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BA77 and a vid on FOXP “1/2/3” molecular trees vs Dawkins’ claim of “You get the same family tree”

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BA77 often posts clips of citations and links here at UD. After a recent noticeable break (we missed you), he has just [–> correction: he posted in a thread some time ago which just got a comment from TJG . . . ]  posted a link to a video on objections to prof Dawkins’ claims that FOXP 2 (let me be exact) etc trees give the same structure:

[youtube IfFZ8lCn5uU]

Key clips include a transcript:

dawk_same famtreemolec

Plus, several family trees, such as FOXP1, showing:

foxp1tree

With FOXP2:

foxp2treeFOXP3:

foxp3tree

The three trees seem to be quite divergent, one putting chimps with squirrels and the like, another putting gorillas on a different branch, and only one putting the three on neighbouring twigs.

This seems to be consistent with the objection that molecular trees are both inconsistent with traditional trees and that they are mutually inconsistent.

So, has Mr Dawkins erred, or is this the grand-daddy of all elaborate Creationist quote mines and hoaxes?

If you assert or imply the latter, what is your evidence? END

63 Replies to “BA77 and a vid on FOXP “1/2/3” molecular trees vs Dawkins’ claim of “You get the same family tree”

  1. 1
    kairosfocus says:

    F/N: I here headline BA77’s vid link on objections to prof Dawkins’ reported claims that FOXP 2 (let me be exact) etc trees give the same “family tree” structure. Molecular tree chaos or the grand daddy of all Creationist Quote Mines? Justify your claims. KF

  2. 2
    GaryGaulin says:

    Larry Moran just posted a response that for the most part agrees with the video, by explaining why Richard Dawkins used a bad example:

    http://sandwalk.blogspot.ca/20.....-when.html

  3. 3
    Mung says:

    This seems like a pretty good answer until you realize who you are dealing with. The creationist crowd isn’t interested in the big picture view of evolution and they’re not interested in making allowances for trivial errors. They are more interested in nitpicking about details and showing that evolutionary biologists are wrong about evolution.

    I just love Larry. 🙂

  4. 4
    kairosfocus says:

    Folks,

    It is worth noting the following revealing 2006 remark in the journal, PNAS, by W. Ford Doolittle and Eric Bapteste:

    Darwin claimed that a unique inclusively hierarchical pattern of relationships between all organisms based on their similarities and differences [the Tree of Life (TOL)] was a fact of nature, for which evolution, and in particular a branching process of descent with modification, was the explanation. However, there is no independent evidence that the natural order is an inclusive hierarchy, and incorporation of prokaryotes into the TOL is especially problematic. The only data sets from which we might construct a universal hierarchy including prokaryotes, the sequences of genes, often disagree and can seldom be proven to agree. Hierarchical structure can always be imposed on or extracted from such data sets by algorithms designed to do so, but at its base the universal TOL rests on an unproven assumption about pattern that, given what we know about process, is unlikely to be broadly true. This is not to say that similarities and differences between organisms are not to be accounted for by evolutionary mechanisms, but descent with modification is only one of these mechanisms, and a single tree-like pattern is not the necessary (or expected) result of their collective operation . . . [[Abstract, “Pattern pluralism and the Tree of Life hypothesis,” PNAS February 13, 2007 vol. 104 no. 7 2043-2049.]

    While these researchers do try to suggest a new evolutionary alternative (much as the punctuated equilibria advocates did in the 1970’s), the basic message is plain.

    Namely, the premier icon of macro-evolutionary theory, the tree of life — one long presented in the august name of science as almost indubitable truth — is in serious trouble and is now unlikely to be sound, once the molecular evidence has spoken.

    All of this grand — even, visionary — tree of life picture, then, has always been a sweeping, extrapolated explanatory inference; one long since projected unto a significantly recalcitrant gap-filled fossil record and now even more recalcitrant genetic/molecular evidence.

    KF

    PS: Worse, there are hints that your tree-form results will vary based on how you parse and process the sequences.

  5. 5
    kairosfocus says:

    F/N: Luskin’s critique here will also be helpful.

    I clip, for reference:

    Evolutionists often claim that universal common ancestry and the “tree of life” are established facts. One recent opinion article argued, “The evidence that all life, plants and animals, humans and fruit flies, evolved from a common ancestor by mutation and natural selection is beyond theory. It is a fact. Anyone who takes the time to read the evidence with an open mind will join scientists and the well-educated.”1 The take-home message is that if you doubt Darwin’s tree of life, you’re ignorant. No one wants to be ridiculed, so it’s a lot easier to buy the rhetoric and “join scientists and the well-educated.” . . . . The truth is that common ancestry is merely an assumption that governs interpretation of the data, not an undeniable conclusion, and whenever data contradicts expectations of common descent, evolutionists resort to a variety of different ad hoc rationalizations to save common descent from being falsified.

    Some of these ad hoc rationalizations may appear reasonable — horizontal gene transfer, convergent evolution, differing rates of evolution (rapid evolution is conveniently said to muddy any phylogenetic signal), fusion of genomes — but at the end of the day, we must call them what they are: ad hoc rationalizations designed to save a theory that has already been falsified. Because it is taken as an assumption, evolutionists effectively treat common ancestry in an unfalsifiable and unscientific fashion, where any data that contradicts the expectations of common descent is simply explained away via one of the above ad hoc rationalizations. But if we treat common descent as it ought to be treated — as a testable hypothesis — then it contradicts much data . . . .

    When speaking to the public, evolutionists are infamous for overstating the evidence for universal common ancestry. For example, when speaking before the Texas State Board of Education in January, 2009, University of Texas evolutionist biologist David Hillis cited himself as one of the “world’s leading experts on the tree of life” and later told the Board that there is “overwhelming agreement correspondence as you go from protein to protein, DNA sequence to DNA sequence” when reconstructing evolutionary history using biological molecules. But this is not accurate. Indeed, in the technical scientific literature, one finds a vast swath of scientific papers that have found contradictions, inconsistencies, and flat out failures of the molecular data to provide a clear picture of phylogenetic history and common descent.

    Indeed, the cover story of the journal New Scientist, published on the very day that Dr. Hillis testified, was titled, “Why Darwin was wrong about the tree of life.” Directly contradicting Hillis’ gross oversimplification of molecular systematics, the article reported that “The problem was that different genes told contradictory evolutionary stories.” The article observed that with the sequencing of the genes and proteins of various living organisms, the tree of life fell apart:

    “For a long time the holy grail was to build a tree of life,” says Eric Bapteste, an evolutionary biologist at the Pierre and Marie Curie University in Paris, France. A few years ago it looked as though the grail was within reach. But today the project lies in tatters, torn to pieces by an onslaught of negative evidence. Many biologists now argue that the tree concept is obsolete and needs to be discarded. “We have no evidence at all that the tree of life is a reality,” says Bapteste. That bombshell has even persuaded some that our fundamental view of biology needs to change.2

    Of course, these scientists are all committed evolutionists, which makes their admissions all the more weighty. To reiterate, the basic problem is that one gene or protein yields one version of the “tree of life,” while another gene or protein yields an entirely different tree. As the New Scientist article stated:

    The problems began in the early 1990s when it became possible to sequence actual bacterial and archaeal genes rather than just RNA. Everybody expected these DNA sequences to confirm the RNA tree, and sometimes they did but, crucially, sometimes they did not. RNA, for example, might suggest that species A was more closely related to species B than species C, but a tree made from DNA would suggest the reverse.3

    [–> this looks a lot like what was just highlighted in the OP from a different set of molecules used in evidence, among primates]

    Likewise, leading evolutionary bioinformatics specialist W. Ford Doolittle explains, “Molecular phylogenists will have failed to find the ‘true tree,’ not because their methods are inadequate or because they have chosen the wrong genes, but because the history of life cannot properly be represented as a tree.”4 Hillis (and others) may claim that this problem is only encountered when one tries to reconstruct the evolutionary relationships of microorganisms, such as bacteria, which can swap genes through a process called “horizontal gene transfer,” thereby muddying any phylogenetic signal. But this objection doesn’t hold water because the tree of life is challenged even among higher organisms where such gene-swapping does not take place. As the article explains:

    Syvanen recently compared 2000 genes that are common to humans, frogs, sea squirts, sea urchins, fruit flies and nematodes. In theory, he should have been able to use the gene sequences to construct an evolutionary tree showing the relationships between the six animals. He failed. The problem was that different genes told contradictory evolutionary stories. This was especially true of sea-squirt genes. Conventionally, sea squirts—also known as tunicates—are lumped together with frogs, humans and other vertebrates in the phylum Chordata, but the genes were sending mixed signals. Some genes did indeed cluster within the chordates, but others indicated that tunicates should be placed with sea urchins, which aren’t chordates. “Roughly 50 per cent of its genes have one evolutionary history and 50 per cent another,” Syvanen says.5

    Even among higher organisms, “[t]he problem was that different genes told contradictory evolutionary stories,” leading Syvanen to say, regarding the relationships of these higher groups, “We’ve just annihilated the tree of life.” This directly contradicts Hillis’ claim that there is “overwhelming agreement correspondence as you go from protein to protein, DNA sequence to DNA sequence.”

    Other scientists agree with the conclusions of the New Scientist article. Looking higher up the tree, a recent study published in Science tried to construct a phylogeny of animal relationships but concluded that “[d]espite the amount of data and breadth of taxa analyzed, relationships among most [animal] phyla remained unresolved.”6 Likewise, Carl Woese, a pioneer of evolutionary molecular systematics, observed that these problems extend well beyond the base of the tree of life: “Phylogenetic incongruities [conflicts] can be seen everywhere in the universal tree, from its root to the major branchings within and among the various taxa to the makeup of the primary groupings themselves.”7

    Likewise, National Academy of Sciences biologist Lynn Margulis has had harsh words for the field of molecular systematics, which Hillis studies. In her article, “The Phylogenetic Tree Topples,” she explains that “many biologists claim they know for sure that random mutation (purposeless chance) is the source of inherited variation that generates new species of life and that life evolved in a single-common-trunk, dichotomously branching-phylogenetic-tree pattern!” But she dissents from that view and attacks the dogmatism of evolutionary systematists, noting, “Especially dogmatic are those molecular modelers of the ‘tree of life’ who, ignorant of alternative topologies (such as webs), don’t study ancestors.”8

    In short, there is a serious problem to be addressed on the merits rather than the dismissals.

    KF

  6. 6
    kairosfocus says:

    PS: In response to one of LM’s commenters, I have headlined a comment BA77 made in the context of a fresh remark by TJGuy, and have therefore laid it on the table for serious discussion i/l/o the trend of quote mining accusations and associated projection of claims that are under reasonable doubt as though they were settled. There is an issue there that needs to be faced, whether BA77 commented in 2014 or more recently (as I had initially thought). Mr Spearshake would do better to refrain from outing tactics and accusations.

  7. 7
    GaryGaulin says:

    Then the question is now: what does your well advertised “theory of intelligent design” add to this?

    http://www.zo.utexas.edu/facul.....e/tree.pdf

    More:
    http://www.science20.com/news_.....red-103142

  8. 8
    kairosfocus says:

    GG, looks to me like there may be a question of a little gash down the side of the ship due to an impact with a floating ice mountain. Under such circumstances, other priorities may be advisable. KF

  9. 9
    GaryGaulin says:

    KF, I have good reason to believe that the “theory of intelligent design” can in fact add to what is shown, which is the result of the theory being properly premised to start at the forces powering the “behavior of matter” that causes a trinity of conscious intelligence levels each in our image/likeness to show in a different color or whatever.

    Darwinian theory is premised for a “natural selection” generalization, not the bigger-picture that Alfred Wallace spoke about that has to account for conscious intelligent minds. I can here recommend this video summary:

    http://www.discovery.org/multi.....ered-life/

  10. 10
    vjtorley says:

    Thanks very much for posting the very interesting video linked to by BA77, kairosfocus. It was quite an eye-opener. I notice that Professor Larry Moran stated in his post that “the FOXP2 example was a bad one for many reasons,” but he didn’t say what they were, which is not very helpful.

    Over at the Sandwalk blog, a commenter named Tom Mueller wrote: “FOXP2 is one of several interesting genes that constitute an EXTRAORDINARY EXCEPTION to the rule when expecting the inexorable ticking of some presumed neutral molecular clock – to wit Human accelerated regions (aka HARs).”

    Professor Joe Felsenstein made another point: “Trees from different genes are not all exactly the same. There is noise owing to accidental convergence, reversals, and parallelism. But they do come out very similar, and when you look at many loci in eukaryotes the signal of an underlying evolutionary tree becomes overwhelming. See, for example, Doug Theobald’s papers on formal tests of common ancestry (here, for example).”

    What do readers think of these points?

    By the way: what’s the name of the Website where you can check out these gene trees, and does anyone have a list of the names of all human genes? (Is there such a list?)

  11. 11
    gpuccio says:

    VJ:

    For what it’s worth, I will restate here a few points which I have always sticked to:

    a) The similarities and differences between homologous genes in different species are an argument in favor of Common Descent, not an argument against ID. Indeed, they are usually a very good argument in favor of ID, because the similarities allow to quantify in some way the functional constraints of proteins.

    b) As an argument for Common Descent, those similarities and differences are in general a very good argument. I agree with our neo darwinian interlocutors that the evidence for Common Descent is very strong (maybe not “overwhelming”, but very strong). That’s why I have always accepted CD as the best explanation for those observations.

    c) I am not an expert (or fan) of trees and nested hierarchies. However, as far as I can understand, the existence of different trees from different genes is not a strong argument against CD, even if it deserves attention. I believe that Joe Felsensteins thoughts, as reported by you, are essentially correct in that regard.

    d) Tom Mueller’s objection is definitely more interesting. I have always argued that differences in homologous genes are probably of two different kinds:

    d1) Differences due to neutral evolution: these are the differences which can be used to build molecular clocks and trees, with some hope of success. They can also help us understand how much of a protein is functionally constrained by purifying selection, which is a basic point for ID theory.

    d2) Differences due to different functional constraints in different species: IOWs, those differences which represent optimizations of the protein in different contexts. Here we have an opposite perspective: the diffferences are evidence of functional constraints, exactly as the homologies. These differences, if unrecognized, will cause strong anomalies in the building of molecular trees.

    e) As far as I can understand, the second type of differences are vastly underestimated. Many “evolutionists” go on with an attitude which seems to assume that almost all differences are due to neutral evolution. That is, IMO, a big mistake. HAR are a rare exception to that, one of the few cases where the problem has been faced explicitly.

    f) The problem is that it’s not easy to distinguish between the two cases. The only “objective” tool, as far as I can understand, could be the Ka/Ks ratio, which has many problems. However, I believe that this issue deserves better understanding, and not only in relation to HARs. We need to understand how much the differences between homologous proteins are due to functional reasons.That is especially important for regulatory proteins, like transcription factors.

    g) Just to make an example: the cited FOXP 2. In humans, it is a 715 AAs long protein. It is a transcritpion factor, with important high level functions, not exactly well understood. It is absolutely true that it is highly conserved in mammals, and I would say in vertebrates:

    Humans – mouse: Identities: 711/715(99%) Similarities: 713/715(99%) Expect: 0

    Humans – shark: Identities: 632/715(88%) Similarities: 673/715(94%) Expect: 0

    That would already cover a span of about 400 Million Years of “neutral” evolution. And most differences here are due to poli-Q sequences whose length varies in different species.

    The interesting thing is that, in this long and highly conserved proteins, only a short conserved domain is clearly recognized: the DNA binding site, about 70 AAs long. That is often the case in transcription factors: only the DNA binding site represents a clearly recognizable and highly conserved domain, while the rest of the molecule is much less understood.

    Indeed, if we go outside the vertebrates, the protein is much less conserved:

    Humans – Drosophila: The Drosophila protein is shorter, 442 AAs, and only part of it (295 AAs) can be aligned to the human form:

    Identities: 152/295(52%) Similarities: 187/295(63%)
    Expect: 1e-90

    Humans – C. Elegans: The protein is even shorter (262 AAs). This is the best alignment:

    Identities: 102/181(56%) Similarities: 123/181(67%)
    Expect: 2e-53

    OK, 2e-53 is still a strong homology: the protein is certainly in some way the same, and what is most conserved is the DNA binding site, as it always happens with transcription factors.

    But what about the rest of the protein? Are those big differences between humans and C. Elegans just the result of Neutral Evolution? Are those very strong identities in all vertebrates non functional? I really don’t think so.

    The point is: transcription factors are regulatory proteins. While the DNA binding site remain almost the same, because it does more or less the same things, the rest of the molecule changes a lot (or very little) in different species and sets of species, because it probably regulates different things in different ways.

    We understand too little of these problems, and I hope that the growing knowledge about epigenetic regulation of cell differentiation will help.

  12. 12
    kairosfocus says:

    VJT, we should ponder the fate of the Ptolemaic and Copernican epicycles when Brahe then Kepler then Newton came along. KF

  13. 13
    Mung says:

    VJT, this is the site he was using:

    http://www.ensembl.org/index.html

    As far as human genes I found a link to this from the above site:

    FASTA: Homo Sapiens

  14. 14
    GaryGaulin says:

    I found it useful to compile a visual side-by-side comparison of electronically banded chromosomes.

    This is my comparison of Orangutan, Gorilla, Chimp and Human chromosomes that correspond to our number 2 which evidences chromosome fusion speciation, hence chromosomal Adam and Eve who were alive in the period of time before chimps existed and our “split” from a common ancestor is estimated to have occurred. There is a separate comparison for each possible base pair triplet combination, codon to show in the picture. Clicking on the image will greatly enlarge it:
    https://sites.google.com/site/digitalchromosomebanding/home/RevComplimentTripletAbundancesForChr2OrangutanGorillaChimpHuman900Bands150kBasesBrightness20.png

    Brightness adjusted:
    https://sites.google.com/site/digitalchromosomebanding/home/RevComplimentTripletAbundancesForChr2OrangutanGorillaChimpHuman900Bands150kBasesBrightnessAdusted.png

    Source Code:
    https://sites.google.com/site/digitalchromosomebanding/home/Codons.zip

  15. 15
    kairosfocus says:

    VJT,

    it is interesting that it is Dawkins who chose this as his named example and asserted that there were consistent trees across the molecules.

    Crevo headlines comments revealingly about algorithms (which will doubtless be adjusted over time given what is about to be cited), in the context of the Doolittle & Bapteste PNAS paper I cited above:

    Darwin’s “Tree of Life” is a myth. It’s based on circular reasoning. It is a pattern imposed on the data, not a fact emerging from the evidence . . . .

    Homologies, for instance, do not comprise independent evidence for a tree of life: [D & B:] “homologies are more often deduced from trees than trees are from homologies,” they explain. “Thus, explanans melds with explanandum, and neither is tested.” The reasoning is circular. The fossil record and biogeography cannot be used to infer a universal tree except by extrapolation of limited evidence from “specific groups, areas, or times.” No evidence, in short, produces a tree pattern necessarily; biologists should be open to other patterns, like networks.

    Growing realizations that lateral gene transfer (LGT) is rampant in biology, at least among the prokaryotes, render the discernment of a tree pattern impossible. One cannot draw a tree out of a scrambled egg. Is it justifiable to infer a tree when only 5% or less of the data conform to the expected pattern? Some evolutionists have tried to dispute the extent of LGT, but commit another circular argument in doing so. Doolittle and Bapteste explain: “to make ‘vertical descent’ the null hypothesis against which claims for LGT must be tested is to assume that which is to be proved: that an inclusive hierarchy exists independently of our beliefs.” In addition, the authors complain that a “phylogenetic signal” in the genetic data is often weak at best. Despite what students have been led to believe, “there is no strong expectation that a universal hierarchy that embraces all life should be produced with molecular markers.” . . . .

    this paper clearly argued that there was no reason inherent from the data that the pattern of relationships we observe must look like a branching tree. It could look like a web, or a network, or something else.2 In fact, some evolutionists have argued for a ring instead of a tree (09/09/2004). The possibility of “pattern pluralism” arising from multiple mechanisms requires that evolutionary biologists rid themselves of the predilection for “tree-thinking.” . . . .

    Carl Woese, the one who reorganized taxonomy into three kingdoms (archaea, bacteria, and eukarya), wrote an article with Nigel Goldenfield in Nature last week that is even more radical.4 They even call it revolutionary. “The emerging picture of microbes as gene-swapping collectives demands a revision of such concepts as organism, species and evolution itself” they said in a Connections article called, “Biology’s next revolution.” . . . .

    The Tree of Life is arguably the central icon of evolution. From the single illustration in Charlie’s book till now, the image of a branching tree from a single root emerging from a primordial soup has been the symbol of evolution. Papers are regularly published with phylogenetic trees. There are whole journals devoted to tree-building. Phylogenists employ elaborate software programs that take genomes and try to decipher the hidden tree within. Is this all for naught? Is it nothing more than playing games, tilting at windmills that don’t fight back and aren’t even aware of you?

    These authors basically said that tree-thinking evolutionists are dreaming. Data don’t build trees, people do! The software programs only succeed in finding a “consensus tree” or “maximum likelihood tree” or “maximum parsimony tree” because that is what biased programmers told them to find (see 07/25/2002). If the program’s job is to find a tree, then find a tree it will. It may have to throw out long-branch attraction (04/30/2005), massage the data to account for molecular clock heterogeneity (05/02/2006), and select between a dozen equally-valid results or whatever, but out pops a tree – whoop-de-doo! The scientist gets a nice graphic to publish in his paper, and everyone is happy except Mother Nature. If you doubt this, look at what they do with evidence in the 06/13/2003 and 04/30/2005 entries.

    CEH should give us sobering pause.

    KF

  16. 16
    GaryGaulin says:

    I have to add that there is another program that goes with it to draw the images, which I’m having trouble finding on the computer I now use after the one I wrote the software with broke down. I’ll see what I can do to recover the files or find a backup somewhere. It will only make the same images already linked to in my previous reply, but I would like to find it.

  17. 17
    GaryGaulin says:

    I found it! Software is now at:

    https://sites.google.com/site/digitalchromosomebanding/home/BandChromosomes.zip

    To make the size of the zip file small enough to upload to Google the software does not include the fasta (.fa) files the program generated DNA files (.DNA) were made from. The .fa files are available in .gz compressed form here:
    ftp://ftp.ncbi.nlm.nih.gov/genomes/

    For example Human chromosome 2 is at:
    ftp://ftp.ncbi.nlm.nih.gov/genomes/Homo_sapiens

    There may be updated assemblies but the software also used:
    Pan_troglodytes.CHIMP2.1.4.68.dna.chromosome.2A.fa
    Pan_troglodytes.CHIMP2.1.4.68.dna.chromosome.2B.fa
    Gorilla_gorilla.gorGor3.1.68.dna.chromosome.2a.fa
    Gorilla_gorilla.gorGor3.1.68.dna.chromosome.2b.fa
    Pongo_abelii.PPYG2.68.dna.chromosome.2a
    Pongo_abelii.PPYG2.68.dna.chromosome.2b

    Into the “DNA” folder: decompress the .fa.gz to a folder you created and named, or use the now empty ones files were once in that are already there.

    The way it works is in the top file list box you select which ChromoType (such as Human or Gorilla) then click on the downloaded .fa file to compile it to a DNA file the program will use. Repeat for all of the chromosomes needed. Human has one. The others have two chromosomes each, a part “A” and “B”.

    After having all the required .DNA files showing up in the middle file list box: select which ChromoTypes to compare together then press the “Create Illustrations” button. The new bitmap will be saved to the “BitMaps” folder.

    The “Codons” directory contains the text files that the earlier linked to software had generated.

    Since the code was written in VB6 and Microsoft no longer supports it there is a small chance you will need something no longer shipped with Windows. If there is a problem then please let me know so I can try to work around it, or where necessary rewrite in the newer VB.Net that replaced VB6.

    There is now a bonobo genome to add to the comparison and other possibilities for this way figuring out what came from what, where when how and why, according to ID. In that case the methodology would be based upon how intelligent systems learn over time, as opposed to selection acting upon this or that approach. A living genetic system then reduces down to sensory, memory (its genome letters that allow reading its mind), confidence (in cells called homeostasis) and motor (protein) force that controls itself and its environment. It’s then clear why the “natural selection” variable and all the “evo” words are only useful in Darwinian theory.

    For cognitive science related work regardless of whether a (multicellular development) human baby or (genetic/molecular development) new species everything “develops” over time, we just have to add a qualifier in front to indicate which intelligence level is being discussed. After this way being as scientifically precise as possible even the word “evolution” is made irrelevant, don’t need it. And the “evo-devo” phrase was created after realizing “development” has to be considered, which caused further bloating of the Darwinian model. It in way creates its own science world that has to link back to the real science world that would now still go on just fine without its metaphors.

  18. 18
    Robert Byers says:

    If molecular data means anything then why not just mean a atomic parts department number for a common blueprint from a creator??
    Its fine with me to have perfect matches for bio itams that are a match.
    If a creator did have a common blueprint with a parts department dna number THEN one would predict likeness in dna relative to likeness in parts.
    Evolutionism is using a line of reasoning that not only denies this option but the better option.
    In fact Darwin had to defeat the piont in his book and possiblt the modern dna scores would cause him distress and not happiness.

    We should have almost perfect dna scores with apes because we look almost alike.
    What else would it be?
    Yet don’t assume the likeness is EVIDENCE SETTLED for common descent.
    Its not evidence for anything but likeness.
    its another presumption that connects the dots. Yet another also connects the dots.
    there is no bio sci evidence for evolution as it never happened.
    Its funny Dawkins embraces this stuff ass his top evidence.
    A other error.

  19. 19
    GaryGaulin says:

    I was able to upload a version that has all the required Fasta files still in it. Each of the .fa files for each ChromoType only needs to be clicked once (then be patient it might take half a minute for the biggest our human 2) to compile to DNA files. It’s 294 megs and after unzipping is a 1.7 gigabyte folder named BandChromosomesFromFastaFiles. The .zip file is then no longer needed and can deleted. Since no files are saved or installed outside of the BandChromosomesFromFastaFiles folder deleting it from your hard drive completely removes everything, including illustrations that were saved to the BitMaps folder so first move any you want to keep to a safe place. A downward pointing arrow should be right above for downloading the .zip file at this link:

    https://drive.google.com/file/d/0ByxeUHZcTIhgazNQcWF0MUJFRnc/view

    I just downloaded and tried it out, works well on at least my Windows 10 machine. This should make it easier for anyone who wants to get started on their own comparison using the newer fasta file assemblies available for download on the internet. There is also a place to write your name so it will display in the credit line at the bottom left of each bitmap you make. Then please make sure to give me a link so I can show them around to others who would be genuinely interested in seeing your work.

    This very visual method for comparing the genetic data of chromosomes does not draw a tree showing what came from what and what “split” from another is not shown.

    Only what we became after long ago going off on our own to become what we now are is shown in the picture. You see what things look like in the year 2016, not what was around when the split occurred.

    Showing what existed at the time of the chromosomal fusion (estimated to have occurred up to around 6 million years ago or so) should lead to what I can best describe as a backtracking of what all the chromosomes learned over time, leading to a morphing where at some point the next thing that happens is the fusion event never happened and there is suddenly a Human “A” and “B” half to our now single chromosome 2. That would require converting the fasta files to new fasta files, then same way compare the banding.

    I expect that at the point in time when the Adam and Eve moment occurs the halves they came from would still not exactly match any of the others shown. A common ancestor would still be further back in time, where at that point what we see is more human looking than chimp. Our common ancestor might even have more smarts than chimps now do, but (not to pick on them) it’s too early to know for sure what went wrong for their lineage. I’m eager to see what bonobos look like, which is at least a step up in social responsibility and civility skills even though all run around naked while thinking about sex all day. The lack of common human sense to run for clothes certainly rules them out as being described by Genesis. It’s in a way funny but according to where the scientific evidence leads that works as an indicator of what our Adam and Eve moment looked like. All of a sudden having 46 chromosome (human) thoughts and a brain that makes the tree of the knowledge of good and evil worth getting kicked out of the more living in trees type Eden that all the other animals are happy with. To us that is a cruel thing to have happen. We even soon enough pave paradise then put up a parking lot, in a way our own worse enemy. But not getting kicked out of that paradise would require us to have been less than we now are, which sets us back to still being an animal happy running around naked all day in a forest like the others.

    Scientific theory that is this much in agreement with Genesis is at least a big improvement over the Darwinian world view, which normally instead ridicules what I consider to be the oldest of origins theory, even though some call it “scripture”. There was not even supposed to an Adam and Eve moment to be found in the scientific evidence.

    What it takes to go even further is to compare chromosomes and other things that do not require a fancy lab or necessarily writing science papers. And where it came from does not matter, so regardless of your possibly not having academic “credentials” all are now scientifically equal. So no matter who you are, have fun trying to make a PhD+ sized dent in science, of your own. At this point we just need more chromosome comparisons that look at biology from the perspective of intelligence, which should not be all that hard for those who are NOT looking at everything from the perspective of “natural selection” that in this case only stops progress. It’s best to not even once mention it, at all.

  20. 20
    Eric Anderson says:

    gpuccio:

    Not necessarily arguing with you at this point, just wanted to get your take and play devil’s advocate for a moment.

    As to this:

    I agree with our neo darwinian interlocutors that the evidence for Common Descent is very strong.

    If similarity is evidence for common descent, then is it not the case that dissimilarity should be evidence against common descent? In other words, why do we get to invoke common descent when we see similarity, but don’t question common descent when we see dissimilarity, even significant dissimilarity?

    I’m not just talking about so-called homologous genes (a definition based essentially on circular reasoning anyway). What about completely different genes? For example, organism A shares a “homologous” gene with organism B. Common descent, we shout! Yet organism B has, say, a dozen completely unique genes from organism A. Do we acknowledge the significant dissimilarity and infer that there is no way a dozen non-homologous genes could have arisen in only organism B, thus casting doubt on the common descent idea? Or do we just ignore the dissimilarities? Do we bring in some other justification, horizontal gene transfer and such, to salvage the common descent story?

    The inference to common descent by looking at similar structures, whether genetic or phenotypic, seems to be so heavily invested with the pre-suppositions of (a) common descent, and (b) only purely natural and material causes allowed, that it begs the question as to whether such similarities actually provide evidence for the presuppositions.

    Unless we are willing to count dissimilarities and discontinuities as evidence against common descent, it seems we should not be saying that similarities constitute evidence that helps prove common descent.

    What really seems to be happening is that if (a) we assume common descent by purely natural causes is the cause of the organisms we see, including A and B, then (b) we can infer that organism A might have a descent relationship with organism B, because we’ve stumbled upon an interesting case of similarity.

  21. 21
    Eric Anderson says:

    gpuccio @11:

    The interesting thing is that, in this long and highly conserved proteins, only a short conserved domain is clearly recognized: the DNA binding site, about 70 AAs long. That is often the case in transcription factors: only the DNA binding site represents a clearly recognizable and highly conserved domain, while the rest of the molecule is much less understood.

    The part I highlighted above is another significant part of the issue. I may be getting cynical, but anytime I hear “poorly understood” or some similar statement with respect to a scientific claim, particularly with respect to evolutionary biology, I can take it to the bank that it means, “not understood at all to the level necessary to draw any rational conclusion,” or, more often, “no-one even has a clue about X.”

    The fact is that no-one has any good knowledge about what it takes to get from organism A to organism B. What we do know is that what it takes is always grossly underestimated by facile, naive evolutionary relationship stories. Casting about the whole of biology to find similarities is, to roughly paraphrase David Berlinski, perhaps more useful for keeping cladists employed than for finding actual answers. 🙂

  22. 22
    Mung says:

    If similarity is evidence for common descent, then is it not the case that dissimilarity should be evidence against common descent? In other words, why do we get to invoke common descent when we see similarity, but don’t question common descent when we see dissimilarity, even significant dissimilarity?

    Personally I don’t follow the logic that says that if you accept that similarities are explicable in terms of common descent that therefore dissimilarities are evidence against common descent.

    I would also say that common descent is what allows us to make sense not just of similarities, but also of dissimilarities.

  23. 23
    Dionisio says:

    GaryGaulin

    Thank you for sharing your interesting software here.
    Seems like an impressive work you’ve done.

  24. 24
    Dionisio says:

    Eric Anderson and gpuccio
    Your insightful comments confirm my enormous ignorance.
    Is the below referenced paper somehow related to your interesting discussion? Maybe not.
    Based on that paper, could HFGT+epigenetics+DNA recombination gene exchange+RM+NS+T+…+(anything else someone could think of in the future) eventually help to change the mentioned fish spatiotemporal developmental process into the spatiotemporal developmental process for a different kind of biological system? How? Thank you.

    Further investigations will lead to a more complete understanding of the biological functions of this gene.

    Horizontal functional gene transfer from bacteria to fishes
    Bao-Fa Sun1, 2 n1, Tong Li3 n1, Jin-Hua Xiao1, Ling-Yi Jia1, Li Liu4, Peng Zhang1, Robert W. Murphy5, Shun-Min He1 & Da-Wei Huang
    Scientific Reports 5, Article number: 18676 (2015)
    doi:10.1038/srep18676
    http://www.nature.com/articles.....discussion

  25. 25
    bill cole says:

    Hi VJT
    The opinion I shared with Dr Moran about common decent is that it does not have meaning without an identified cause of change or mechanism. Common decent implies that the change happened in nature. If we can mathematically model these changes then common decent becomes a credible argument. Until then it remains an untested hypothesis. I think the evidence is strong for common biochemistry.

  26. 26
    Eric Anderson says:

    Mung, as I said in 20, if we assume common descent, then similarities seem helpful in putting together the tree of descent.

    But wouldn’t it be a little strange to say that similarities are evidence of common descent (because, the thinking goes, certain characteristics will tend to be preserved), but then to ignore the other side of the coin, namely, if there are lots of dissimilarities, then perhaps we do not have common descent.

    We don’t just get to say common descent will produce similarities . . . except when it doesn’t. I admit, that is a standard approach in evolutionary thinking, but it is unbecoming anyone who is serious about rational thought.

    Furthermore, what most people mean when they say “common descent” is a purely naturalistic and materialistic storyline. And it is a storyline without a realistic mechanism, as bill cole notes @25.

    Obviously some on this site and elsewhere in the Darwinian-skeptical realm take the view that common descent is true, but that some other mechanism, such as front-loading or guided evolution, is in play. Even setting aside for a moment that this desire to conclude common descent is often driven by a philosophical/religious preference, a proposal of some kind of pre-programmed or guided evolution is certainly far preferable to the facile, materialistic evolutionary approach of stuff-happens-and-here-we-are.

    However, it still begs the question. We are still left with all the dissimilarities and discontinuities, the questionable and contradictory trees. We can’t simply ignore them. They are real evidence, just as much as the similarities.

    Common descent may indeed be true (though we would need to tighten up our definitions a lot to determine whether we are talking about limited common descent, universal common descent, or something else), but there is certainly no known mechanism to go from organism A to B to C to Z. Nobody has a clue how to get from A to Z.

    Without a realistic mechanism, without knowing how it could occur, and without evidence that such a thing is even possible in the real world, a conclusion of common descent becomes, at very best, a tentative idea.

    I, for one, am singularly unimpressed with our ability to identify so-called “homologous” characteristics by scouring the realm of nature. Searching for similarities and cataloging and labeling and nesting and drawing trees are interesting exercises, but we must not lead ourselves to believe that they necessarily represent reality.

  27. 27
    bill cole says:

    VJT
    From Joe’s paper cited:

    Thus, a more stringent and rigorous way to test the common ancestry for more than two proteins would be to model the possible relationships among the proteins, which may conflict. It is plausible, then, that the extra INFORMATION IMPARTED BY A PHYLOGENETIC MODEL MAY FAVOR INDEPENDENT ORIGINS OVER COMMON ANCESTRY, even for a set of proteins with low BLAST E-values.

    SO INDEPENDENT ORIGINS A POSSIBLE CONCLUSION….
    DNA data is just part of the story. Must also look a splicing patterns and gene expression for multi cellular species.

  28. 28
    Dionisio says:

    Eric Anderson

    Nobody has a clue how to get from A to Z.

    Well, the situation gets even worse when they try to explain in detail how to get from Z* to B**. 🙂

    (*) Zygote
    (**) Birth

  29. 29
    GaryGaulin says:

    Thanks for the compliment (at #23) Dionisio!

  30. 30
    gpuccio says:

    Eric:

    Thank you for your interesting comments. Discussing CD here is always a little difficult for me, because it seems that I cannot easily explain what I think about the issue. I will try to clarify.

    I have said many times that, IMO, the strongest argument at the molecular level for CD is not the homologies, but the differences.

    My point is: I accept that neutral variation happens, if there is not a strong functional constraint which translates into negative (purifying) selection.

    IOWs, take histone H3, a 136 AAs protein which is practically the same in all eukaryotes: it does not change, except for really trivial differences, throughout something like 1 – 2 billion years (impossible to say exactly when eukaryotes first appeared).

    Is that an argument for CD? Yes and no. It is an argument for a very strong functional conatrint on histone H3, and if we accept CD it is an argument for extremely strong purifying selection on the protein. IOWs, it is an argument for the designed origin of the protein (a sequence of 136 AAs which has to be, in some way, almost exactly that specific sequence has a lot of functional information in it).

    But the fans of common design could simply argue that, exactly because there is such a functional constraint, a designer who redesigns each living species can only use that sequence.

    So, simple strong homology and conservation is not the best argument fro CD.

    Now, tale myoglobin. Human myoglobin is 154 AAs long. Globins are rather “simple” globular proteins, whose 3D structure is rather well conserved even in presence of great differences in sequence.

    Now, if we blast human myoglobin against chimp, we have 153/154 identities (99%), expect 2e-108. IOWs, almost the same sequence. And a few million years of chronological split.

    Let’s go to mouse. Against human, we have 129/154 identities (89%), expect 1e-89. The two proteins are still very similar, but less. And we have 80 – 100 million years of chronological split.

    Let’s go to bony fishes. We have 71/149 identities (48%), with an expect of 6e-37. And a time split of about 400 million years.

    And so on.

    Now, my point is: these molecules are rather similar. They do more or less the same thing in different species. They have similar 3d structure. OK, there could be different functional constraint to explain some of the sequence differences, but… frankly, the best explanation for the growing differences at sequence level between homologue molecules with the same function and 3d structure is simply: neutral variation through time. And indeed, as the time split grows, so grows the sequence difference.

    This is a good argument for CD: not the homologies, but the differences in similar molecules, differences which are proportional to time separation between species.

    OK, this is the first point. I will go on in next post.

  31. 31
    gpuccio says:

    Eric:

    However, if you read carefully my post #11, you will see that I don’t believe that all differences in homologue proteins are due to neutral variation.

    My point is, some of the differences are certainly due to neutral variation, and my example of myoglobin is a good example of the. Those differences are an argument for CD.

    But many other differences are due to different functional constraints in different species. That is the case, IMO, with transcription factors.

    As I have said, usually TFs are made of two different “parts”: at least one DNA binding domain, and the rest of the molecule.

    In general, the DNA binding domain in very conserved. Not so the rest of the protein.

    Does that mean that only the DNA binding domain is functionally constrained? I don’t think so. Usually, the “rest” is the greatest part of the molecule, and often no conserved domains can be recognized there.

    My point is: TFs are regulatory proteins, which act combinatorially to change the transcriptome not only in different species, but also in different cells of the same species. IOWs, they are master actors of the epigenetic landscape.

    So, while the DNA binding site works in similar ways in different species, the “rest” regulates different procedures in different species. That’s why the “rest” changes so much: not because it is not functional and neutral variation acts on it, but because its functions vary from species to species.

    So, restricting function to conserved sequences is a potential error. Different functions require different sequences.

    However, we cannot deny that neutral variation happens: we see it happening even in the human genome, and generating functional polymorphisms, exactly as negative variation generates genetic diseases.

    We know that not all protein sequence have the degree of functional constraints that we see in histones. Myoglobins certainly behave very differently. Some kinds of proteins can be even less constrained.

    So, neutral variation, when it is really neutral variation, tells us that proteins pass from one species to another, and bring with them the neutral differences which have accumulated through time.

    More in next post.

  32. 32
    gpuccio says:

    Eric:

    You say:

    “The fact is that no-one has any good knowledge about what it takes to get from organism A to organism B. What we do know is that what it takes is always grossly underestimated by facile, naive evolutionary relationship stories.”

    I must disagree. I believe that I have a very good knowledge about what it takes “to get from organism A to organism B”: it takes design, the input of new original functional information. And you may probably agree with that.

    The point is: when I say that there is strong evidence for CD, in no way I am saying that CD explains the evolution of species. What I am saying is:

    a) There is CD

    and

    b) New species appear by design, and reuse some previous information by CD.

    IOWs, CD is guided CD, engineered CD. It is like developing Windows 11 by working physically on the code of Windows 10 in a disk which contains that code. IOWs, the designer does not start from scratch to design Windows 11: he takes the code of Windows 10, and changes what has to be changed, writes from scratch what is really new, and keeps what remains more or less the same.

    Now, if there is some minor error in Windows 10, which is not important for the basic work (let’s say a quasi-neutral error), and the designer is not aware of that error, or simply is not really interested in taking the time to correct it, he will “bring” that error into Windows 11. That is evidence of physical descent of Windows 11 from Windows 10. But Windows 11 is a new design, with inertial parts derived from the previous system.

    OK, I will wait for your comments.

  33. 33
    gpuccio says:

    Mung:

    “I would also say that common descent is what allows us to make sense not just of similarities, but also of dissimilarities.”

    I absolutely agree, as I have tried to explain in detail in my last posts. 🙂

  34. 34
    Mung says:

    Windows 11, like the humanatee, is a mythical creature.

  35. 35
    Eric Anderson says:

    gpuccio:

    I have said many times that, IMO, the strongest argument at the molecular level for CD is not the homologies, but the differences.

    OK, but if I read the rest of your first post correctly, you are talking about differences within a similar structure, correct? In other words, what we might call “small differences in a similarity,” rather than stark differences. I was more focused on the latter, but let’s see where else we agree . . .

    My point is: I accept that neutral variation happens, if there is not a strong functional constraint which translates into negative (purifying) selection.

    Agreed.

    So, simple strong homology and conservation is not the best argument [for] CD.

    Agreed.

    [Talking about various splits in time between humans and other organisms] . . . we have [x] million years of chronological split.]

    How is the chronological split determined?

    … frankly, the best explanation for the growing differences at sequence level between homologue molecules with the same function and 3d structure is simply: neutral variation through time. And indeed, as the time split grows, so grows the sequence difference.

    I think that is a reasonable position, if (a) the time split is independently known, at least to a reasonable level, and (b) we are confident that the sequence differences do not meaningfully impact function and are not necessary to the particular organisms in question.

    But many other differences are due to different functional constraints in different species. That is the case, IMO, with transcription factors. . . .

    So, while the DNA binding site works in similar ways in different species, the “rest” regulates different procedures in different species. That’s why the “rest” changes so much: not because it is not functional and neutral variation acts on it, but because its functions vary from species to species.

    I presume you mean “is so different” rather than “changes so much.” Again, the source of the change or whether there has been a “change” is the question at issue. 🙂

    So, restricting function to conserved sequences is a potential error. Different functions require different sequences.

    Absolutely.

    However, we cannot deny that neutral variation happens: we see it happening even in the human genome, and generating functional polymorphisms, exactly as negative variation generates genetic diseases.

    Agreed.

    So, neutral variation, when it is really neutral variation, tells us that proteins pass from one species to another, and bring with them the neutral differences which have accumulated through time.

    I would tend to agree, if (a) we know that variation is actually neutral (probably much less clear in most cases than we might be inclined think), and (b) we assume that there was only one original single sequence. This brings in the whole issue of how we define similarity-by-descent versus independent/convergent origins.

    I must disagree. I believe that I have a very good knowledge about what it takes “to get from organism A to organism B”: it takes design, the input of new original functional information. And you may probably agree with that.

    Of course! 🙂

    What I mean is that we don’t know how to build an organism. We don’t know the details. No-one has any reasonable level of knowledge about how all the various structures work together, or how tweaks to DNA could possibly lead to large-scale changes. Thus, it is simply factually false for a Darwinist to claim that something like random mutations and natural selection can change an organism from A to B. They have no idea, even in principle, whether it is possible.

    The point is: when I say that there is strong evidence for CD, in no way I am saying that CD explains the evolution of species. What I am saying is:

    a) There is CD

    and

    b) New species appear by design, and reuse some previous information by CD.

    IOWs, CD is guided CD, engineered CD.

    I would say that is certainly a reasonable position to take. And is far stronger than the purely naturalistic story.

    —–

    I think you have some reasonable and well-considered thoughts on the topic. You’ve probably followed some of the issues around common descent more closely than I, but to the extent I’ve looked into them, I think we are largely on the same page.

    If you’ll permit me, I just wanted to clarify my earlier comment about dissimilarities. We can look at it from a high-level perspective as follows:

    Organism A and organism B share a similar structure, say, a similar gene, based on genetic sequence. We look at this and conclude that there is a descent relationship between A and B (or, from a common ancestor). Yet at the same time, A and B have a number of unique genes, say, a dozen of them. What do we make of that?

    If a similar gene counts as evidence for a descent relationship, then unique genes suggest something else entirely. I can’t just say that a similar gene in organism B came from organism A (explained by the alleged descent relationship) and at the same time ignore the many more genes that don’t have similarities in organism A. After all, where did they come from? From the same descent relationship? Obviously not. Unfortunately, if an answer is given it is usually some vague claim about horizontal gene transfer and the like. More often than not, the point is simply ignored.

    Yet it is precisely the differences that evolution is supposed to be able to explain. Similarities from generation to generation are not a smoking gun for evolution. As you well point out, we can explain small differences in the same gene by neutral variation. It is precisely the claim of novelty, the claim of ability to generate new, specified, functional structures that lies at the heart of evolutionary theory – at least the grand claims of the theory. So we might be able to explain a few tweaks in the same gene accumulating by neutral variation over time, but where did all the unique new stuff come from?

    You have proposed an answer in the claim of design – if not a completely satisfactory answer, at least a rational one. The materialist creation story has no rational answer.

    (Two further points to follow.)

  36. 36
    Eric Anderson says:

    #2:

    Homology has an extremely poor track record as a tool for determining common descent. It is essentially a circular definition with as many exceptions as rules, is fraught with subjectivity, and is salvaged only with a host of ad hoc rationalizations, such as convergent evolution and the like.

    Personally, I am very unimpressed with a tool that claims similar structures point to common descent . . .

    Except when they don’t.

    Thus, given that everyone seems to recognize that similar structures might be due to common descent but might not, when presented with a similarity between organisms that is supposed to demonstrate some common descent relationship, I feel perfectly comfortable asking, “Perhaps. But what if it doesn’t?”

    This is not to say that we just throw the whole enterprise out the door. Some interesting facts can be collected, some interesting similarities can be noted, we might even learn some biology in the process. But as a general matter, I think we have to view the collection, cataloging, and relationship-tree-drawing exercise as highly tentative and subject to massive error bars.

  37. 37
    Eric Anderson says:

    #3:

    You mentioned getting from organism A to B is a matter of common descent and design. I wanted to push on the design aspect, if perhaps just definitionally.

    Specifically, when we look at designed systems, we can find many similarities across systems of the same domain (transportation, for example), but that does not necessarily mean there is a descent relationship. For example, compare the wheels on my car and the wheels on the Space Shuttle. Lots of similarities.

    We could argue that there is a descent relationship. We could analyze various characteristics and come up with a tree. We could create nested hierarchies to show where my wheel and the Space Shuttle wheel each lie in the tree. We could call them part of a family. We could make claims about one giving rise to the other or about some common wheel giving rise to both.

    But it would all be nothing more than an analogy, a creative description, a made-up tree and a made-up hierarchy and a made-up story of descent. Because design does not work that way.

    Design is not, fundamentally, a process of descent from A to B to C. Yes, products change over time, but they do so not on the basis of some natural process. Design works by understanding the field, being aware of and analyzing various options, considering prior systems, applying principles, re-using parts or approaches, and so on. A new design might bear striking similarity to something that came before. Or it might scrap everything and start all over with a wildly different approach. That is how design works. It is an intellectual, creative effort. Any attempt to create a genealogy or a tree or a nested hierarchy is just a matter of descriptive convenience.

    So . . .

    When you say that organisms came about through common descent plus design, what does that really mean in practice? If, despite the similarities between organism A and B, organism B exists only as a result of additional engineering, including, we must not forget, making sure that even the similarities are properly integrated into the new functional whole – if it requires a substantial re-engineering exercise to get from A to B, then how does that differ from design generally? Does it even make sense to say that there is a descent relationship between A and B?

    Is the only reason to refer to common descent in such a case just to give lip service to the concept? Or are we really talking about regular injections of design tweaks over time? Keeping in mind that the fossil record is largely discontinuous, is the design process one of “slight, successive modifications” or one of larger-scale, discreet creative bursts?

    Asked perhaps another way, do you view the design as being introduced (i) in tiny incremental variations, (ii) in somewhat larger creative events throughout the history of life, or (iii) as front-loading only?

  38. 38
    gpuccio says:

    Eric at #35:

    OK, but if I read the rest of your first post correctly, you are talking about differences within a similar structure, correct?

    Yes.

    In other words, what we might call “small differences in a similarity,” rather than stark differences. I was more focused on the latter, but let’s see where else we agree

    Well, as I have tried to show with the example of myoglobin, we can have rather big differences due to neutral variation. However, I agree with you that big functional differences can only appear by design.

    How is the chronological split determined?

    From known facts about natural history: fossils, reasonable morphological inference, and so on. IOWs, independently from the molecular issue itself. In my reasoning, I have used only very obvious splits: I think we cannot argue about the different times of appearance of mammals and bony fishes, for example. And it seems obvious that single celled eukaryotes like fungi appeared before metazoa. We also know that primates and humans are very recent in natural history.

    So, if I compare mouse and humans, I assume a split of about 80 – 100 million years, because mammals first appeared at that time, while humans only a few millions years ago. So, I compare two different mammals, one of them certainly very recent, and the chronological split between possible common ancestors in mammalian line (which is the assumption we are reasoning about) should be approximately that. I think this kind of reasoning is absolutely acceptable.

    I think that is a reasonable position, if (a) the time split is independently known, at least to a reasonable level,

    I have tried to show that in my reasoning it is independently determined, to a reasonable level.

    (b) we are confident that the sequence differences do not meaningfully impact function and are not necessary to the particular organisms in question.

    That should be reasonably evaluated from case to case. In the case of myoglobin, which is very well studied, it is IMO very reasonable that most of the differences are not functional, even if part of them can be functional. In other cases, it is not so obvious. But again the point is: we certainly have neutral variation, and where we can reasonably recognize it, it points to continuity and CD.

    I presume you mean “is so different” rather than “changes so much.”

    Yes, that’s what I meant.

    I would tend to agree, if (a) we know that variation is actually neutral (probably much less clear in most cases than we might be inclined think),

    OK, I have already discussed that, and I think we agree.

    (b) we assume that there was only one original single sequence. This brings in the whole issue of how we define similarity-by-descent versus independent/convergent origins.

    No, here the point is different: it’s the growing difference in time between similar sequences which points to continuity and CD. I can’t see how you can explain it in other ways. In the case of independent/ convergent origins we would expect convergence towards function in time, but that is not what we observe: function is there from the beginning. Myoglobins are functional. ATP synthase is functional. In all species. And the functional parts are conserved at sequence level (in the case of some chains of ATP synthase, even for billions of years, as I have often debated). Histones are the same in all eukaryotes, which gives us a reasonable time span of at least one billion years.

    One of the great unsupported points of neo darwinian theory is that function gradually increases. That is not what we observe in the general case. We observe highly optimized proteins which often share almost the same sequence between distantly related organisms. And in those sequences, we observe often differences which increase with time, and which seem not to affect the function, which remains essentially similar.

    That’s the correct argument for CD.

    What I mean is that we don’t know how to build an organism. We don’t know the details. No-one has any reasonable level of knowledge about how all the various structures work together, or how tweaks to DNA could possibly lead to large-scale changes. Thus, it is simply factually false for a Darwinist to claim that something like random mutations and natural selection can change an organism from A to B. They have no idea, even in principle, whether it is possible.

    Agreed!

    If a similar gene counts as evidence for a descent relationship, then unique genes suggest something else entirely.

    Yes. New genes with new functions suggest design from scratch. I absolutely agree with that, and with the rest of what you say here.

    But I would add that the assumption of common descent + design allows us to test some interesting possibilities about design procedures in natural history. For example, as I have discussed many times, there are many clues which seem to suggest that, at least in some cases, new functional genes arise from non coding DNA, often by the working of transposone activity. Now, if that is confirmed (and I believe it will be), we can find homologies between the functional sequence in the more recent species (let’s say humans) and the non coding sequence in older species (let’s say primates). If probabilities can well exclude sheer luck, in the light of the CD hypothesis that can mean only one thing: gradual design which prepares a functional sequence in non coding form, and at some point, when it is requested, activates it in coding form. By transposone activity, which is a very good candidate for a consciousness – matter interface at quantum level.

  39. 39
    gpuccio says:

    Eric at #36:

    Homology has an extremely poor track record as a tool for determining common descent. It is essentially a circular definition with as many exceptions as rules, is fraught with subjectivity, and is salvaged only with a host of ad hoc rationalizations, such as convergent evolution and the like.

    OK, but even in the field of darwinian biologists, descent is not usually based on homology alone, rather on homology and differences. For example, at the molecular level the common principle is to compare differences in homologues. I am not saying that there are not inconsistencies. I am not a big fun of trees, either morphological or molecular. However, at the molecular level, definite techniques can be used, with all their limits, for example the Ka/Ks ratio. I agree with you that homology should never be used alone to infer CD. There is also the HGT issue which complicates things!

  40. 40
    gpuccio says:

    Eric at #37:

    Well, I can agree with much of what you say here, but…

    My reasonings are always about molecular data, and molecular data are digital information.

    In digital information, development by continuity is often the rule. That’s why I offered the example of Windows 11.

    In digital information, it is rather easy to distinguish, at the level of the source code, whether a new software was designed independently from an existing one, or if it is simply derived from an existing one. That kind of “design detection” can also be used in legal trials. There are simply a lot of signatures of the precious design which would never have occurred in a new design from scratch.

    Wheels can be redesigned independently, but if you build a new computer with new components, but you reuse the same video card, maybe adding just a couple of new features, the old video card will be easily recognizable.

    Indeed, software design is usually object oriented now. Why? Because that allows to reuse the precious parts of the software more easily, in new contexts and with the minimum quantity of modifications.

    That’s what we usually observe in the biological scenario: reuse of the software, with designed modifications.

    OK, that was certainly a very interesting discussion. I really thank you for your points, and obviously I remain open to new ones! 🙂

  41. 41
    gpuccio says:

    Eric:

    Ah, I forgot to answer your last question!

    “Asked perhaps another way, do you view the design as being introduced (i) in tiny incremental variations, (ii) in somewhat larger creative events throughout the history of life, or (iii) as front-loading only?”

    I don’t believe in front loading. It is a possibility, but I am not aware of any real empiric support to it.

    That said, I believe in active design interventions throughout natural history. Only data and good inferences can distinguish between gradual and rather sudden interventions. I think that what we know at present data support both scenarios, even if the second seems more common.

  42. 42
    bill cole says:

    Hi Eric gpuccio
    Thanks to both you guys for the interesting posts. I think we need to keep in mind that DNA protein sequences are a small part of the genome and that how genes are expressed and how RNA is alternatively spliced may be a bigger part of the story.

    http://www.sciencemag.org
    Science 21 December 2012:
    Vol. 338 no. 6114 pp. 1587-1593 DOI: 10.1126/science.1230612

    From this paper you will see very different alternative splicing sequences among vertebrates which may tell us more about evolution then the DNA sequences.

  43. 43
    gpuccio says:

    bill cole:

    Thank you, and thank you for the very interesting link.

    Of course alternative splicing is a big part of the picture, and so are all epigenetic regulation mechanisms.

    Unfortunately, while much is known of the different final procedures which contribute to those mechanisms, very little is still understood of the general control of those mechanisms. This is a very important field for the application of ID theory, but we really need to understand more. For proteins, at least, we have the sequence data and understand a little (sometimes too little) of the sequence – structure – function relationship.

    Much less is understood of transcriptional regulation, which is the key to everything. For example, regarding alternative splicing, it is still not clear what regulates the different splicing in different situations (even if there are interesting data about a “splicing code” in the paper you linked).

    I think that, when we understand more of the general control of those mechanisms, we will be able to apply a quantitative design detection analysis to the codes and sequences implied. And that will be bad news for the neo-darwinian theory. Again.

  44. 44
    Mung says:

    If you think GA’s are powerful now, just think what they will be able to do once they are programmed to use epigenetic and natural genetic engineering techniques!

  45. 45
    bill cole says:

    gpuccio

    Good points regarding how little is known about transcriptional regulation and alternative splicing codes.

    Do you think this makes trying to form a tree bush etc of life premature?

  46. 46
    drc466 says:

    Gpuccio @38,
    I have a question. You make some good points regarding common descent but I don’t understand why some genes would remain in stasis for 80 – 100 million years while others undergo large changes. For your mouse human comparison to work, you must assume that that particular genetic code is the same in modern mouse as a mouse of 100 million years ago. If the modern mouse has not changed, then all its genetic code should have the same relationship to human genetic code. By pointing to one piece of code and saying look this has not changed in a long time and shows the proper amount of neutral evolution while ignoring other genetic code that has changed a lot and shows much greater variation, are you guilty of cherry picking code to support your common descent assumption?

  47. 47
    drc466 says:

    gpuccio further,

    I’m not expressing my concern very well, so let me try to elaborate further. In order for your mouse-human myoglobin correlation to be valid, you must assume that modern mouse myoglobin is identical to that of a mouse 80-100 million years ago. In other words, that myoglobin is immutable in mice (if not, the % difference between mouse/human myoglobin is…irrelevant).
    But, if we assume that mouse myoglobin is a foundation for, or an evidence of CD for human myoglobin, we must admit that myoglobin can change neutrally – that merely changing myoglobin is not a death warrant for a species.
    This leads us to a logical conclusion that if myoglobin evidences change, then there MUST be a corresponding species change – e.g. a mouse of 50million years ago shared identical myoglobin with modern and 100myo mice, but for a 50myo descendant of mice, myoglobin evidences 50my of neutral change.
    Further, since a single data point doesn’t make a trend, you must make this same argument for any other protein that supposedly shows the same time/change correlation between mice and humans – the mouse version is immutable from 80-100my ago, but the human version evidences 100my of neutral change. How can this be?

    As a logical argument:
    1) Mouse myoglobin is immutable in mice – changes in myoglobin must result in either a species change or evolutionary dead-end. (see above)
    2) Non-mouse myoglobin shows “neutral” changes corresponding to evolutionary time (assertion required for CD)
    3) All similar proteins that are evidence for CD have the same pattern – immutable in original species, but evidencing gradual change in descendants. (logical expansion of 1st two points from myoglobin)
    Forced Logical Conclusion: Descendants of ancient species accumulate neutral changes in synchronization with their change in species – all proteins that evidence CD simultaneously change when, and only when, the species changes.

    True or False? This seems like an incredible stretch to me.

    Further – for myoglobin (and other similar proteins) to be a valid indicator of CD, you should be able to plot the differences of myoglobin over time for ALL mammals and show a direct correlation between change accumulation and time of evolutionary appearance, using a rodent like the mouse as your starting point. Otherwise, mouse/chimp/human simply represent cherry-picked data – in this case, 3 points out of thousands don’t make a trend.

    The logic doesn’t make sense to me – what am I missing?

  48. 48
    Dionisio says:

    gpuccio @43

    Of course alternative splicing is a big part of the picture, and so are all epigenetic regulation mechanisms.

    […] while much is known of the different final procedures which contribute to those mechanisms, very little is still understood of the general control of those mechanisms. […]

    For proteins, at least, we have the sequence data and understand a little (sometimes too little) of the sequence – structure – function relationship.

    Much less is understood of transcriptional regulation, […]

    For example, regarding alternative splicing, it is still not clear what regulates the different splicing in different situations […]

    esattamente eccellente mio caro Dottore!!!

  49. 49
    Dionisio says:

    Eric, bill cole, gpuccio

    When the term ‘code’ is mentioned, can we make any association with the multiple layers of different code that is seen in computers? For example, in a laptop an engineer could enter a code written in some kind of specialized engineering language, which would be understood and translated by an engineering design program in order to adapt its general procedures to the given engineer’s conditions, standards and methods. The engineering design software might have been written in C# linked to some utility libraries written in C++, all compiled/assembled on .NET framework, which runs on Microsoft Windows 10, running on the Intel microprocessor code and the drivers for separate devices. All that still requires an external source of energy to run. But most importantly, it depends on the actions of someone to start it.
    The biological systems might not be comparable to the described computer software, but perhaps some analogies could be made for illustration?
    As gpuccio stated so clearly, in the biological systems we still don’t understand well enough their entire controlling architecture. However, as more data keeps coming at an accelerated pace out of the ongoing research, perhaps more light could be shed on the details in order to have a better idea of the big picture?

  50. 50
    gpuccio says:

    bill cole:

    “Do you think this makes trying to form a tree bush etc of life premature?”

    Probably. And I believe that trees and bushes should always be considered tentative, as should be all scientific inferences. We should always be looking for the best available inference. And just avoid making the worst available inference ! 🙂

  51. 51
    gpuccio says:

    drc466:

    I have not been clear enough. My reasoning about neutral variation is similar to the general reasoning about neutral variation in evolutionary thought, because that is the only part of traditional evolutionary thought that I accept as credible (with the differences that I have tried to highlight in my previous posts.

    Therefore, the reasoning is not that the sequence does not change in one species and changes in the other: that would be unreasonable, as you correctly point out.

    Let’s take the myoglobin example in mouse and humans. We observe similarities, and also differences. The 3d structure and the function are very similar, while the sequence is 89% identical. There are some differences.

    If instead we compare myoglobin in humans and bony fishes, we still have a strong homology, but it is only, at best, 48%.

    Now, let’s say for simplicity that the time split between mice and humans is about 100 million years, while between fishes and humans it is about 400 million years. And let’s say that the “relationship” between differences in that homologue protein and time from the split is consistent in most species (which, for myoglobin, seems to be the case).

    The question is: how so we explain that pattern?

    The best explanation. IMO, is CD (probably, the only credible explanation that I can think of for this particular pattern).

    It goes this way. We assume CD, and we assume that the species we consider shared a common ancestor up to the moment of the split. We also assume, reasonably, that the function and 3d structure of myoglobin do not change significantly in species, and that most differences observed between species are due to neutral variation.
    That means that in the last common ancestor of mouse and human, myoglobin had a certain sequence, which was perfectly compatible with its 3d structure and function.

    In the time from the split, both lines undergo neutral variation at a rate which is more or less “proportional” to time, and retain the same 3d structure and function (with possible slight adaptations).

    So, the difference we observe between mice and humans is the result of neutral variation acting on both evolutionary lines in 100 million years. While the difference we observe between bony fishes and humans is the result of neutral variation acting on both evolutionary lines in 400 million years. Therefore, it is much greater.

    This explanation is good. Can you offer a better one?

    Of course, myoglobin is a good case for this reasoning, because it apparently satisfies the premises: its 3d structure and function do not vary much in time and between species, and the 3d strucutre and function are compatible with big sequence variation (IOWs, myoglobin is a protein which allows big neutral sequence changes).

    Histone H3 is not a good case for our reasoning, because its structure and function do reamin the same, but its sequence also remains the same. As we know that neutral variation happens (when it can happen), the only possible explanation for that is that the molecule is under such functional restraints that purifying (negative) selection keeps it the same. IOWs. it tells us all about similarities, and nothing about differences.

    Transcription factors are not a good case for our reasoning, because they reasonably change their function in different species: they are regulatory proteins, and they have to regulate different things in different contexts. In this case, it is reasonable that most of the differences we observe are due to different functions. However, the DNA binding site in TFs (which is often a minor part of the sequence) usually is much more conserved, because it works in the same way in different species.

    I hope that I have been more clear.

  52. 52
    gpuccio says:

    Dionisio at #49:

    Very good points!

    Let’s try to make an example with what we know.

    a) The classical genetic code allows to write proteins sequences by a strict link between the symbolic sequence of codons in the gene and the sequence of AAs in the protein, which is the main cause of some biochemical activities. So, if I want to change the activity, I can change the coded nucleotide sequence and that will change the protein and its activities.

    b) Histone post translational modifications contribute strongly to determine chromatine status, and therefore transcription (what is usually called the “histone code). Let’s say that we understand well what parts of DNA or else controls different histone modifications, and how the code works. That is not yet completely true, but we know something about those mechanisms.

    So, let’s say that I am an engineer, and that I want to change some transcriptional scenario from species A to species B. I can act at least in two different ways:

    1) I change the sequence of some transcription factor, so that it interacts differently with other transcription factors, and the different combinatorial effect changes what is transcribed. As trasncription factors are proteins, to do that I can simply change appropriately the sequence of my TF, not so much the part which binds DNA (the DNA binding site), but rather the part which interacts with other TFs (the “rest”). To do that, I must change the nucleotide sequence in the coding gene of my TF, so that the modified TF will have a different AA sequence and interact differently with other TFs. IOWs, I write my variation by changing the nucleotide sequence in its gene: I am writing my new code in the language of the classical genetic code.

    2) In alternative, I can change histone modifications in the appropriate situation, so that different chromatin configuration will be active at the appropriate time. To do that, I can act on those parts of the genome which control histone modifications at different times. While we don’t know well what those parts are and how they work, it is reasonable that much of the information is not in the gene coding part, and does not work by coding AA sequences. DNA sequences which act as signals in the non coding part of the genome, for example, could have important roles to “guide” histone modifications in different states. That is already known in part.

    So, if I choose to act in this way, I will change sequences of nucleotides in the appropriate non coding parts of the genome, and I will not use the classical genetic code, which only serves to build proteins, but rather the biochemical code which allows to guide histone modifications by non protein coding DNA sequences, and therefore to achieve modifications of the histone code active at particular times. IOWs, I am using a different language to achieve the same result.

    3) In alternative, I can do both things. That can give me functional redundancy, and allow finer levels of regulation which benefit of the interaction between the two levels. That is what commonly happens in epigenetic regulation, and we already know that it happens: only, the levels are not just two, but many more (just add alternative splicing, microRNA control, long RNAs control and all the other forms of RNA control, DNA methylations, chromatine modifying enzymes, post translational modifications of proteins, regulation of transport between nucleus and cytoplasm, differences in localization, and many others which are all coming out as our understanding grows).

  53. 53
    Dionisio says:

    gpuccio,

    Thank you for the very insightful explanation.

    Here are a few additional questions -which might sound kind of senseless:

    1. Are all the “coding”/”controlling” mechanisms stochastic? IOW, are there any spatiotemporal cases of “coding”/”controlling” mechanisms?

    If there are spatiotemporal “coding”/”controlling” mechanisms, then

    2. what would be the spatial component(s)? Could it be (for example) the location of certain things relative to other things within each given scenario?

    3. what would be the temporal component(s)? Could it be (for example) the timing for certain biochemical/biological events to take place?

    4. What mechanisms of spatiotemporal control could determine the occurrence of certain biochemical/biological events in the right place at the right time?

    Mile grazie! again for taking your time to explain things here.

  54. 54
    Dionisio says:

    gpuccio,

    would it help to open a separate thread for this discussion related to your post @52?

  55. 55
    Dionisio says:

    gpuccio,

    Thank you for the clear explanation you wrote @51.
    BTW, would it be reasonable to associate the last paragraph of your comments @51 (related to TFs) with any of the things you explained @52 and my follow up questions @53?
    Sometimes my visible ignorance makes me ask questions that may not make too much sense (if any). But that’s how I learn some things. 🙂

  56. 56
    gpuccio says:

    Dionisio:

    Thank you for your always careful interest!

    Yes, probably I should collect some of these ideas in a thread. I am thinking about these things almost daily, and always checking the literature for pertinent news (with your precious help, obviously 🙂 ).

    Regarding your questions at #53, this is one of the most interesting aspects which are coming out from recent research. As you know, it seems that many “decisions” about cell fate, especially in stem cells, happen as “events” which are superimposed to some basic oscillating state. That is really very interesting. So, that could really be a basic procedure in cell differentiation: the establishment of oscillations in time and space of important patterns (TFs and other epigenetic components), whose purpose would be to generate a range of possible states from which the cell can “choose” at appropriate times.

    Of course, both the ways that oscillations in time and space are established, and the mechanisms of control and choice, remain vastly unknown. 🙂

  57. 57
    Dionisio says:

    gpuccio @ 56

    […] this is one of the most interesting aspects which are coming out from recent research. As you know, it seems that many “decisions” about cell fate, especially in stem cells, happen as “events” which are superimposed to some basic oscillating state. That is really very interesting. So, that could really be a basic procedure in cell differentiation: the establishment of oscillations in time and space of important patterns (TFs and other epigenetic components), whose purpose would be to generate a range of possible states from which the cell can “choose” at appropriate times.

    Of course, both the ways that oscillations in time and space are established, and the mechanisms of control and choice, remain vastly unknown. 🙂

    Esattamente eccellente mio caro Dottore!

  58. 58
    Eric Anderson says:

    gpuccio:

    I know this thread is getting a little old, but I’m finally getting a few moments to continue our discussion and wanted to offer a couple of additional thoughts for consideration.

    1. There is a logical separation between common descent and design. We know that design can either incorporate prior elements or not, at the decision of the designer.

    2. Building an organism requires significant integrated complexity and functionality. When thinking of common descent we need to consider the whole organism. We can’t follow the naive approach that seems to be taken by some evolutionary proponents of considering each gene as though it were some independent, isolated construct. A gene doesn’t descend from generation to generation in a vacuum.

    Although a gene may change over time, we have to remember that the mental picture we sometimes have of a gene descending through time is essentially a hypothetical construct. The only thing that ever descends is a complete, functional organism, with all its code, parts and functions intact.

    3. If we look at organism A and organism B and note that (a) some gene or other small element is highly similar, and (b) there are a host of other elements that are unique, then, under your proposal, we are looking at significant redesign. But in that case, and considering #1 and #2 above, what sense does it make to say that the small element came about by common descent?

    If there were a piece of code in the latest iPhone that was also in the first iPhone and, before that, even in the iPod, it still wouldn’t make sense to say the latest iPhone came about by common descent from the iPod. Of course not. Rather, we are dealing with a new design, a massive exercise in building integrated functional complexity that took years and hundreds of millions of dollars. Yes, it happens to incorporate an element that was in an earlier entity, but by any rational use of language the latter entity came about through design, not common descent.

    Furthermore, it wouldn’t make sense to say that most of the iPhone came about by design, and a small part came about by common descent. The prior coding element (in our example) was included as part of the new entity and integrated into the functionality of the new entity on purpose, not via some parallel accidental development process.* It would stretch common sense to say that an element was included by accident, but integrated on purpose. Finally, in a situation like this it just confuses things to refer to common descent, particularly when that term typically carries an implication of purely natural and material causes.

    —–

    I’m not saying there is a simple, satisfactory answer to all this. You have provided some interesting and intriguing examples. There might even be some valuable clues to be found. But perhaps we still have no clear answers.

    —–

    * It is possible that a designer might include a piece of old code by accident, but that would be unusual, particularly if the piece of code performs an essential function in the new entity. Most of the cases don’t seem to be of that sort and would not support an accidental-inclusion hypothesis.

  59. 59
    Eric Anderson says:

    Dionosio @49:

    gpuccio has already provided a good response, but just wanted to add a few thoughts.

    When the term ‘code’ is mentioned, can we make any association with the multiple layers of different code that is seen in computers?

    Absolutely. Indeed, one of the unfortunate side effects of all the emphasis for decades on the “genetic code” is that it has really hampered some people’s ability to think clearly about what is required for an integrated, functional system. In hindsight we are starting to see that the Central Dogma of “DNA makes RNA makes protein makes us” is not just incomplete, not just too simplistic, but in very substantive ways is fundamentally misguided.

    Notwithstanding the value of hindsight, it is nevertheless rather embarrassing that it has taken so long for the scientific community in general to catch up to what should have been anticipated and predicted long before, just by thinking through in detail what might be required to build an organism. And I am convinced that a researcher today with the tools and the willingness to look has the opportunity to make many profound discoveries in biology by going through a design exercise beforehand.

    Unfortunately, we still see biological science being dragged down by the simplistic and naive evolutionary baggage of yesteryear, with its creation story focused on happenstance tweaks to DNA, as though nucleotide sequences alone were the be-all-and-end-all of biology.

    Might as well try to build a new server by making random changes to files on the hard drive . . .

    That is not an exaggeration. If anything, it is probably still an underestimation. There are layers upon layers of functional integration and feedbacks and sensors — nearly all of which require coding, not to mention precisely interconnected physical systems. We are barely scratching the surface and will one day look back on the “protein-coding DNA determines the organism” idea as a reflection of an incredibly backward and primitive time in biological science.

    The sooner we shed the “tweak nucleotides and build a new organism” school of thought and start approaching biology with a real eye toward design — including by going through detailed design analysis exercises — the better off the whole of biological science will be.

  60. 60
    Dionisio says:

    Eric Anderson @59

    Thank you for the insightful analysis of such an important aspect of the current state of affairs in scientific research: how to approach the object of study.

    Please, help me with organizing/streamlining/refining/correcting these (overlapping/colliding/redundant/senseless/vague/ambiguous?) thoughts:

    Could we dare to say that -at least in part- the “unfortunate” situation you have pointed at and so concisely described may have to do with our natural human condition that makes us lose the sense of wonder we had (in different degrees) in our childhood?

    Can we say that such a natural loss of our infantile sense of wonder be partially associated with our lack of humility (any chicken-egg dilemma here?), which may lead us to narrow-minded thinking that keeps us from putting everything to test and thinking out of any box others might have established previously?

    Perhaps an additional (and kind of more earthly ‘pragmatic’ and less philosophical) reason for that “embarrassingly” confusing approach seen through the recent history of scientific research is the university undergrad students’ lack of exposure to at least basic courses on math logic, systems theory, set theory, (regardless of what they’re majoring on) that could help them look at certain things from a slightly different perspective?

    Could we risk much by saying that the above situation might explain -at least partially- the cases where outsiders, who in most occasions lack the required deep technical knowledge and expertise, end up noticing and pointing at obvious basic things the experts could not or did not want to see?

    In any case, you have brought up very important points that provide much food for thoughts that could lead to very interesting extensive discussions.

    However, in all this there’s an important caveat: we should ask honest questions -whatever that means according to a distinguished professor from the U. of Toronto who has commented here in this forum. 🙂

  61. 61
    gpuccio says:

    Eric:

    Your comments at #58 are very interesting, and I certainly agree with many of the things that you say.

    Still, I think that the concept of Common Descent has its importance, even if we agree that new species are (maybe mostly) the result of new design.

    Let’s simplify the problem. Let’s say that there is species A, and at some time, a new species, B, appears.

    Let’s say that B has many new features: differences in body plan, new proteins, new networks. And yet, it also reuses many basic biological structures which were already in species A.

    I have also discussed that simple fact that there is strong evidence that events which happen in species A along time, like neutral variation in many of its already existing proteins, are often “inherited” by species B, where the same proteins will again undergo further neutral variation which will be “inherited” by some future species C, and so on. That is, IMO, the best explanation for a significant part of the similarities and differences which we can observe in the proteome.

    OK, Common descent, even in the context of new engineering and design, mean one important thing: there is physical continuity between species. Not only the continuity of the reuse of some software which was written in some non physical world, but rather the reuse of biological software as written in the physical bodies of existing species.

    Let’s simplify again, and suppose that we have a human biological designer who has succeeded in engineering from scratch a new species, maybe even a simple one, let’s say a new form of prokaryote, in his lab. Let’s say that this new species, that we call A, has its new proteins, engineered in the lab, and it is a satisfactory achievement for our biological engineer.

    Now, our engineer plans a further advancement, a new new prokaryote, with even more surprising abilities, which will be, in part, based on what he has already achieved. Let’s call this new project species B.

    Now, even admitting that B will be a new example of original design, there are two different ways for the engineer to bring B into existence:

    a) He designs B from scratch, if necessary by reusing some notes that he has in his lab.

    b) He works on A, transforming it into B by new engineering work.

    The two scenarios have different implications, and are recognizable from the results.

    In a) there is no common descent, only common design.

    In b), there is common descent (physical continuity) and new design.

    My point is that the aspects which I have discussed in my previous posts definitely point to b, and not to a). That’s what I mean when I say that observations in the proteome strongly favor Common Descent.

    I am convinced that there are many patterns which cannot be reasonably explained by the a) scenario. As my only commitment, in this kind of reasoning, is to scientific facts and good inferences from those facts, I remain convinced that CD is at present the best explanation for those patterns. It’s as simple as that.

  62. 62
    Eric Anderson says:

    gpuccio:

    Your example of (a) building from scratch versus (b) transforming into a new engineering work is well stated. Indeed, with anything even semi-complicated, design is typically done as a transformative work, as in (b).

    I think I’m in agreement with you there, and you may well be right that this could account for some of the interesting data. Definitely an approach worth considering.

    I just want to press a little bit, however, on your definitions. You mentioned that in case (b) there is physical continuity. But is there really physical continuity? In what sense?

    If there is meaningful redesign between A and B (which you seem to agree is likely, as opposed to Darwin’s slight, successive modifications), then presumably we aren’t suggesting that — to give a grossly-oversimplified example — a dinosaur gave birth to a bird, thus preserving the physical continuity, as well as the common descent.

    Meaning, we could indeed have a situation in which a designer takes an existing species and significantly modifies it, accounting (as you note) for some of the genetic continuity. But surely we wouldn’t be proposing that there was an actual, physical parent-child relationship between A and B?

    In other words, perhaps we are dealing with continuity of design or continuity of features, rather than what is commonly referred to as “common descent” — a physical, parent-child relationship from A to B.

  63. 63
    gpuccio says:

    Eric:

    OK, I think of physical continuity in the sense that design happens, more or less gradually, or even suddenly, by modifying information in existing species while those species go on reproducing. IOWs, even if design is realized by the input of information, the continuity of reproduction is not interrupted.

    This has many advantages on designing new living beings from non living parts, even if we reuse design features. I think it’s also the way we would act, in modifying living cells: just input the modifications in the existing cells, and then relying on their reproduction.

    And again, the point is that my argument for CD is based on the heredity of neutral variation. Now, the important issue is that neutral variation happens mainly because of random errors in reproduction: it is not part of the original design.

    So, let’s say that the designer design A. Then A lives for a few million years, and in that time some of the proteins in A undergo neutral variation, and some of those modifications survive in the population, or even become fixed by genetic drift. That’s what happens to neutral variation.

    Now, the designer designs B, which is in part similar to A, but has many new features.

    Now, the point is: if the designer rebuild B physically from scratch, even reusing his plans for A, there is no reason why we should observe in B, in the proteins which are common to A, any neutral variation. Why? Because the neutral variation has accumulated in A through time, after the initial design.

    But, if the designer inputs his new information in some member of the A population, and then lets it reproduce, then the neutral variation which was present in that organism will be inherited by the new species.

    And that is exactly what we observe in the proteome, at least IMO.

    By the way, I have posted an OP which is in some way an expansion of our discussion here. I would be happy if you could give it a look:

    http://www.uncommondescent.com.....ion-jumps/

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