (for example) will be grouped together. Rodents will always be inside the larger mammal clade. Primates will always be grouped together, and they’ll always be inside mammals. And so on and so forth.

    Now you come along, and you say: I can explain that, it’s because there’s a designer that is re-using parts. Okay, let’s see if that’s correct.

    So the designer has this “part”, a gene. She takes this gene-part she’s created, for this new organism she’s created, and copies it, because she intends to re-use it in a new organism. She does so. Creates a new organism, but re-uses the gene. So now two identical copies of the gene exist, one in each species. She does it again when creating the third species. Now three identical copies of the gene exists. She does it again for the fourth species, re-uses the gene-part. Now four identical copies exist. And so on and so forth until she’s created ten species with ten identical copies of that gene-part.

    Maybe the gene looks like this:
    CGTACGATACA

    Now biologists come along and submit those ten identical copies of the gene to the above-mentioned phylogenetic algorithm. What do they get Bill? They get a star-tree without any groupings. Nothing is any further or any closer to any other member, than to anything else. They’re all equally distant from each other, because the gene is identical in all twenty species. So the tree is just a star with ten branches all connected to the same node (actually it comes out as a dot, because the branches has zero length).

    Okay, so simply re-using the part doesn’t explain the nested hiearchy. Much less why different genes would ever yield similar trees.

    Old on! You say. Perhaps the designer slightly tweaks the re-used part every time for functional reasons? Perhaps the part NEEDS to be sliightly different in a specific way, in order to function in a slightly different way in the new species the designer creates? And THEN you’d get differences that give hiearchical structure to the tree. Okay, let’s run with that.

    So the designer copies the gene from the first organism, then slightly alters it in a particular location in order for it to function in a particular way. Then she does the same thing again for the third species. But does she take the first gene again and copy it, and then slightly alter it? Or does she take the second gene, the one that was already altered a bit? Either way, we end up with a third copy that is not identical to the 1st or 2nd copy. And so on and so forth, until we have ten copies of the gene, but all of them slightly different from each other.

    Maybe the first gene the designer made looks like this:
    CGTACGATACA

    And then She makes another 10 altered versions of it. The copy she makes for species #2 needs a particular change to function. Like this:
    GGTACGATACA
    That first G there is important for function in species #2. It isn’t randomly chosen, it’s chosen for a functional reason.
    Then she makes one for species #3:
    CGTACGTTTCA
    Those T’s are important, they were chosen for a functional reason. That’s the idea. Moving on.
    #4
    CGTGCGATACT
    #5
    AGTACGTTTCG
    #6
    CGTACGCTACA
    #7
    CTTACGATTCA
    #8
    CGAACGATACC
    #9
    CGAAGGATACG
    #10
    TTTGCGATACT

    So there we go, 10 sequences. And they were designed by re-using a common template and then altered to suit particular functions in their respective species.

    Now biologists come along and take this gene from the 10 organisms and make an alignment, and then use the algorithm to make a tree from the alignment. They get a particular tree this time, with some being closer to others. There are groups this time. I used an actual maximum parsimony algorithm to get this tree. Luckily we only get one tree that is better than all others for this gene. (Link the online maximum parsimony tool I used.)

    But of course it takes more than one gene to make an organism, so the designer makes lots of genes by the same method for her 10 different species. She takes the 2nd gene and goes through a similar process as for the 1st gene. Copies it, makes some changes to it for functional reasons, inserts it into organism #2. Then copies it again, makes some more changes to it, inserts it into organism #3. And so on, until all 10 organisms now have two genes each. And the genes are all different, but sort of derivations of each other.
    So let me do that, here’s 10 versions of Gene #2:

    Species 1 ACATATAGCGG
    Species 2 TCTTATAGCGG
    Species 3 ACATATAGCTT
    Species 4 ACCGCTAGCGG
    Species 5 ACATCTAGCGG
    Species 6 ACATATGGGGG
    Species 7 CCGTATAGCGG
    Species 8 ACATGGAGCGG
    Species 9 TCATATAGCGG
    Species 10 GCATAAGGGCG

    She repeats this again with a third gene, makes ten versions of the third gene. Etc. etc.

    Here’s a list of 10 versions of Gene #3

    Species 1 AGCACACAAAC
    Species 2 AGGGCACAAAC
    Species 3 TGCACACTAAC
    Species 4 AGCACATAAAT
    Species 5 ATCACTCAAAC
    Species 6 AGCACACAGGC
    Species 7 CGCACATCTAC
    Species 8 GGCCCACAATC
    Species 9 AGCTCACATAC
    Species 10 AGCTGAGATAC

    (This is where I can’t be bothered making more genes up for this post, you get the point).

    Now biologists come along again and see the 2nd and 3rd gene in the ten different organisms. They make a new alignment for the 2nd and 3rd gene and submit it to the algorithm. The algorithm produces a tree for each (the one that explains the 10 different sequences using the fewest number of mutations). What trees do we get for genes #2 and #3?

    Let’s see:
    Maximum parsimony tree for gene #2.*
    Maximum parsimony tree for gene #3.**

    Even by just eyeballing this we can see that these trees aren’t remotely similar.

    * Note, the algorithm output four trees of equal score, but I just chose the first one of them for graphical representation. I have a text file that shows the 3 others.
    ** For gene 3 the algorithm output 22 different trees with equal scores, again I just chose the first one for graphical representation but have a text file that shows all 22.

    But remember, the number of possible unrooted trees for 10 species is 2,027,025.

    None of the trees output for these three genes, by the same algorithm, are remotely similar. So even if the designer re-uses the same general gene-template, and slightly alters it for functional reasons (or even aesthetic reason, like “hmm I like G’s here”), there’s still no reason they should yield highly similar branching patterns.

    And remember also, in real life there are many many more genes and many many more species. And the genes are much much longer than my genes made of only 11 nucleotides.

    Statistically speaking, there are only two options here. Either the designer is being deliberately deceptive with the real data sets from the diversity of life, and goes back on purpose and re-tweaks the copied genes with intent such that they yield similar trees when analyzed by the algorithm, or there was common descent. Is your designer deceptive on purpose, Bill?

  12. colewd:
    Rumraket,

    First, thank you for the very thoughtful argument.I am going to spend some time with it but I have one question.

    You are assuming here the design process to set up your argument. What if the process is different then you imagine. In the computer world with perfect simulation as an assumption we would create the widget in software based on design rules. The sequences would be interdependent and a copy an individual sequence and modify process is not what we would use.

    It is very hard to understand what you try to argue, but from the last sentence I gather that you suggest the sequences are actually interdependent. As in there are functional constraints on one sequence, that makes it so you have to make a particular set of changes to the other.

    Put another way, you’re asking: What if the changes you make in the sequence of gene #1, makes it so you have to make a specific set of changes to the sequence of gene #2, otherwise they won’t work in combination. Do I have that correctly?

  13. I just noticed something funny about the maximum parsimony phylogenies I got. The algorithm has in some cases correctly identified how I took a sequence, then copied it and introduced mutations into it in serial fashion. For example, for Gene 2, I generated the species-10 sequence, by copying and then mutating the species-6 sequence, which was itself copied and then mutated from the species-1 sequence.

    This is reflected in the tree by the algorithm, which put species 6 sequence on an internal node between species 1 and 10. This is just another way in which my made-up data sets fails to mimick a phylogeny derived from real data. In the real world, the species we see are not derived from each other, but from common ancestors. Chimpanzee isn’t an internal node that sits between human and Gorilla.

    Real data from living organisms exhibits hierarchical structure in a way it takes real effort and knowledge to “happen to” create by design. Due to the number of possible trees, it’s unbelievably unlikely to be due to chance, and it can’t be due to functional constraint.

    This really just puts another layer of preposterous deceptiveness to any purported designer of the “twin nested hiearchy” of life. It can’t be believed by a thinking person.

  14. Rumraket,

    Put another way, you’re asking: What if the changes you make in the sequence of gene #1, makes it so you have to make a specific set of changes to the sequence of gene #2, otherwise they won’t work in combination. Do I have that correctly?

    Yes. The genome ( like a software program) is built on interdependent sequences. A designer, especially knows the connection between sequence change and function would be dealing with this as he moves from a mouse to a rat assuming each are independent designs. The genetic changes between humans and chimps is across 70% of the protein coding genes.

  15. colewd:
    Rumraket,

    Yes.The genome ( like a software program) is built on interdependent sequences. A designer, especially knows the connection between sequence change and function would be dealing with this as he moves from a mouse to a rat assuming each are independent designs.The genetic changes between humans and chimps is across 70% of the protein coding genes.

    Alright, glad I understood it correctly. I will try to answer it tomorrow as I have to sleep now. Laterz!

  16. Corneel: Only created alleles are tolerated?

    The alleles God did not create are an important part of the signal for a nested hierarchy due to common design.

  17. colewd:
    Rumraket,

    Yes.The genome ( like a software program) is built on interdependent sequences. A designer, especially knows the connection between sequence change and function would be dealing with this as he moves from a mouse to a rat assuming each are independent designs.The genetic changes between humans and chimps is across 70% of the protein coding genes.

    What is the difference in coding genes within the species?

  18. Mung: The alleles God did not create are an important part of the signal for a nested hierarchy due to common design.

    How do you tell the difference?

  19. colewd:
    Rumraket,

    Yes.The genome ( like a software program) is built on interdependent sequences. A designer, especially knows the connection between sequence change and function would be dealing with this as he moves from a mouse to a rat assuming each are independent designs.The genetic changes between humans and chimps is across 70% of the protein coding genes.

    That’s not an independent design at all. You’re assuming a kind of evolution by an overwhelmingly intelligent designer, and you haven’t begun to suggest why this would be done by such an entity at all.

    You believe in essentially poofed (even if, unaccountably, dependent on past “designs”) organisms like the first eukaryotes. Well, why not? Why would anyone with the Designer’s intelligence be tinkering with old sequences in order to make new designs?

    As usual, there’s simply no sense to the “design argument.”

    Glen Davidson

  20. colewd: Yes. The genome ( like a software program) is built on interdependent sequences. A designer, especially knows the connection between sequence change and function would be dealing with this as he moves from a mouse to a rat assuming each are independent designs. The genetic changes between humans and chimps is across 70% of the protein coding genes.

    That might work, but mouse and rat are clearly not independent designs. The differences between mouse and rat are nested within differences that distinguish murids from other rodents. The only explanation I can think of in your computer-analogy world is a strict adherence to legacy, which would be indistinguishable from common descent.

  21. Mung: The alleles God did not create are an important part of the signal for a nested hierarchy due to common design.

    Sure, but Sal’s rigid interlaced molecular systems are not tolerant of variation at all. That was what supposedly prevented them from evolving. OMagain spotted the contradiction as well and started a thread on it, so I suggest we take this discussion there.

    ETA: It appears OMagain is discussing something different, i.e. the occurence of beneficial mutations. That’s not what interests me here. I wonder how variation is tolerated in constrained and highly interlaced molecular systems.

  22. colewd:
    Rumraket,

    Yes. The genome ( like a software program) is built on interdependent sequences.

    Okay, back to this. Yes it is true, genes often times “cooperate” to yield certain functions, and can some times be constrained at some sites to be intercompatible. A very simple example I can think of is a transcription factor that has to bind a particular stretch of DNA and thereby regulate a downstream gene. In this situation, the sequence of the DNA to which the TF binds, and the amino acid sequence of the TF itself are co-dependent.

    However, this there are at least two very important caveats to this that render your suggestion ineffective. First of all, the number of possible TF-to-DNA relationships that are possible, so unbelievably vastly outnumber the number of extant TF and DNA sequences, makes it incredibly unlikely that phylogenies constructed from orthologoues of each will end up exhibiting similar branching patterns.
    So there is sequence-constraint on both. But this relationship between them doesn’t dictate that if you change the sequence of the DNA in a particular way, that the changes to the sequence of the associated TF must be changed in a way that gives a phylogeny constructed from it a similar branching order to the DNA. The constraint is in the direction of whether the TF will function. It is not in the direction of what kind of branching pattern a likelihood or parsimony algorithm makes. So on this fact alone, the suggestion you make doesn’t rescue a “design-plan” rationalization from the “twin nested hiearchy”.

    Second. Even if there were such associations that are constrained to yield similar branching patterns. And to be clear, there are and the most obvious example is RNA-based transcription factors that bind complementarily to DNA, you wouldn’t compare the RNA TF to the DNA it binds, as they are directly complementary. We can simply detect such associations and avoid using them when inferring phylogenetic relationships. In other words, we just have to think about what data sets to use and pick the independent ones.
    To pick an example, we can compare trees from genes that are demonstrably independent in their sequences, like two enzymes in some metabolic pathway. The gene-sequence of enzyme 1 does not cause, nor is it caused, by the gene sequence in enzyme 8, in some long pathway. These two enzymes are constrained by the function they have, not by the order of amino acids in each other. Or we can just compare the RNA based transcription factor tree, to a tree derived from a locus elsewhere in the genome to which this RNA doesn’t bind. Or we can use SINE insertions, and compare them to enzymes, or to transcription factors and so on and so forth.

    So no, it doesn’t work Bill. The fact that different genes are interdependent doesn’t explain why they should yield similar branching orders. Only if they went through the same genealogical relationship would you expect that.

  24. Rumraket: even if you do that, it doesn’t explain why the trees you get are so similar. This is what you are supposed to explain, and which common descent does explain. Let’s try to cut it into tiny little bits so the logic becomes more obvious.

    To help colewd out a bit, while Rumraket’s argument does eliminate the plausibility of separate creation events, it does allow for guided evolution from common ancestors.

  25. Rumraket,

    We can simply detect such associations and avoid using them when inferring phylogenetic relationships. In other words, we just have to think about what data sets to use and pick the independent ones.

    This is easier said then done. I know you are aware the TFs are not a single protein but a complex set of proteins. So you need to take account of binding to each other not just binding to DNA. Very few proteins in Eukaryotic cells are independent. It is possible to find proteins that don’t interact but with design I still don’t see any reason for the trees not to correlate.

    With inheritance along with random mutations due to cell division I would not expect the trees to correlate. Without mutation they would be the same but with mutation that is random I would expect divergence in the gene trees especially with neutral mutations. I think you demonstrated this because you did not take interdependence into account in your simulation.

  26. colewd:
    Rumraket,

    This is easier said then done.

    Not really, no. It’s actually extremely easy. It is incredibly unlikely that there is mutual sequence-constraint that forces different sequences towards yielding a similar branching order if analyzed by a genetic algorithm. Unless you know there is direct complementary templating going on between the two polymers, the basic condition is that there is no such contraint towards mutually corroborating branching orders. Why would there be? The fact that protein A has to bind to protein B at some portion of it’s surface doesn’t explain why an analysis of a large number of variants of protein A from a collection of species, would yield a tree that is similar to a tree derived from variants of protein B in the same collection of species.

    And it is extremely easy to pick genes that don’t associate with each other in any way. Again, you can just use different enzymes for example. Or different transcription factors that don’t bind each other in any way. Or an enzymes and a transcription factor. Or a TF parking spot and a SINE and an enzyme. Or lysozomal metabolic enzyme and a nuclear protein (meaning they have jobs in different cellular compartments/organelles and therefore never interact with each other directly). There’s absolutely no reason why three such arbitrarily picked entities should constrain each other’s sequence towards yielding similar branching orders.

    I know you are aware the TFs are not a single protein but a complex set of proteins.

    I know that TFs can assemble into larger structures that interact with each other. That would still not even remotely indicate that they are constrained towards yielding a similar branching order if analyzed by a genetic algorithm. At best it just indicates that the binding spots have to be compatible in polarity and 3dimensional structure.

    So you need to take account of binding to each other not just binding to DNA.Very few proteins in Eukaryotic cells are independent.

    That’s actually not true, not that it makes a difference for the reasons explained.

    It is possible to find proteins that don’t interact but with design I still don’t see any reason for the trees not to correlate.

    Of course you see that, because I explained that in the long post to you. And none of your later excuses to try to save your design rationalization are successful.

    With inheritance along with random mutations due to cell division I would not expect the trees to correlate.

    Really? At this stage I wish I knew how to code because it would be trivial to demonstrate that your intuition about this is failing you. It is simply demonstrably incorrect.

    Without mutation they would be the same but with mutation that is random I would expect divergence in the gene trees especially with neutral mutations.

    Why? Seriously, please just think about it.

    I think you demonstrated this because you did not take interdependence into account in your simulation.

    *massages forehead*

  27. colewd,

    With inheritance along with random mutations due to cell division I would not expect the trees to correlate.

    Why not? If you create lineages of photocopies, you get an accumulation of random bits of toner. They get copied to all ‘descendants’. You could generate a tree based upon the sharing of these random blobs among branching lineages. I would expect the tree built on the top halves of such sets of copies to correlate with that built on the bottom half. Likewise quarters, and so on.

    I don’t see why you wouldn’t expect copied genes to correlate likewise.

  28. Allan Miller,

    Why not? If you create lineages of photocopies, you get an accumulation of random bits of toner. They get copied to all ‘descendants’. You could generate a tree based upon the sharing of these random blobs among branching lineages. I would expect the tree built on the top halves of such sets of copies to correlate with that built on the bottom half. Likewise quarters, and so on.

    I don’t see why you wouldn’t expect copied genes to correlate likewise.

    I would expect 100% correlation with no copying errors. If the errors are random I would expect the correlation to break down. If we are comparing 2 genes one error in one gene coming from a random mutation would not likely correlate with a random mutation in the second gene especially in a neutral site.

    The theory says that divergence comes from isolated populations so if the mutations are random and there is a break in inheritance from isolation I would expect almost no correlations in the mutated sites again especially from neutral mutations.

    I think Rum may become famous for validating the common design hypothesis 🙂

  29. Now, just to show that I try to deal fairly with my opponents arguments, I’ll show a flower diagram for E. Coli which I believe is because of common descent. It shows something like an Incomplete Lineage Sort.

    Why doesn’t this apply to the flower diagram of chickens and humans. Chickens and humans aren’t the same species, E. coli is. There is the problem of orphan systems that prevent macro evolution from one kind to another.

    The problem for invoking a Pan Genome for tetrapods is that the ancestor genome then becomes immense, not to mention, E. coli’s pan genome can be supported by HGT, which is not generally as available to Eukaryotes.

    But anyway, before someone lays out the pan genome claim and tries to slap me on the head with it, I’ll put it on the table myself.

  35. Corneel:

    Because the biological species concept doesn’t apply to asexual organisms.

    Hey, I learned something today! Seriously, didn’t know that was a prevailing viewpoint. Thanks. Hugs.

  36. … and E. coli is a hodgepodge

    In the Enterobacteriaceae family of the class Gammaproteobacteria, the species in the genus Shigella (S. dysenteriae, S. flexneri, S. boydii, S. sonnei) from an evolutionary point of view are strains of the species Escherichia coli (polyphyletic), but due to genetic differences cause different medical conditions in the case of the pathogenic strains.[86] Escherichia coli is a badly classified species as some strains share only 20% of their genome. Being so diverse it should be given a higher taxonomic ranking. However, due to the medical conditions associated with the species, it will not be changed to avoid confusion in medical context.

  37. stcordova:
    Now, just to show that I try to deal fairly with my opponents arguments, I’ll show a flower diagram for E. Coli which I believe is because of common descent.It shows something like an Incomplete Lineage Sort.

    Sal, you continually fail to explain what your point is, if you have one. What is different about this diagram than about your vertebrate diagram? What is your interpretation of the reason for these differences? What is the evidence that your interpretation is correct? If the vertebrate diagram shows “orphan systems”, what makes you suppose that the E. coli diagram doesn’t also show them? Why do you think that all the E. coli belong to a single kind?

    Incidentally, nobody has proposed that the original vertebrate genome was enormous except you, due to your misinterpretation of the data.

  38. stcordova: Hey, I learned something today!Seriously, didn’t know that was a prevailing viewpoint.Thanks.Hugs.

    This just shows that you either don’t know what the biological species concept is or you don’t know how to reason. How can an asexual population be “interbreeding or potentially interbreeding”?

  39. There is something about that diagram, E. Coli that is. How many genes beyond the core were evolved additions within E. Coli, not HGT additions? If anything this looks like a reductive process of creating strains from an ancestral pan genome.

    That is, any given strain looks like it descended from an ancestor that had the pan genome. If many of those gene in the diagram that aren’t in the core, but are found in other bacterial lines (like Salmonella), well, that would only strengthen the case a reductive process was in play, not a constructive one to account for genes unique only to certain strains.

    On the other hand if some of those genes are true orphans, how did they evolve since there is a combinatoric problem of evolving such novel functionality.

  40. This study suggests the flower diagram is due to gene loss more than creation of novel genes. Some of it is due to HGT. The problem of the evolution of novel proteins remains. So if one thinks the pan-genome rescues evolution, it only rescues the reductive aspects of evolution, it doesn’t say much about constructive processes. If reductive process are the dominant mode of evolution, then how did complexity evolve?

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688493/

    Convergent reductive evolution of obligate intracellular bacteria

    When considering the presence or absence of a COG, we found that facultative host-associated bacteria have 264 COGs less than the free-living bacteria and 615 COGs more than the obligate intracellular bacteria. The differences observed between the different bacterial communities correspond to the COGs lost in relation with the level of host-dependency (mean loss ratio ± sd: 6 ± 11% and 16 ± 17%, Figure ​Figure2).2). Thus, on the first level of dependency (i.e., facultative host-associated lifestyle) bacteria have already lost 264 COGs. To achieve the second level of host-dependency (i.e., obligate intracellular lifestyle) bacteria undergo an additional loss of 615 COGs significantly greater than the previous loss (unpaired Student’s t-test, p < 10-6). Moreover, the number of genes assigned to each COG category decreased in each step of specialization to an intracellular lifestyle (Figure ​(Figure4).4). However, we suspected that gene loss was not random and resulted from a converging evolutionary process.

  41. colewd,

    I would expect 100% correlation with no copying errors.

    With no copying errors, there would be no phylogenetic information. You’d get a series of perfect copies. That’s not what I was talking about. But anyway, there is no correlation between the bits of toner that mark the sheets as you go, but you would still get roughly congruent trees on separate marks.

    If the errors are random I would expect the correlation to break down.

    I don’t quite know what you mean by correlation. There isn’t any between the errors, but there is between the trees built on separate errors, because they’re copied together. If I divide the sheets into quarters, and build a phylogeny on the toner marks in the top left, it would give the same approximate tree as if I built one on one of the other quadrants. Because it’s not correlation between the marks that counts, it’s the way each separate mark gets swept into the same copying lineage once made.

    You do realise that you are effectively arguing that everyone in the entire field of molecular systematics is just plain dumb? There is an explanation for this peculiar mismatch of viewpoints that involves far fewer assumptions that you may like to consider.

  42. Allan Miller,

    You do realise that you are effectively arguing that everyone in the entire field of molecular systematics is just plain dumb? There is an explanation for this peculiar mismatch of viewpoints that involves far fewer assumptions that you may like to consider.

    Fair enough, but make an argument. Please don’t appeal to the masses. When Rum made random changes to his different gene sequences the trees no longer correlated. This is what I would expect from random change. If we are indeed seeing separate species with multi gene sequence correlation my conclusion is the changes are non random a can be attributed to design changes.

  43. colewd,

    Fair enough, but make an argument. Please don’t appeal to the masses.

    I just did, in the statement immediately preceding the paragraph you chose to respond to instead. Care to address it?

  44. stcordova:
    There is something about that diagram, E. Coli that is.How many genes beyond the core were evolved additions within E. Coli, not HGT additions?If anything this looks like a reductive process of creating strains from an ancestral pan genome.

    What is your argument for any of that?

    So if one thinks the pan-genome rescues evolution, it only rescues the reductive aspects of evolution, it doesn’t say much about constructive processes. If reductive process are the dominant mode of evolution, then how did complexity evolve?

    Who thinks the pan-genome rescues evolution? Who thinks reductive processes are the dominant mode of evolution? Why the strawman?

  45. Allan Miller,

    I don’t quite know what you mean by correlation.

    A cause a effect relationship.

    The claim is a nested hierarchy is caused by inheritance yet according to the theory speciation occurs with isolated populations. Once the populations become isolated then random mutation starts to break down correlation and I would expect Rum’s result.

  46. colewd: If we are indeed seeing separate species with multi gene sequence correlation my conclusion is the changes are non random a can be attributed to design changes.

    Because that’s your belief.

    We get that. We just don’t get any evidence for that belief.

    Glen Davidson

  47. colewd: When Rum made random changes to his different gene sequences the trees no longer correlated. This is what I would expect from random change. If we are indeed seeing separate species with multi gene sequence correlation my conclusion is the changes are non random a can be attributed to design changes.

    You are completely missing the point of Rumraket’s exercise. He made random changes in gene sequences without common descent of the sequences. If he had instead made random changes on different branches of the same tree, the trees from those sequences would be identical. Random changes in the context of common descent produce a non-random pattern, which happens to be just the sort of pattern we observe in nature. On the other hand, non-random changes outside the context of common descent produce a completely different sort of pattern, one we don’t observe in nature.

  48. colewd: The claim is a nested hierarchy is caused by inheritance yet according to the theory speciation occurs with isolated populations. Once the populations become isolated then random mutation starts to break down correlation and I would expect Rum’s result.

    That’s so stupid, because the whole point of the nested hierarchy is to break down some correlation (while maintaining much) and at the same time producing new correlations within a divergent clade.

    So it’s how it’s supposed to be, and, as usual, you simply fail to understand.

    Glen Davidson

  49. colewd,

    A cause a effect relationship.

    The claim is a nested hierarchy is caused by inheritance yet according to the theory speciation occurs with isolated populations. Once the populations become isolated then random mutation starts to break down correlation and I would expect Rum’s result.

    I don’t know what you mean by Rum’s result, now. One shouldn’t have to construct your argument from multiple posts.

    There is no correlation between uncorrelated parts of the genome, of course. In the photocopier example, there is no correlation between the marks. If one adds an analogue of speciation *** – takes some of the papers to the photocopier next door – one still has the phylogenetic information, till the entire thing gets covered in toner flecks.

    [*** Yes, I know, photocopying lineages are asexual, before someone pulls me up on this!]

  50. Allan Miller: You do realise that you are effectively arguing that everyone in the entire field of molecular systematics is just plain dumb?

    If the shoe fits …

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