Common Design vs. Common Descent

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

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

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

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

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

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

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

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

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

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

3,738 thoughts on “Common Design vs. Common Descent

  1. colewd:
    Alan Fox,

    If there was descent based on inheritance I would expect genes to be inherited by different classes in a similar manner.From fish we have 2056 genes being inherited by mammals but not birds and 129 being inherited by birds but not mammals.The gene loss in birds is 10% of the total.Where in world did 10% of those genes go?

    How many times do you have to be told? They degraded into non-functionality, and some likely still exist as pseudogenes.

    If you began to read and comprehend competent people, rather than doubling down on denial and incompetent claims by Sal, you might begin to be able to discuss these things in something other than your annoying obtuseness.

    Glen Davidson

  2. colewd:
    Alan Fox,
    If there was descent based on inheritance I would expect genes to be inherited by different classes in a similar manner.

    Why would you expect that? Genes can disappear from lineages analogously to species becoming extinct. If a gene becomes deleterious in a new niche, selection will tend to remove it.

    From fish we have 2056 genes being inherited by mammals but not birds and 129 being inherited by birds but not mammals.The gene loss in birds is 10% of the total. Where in world did 10% of those genes go?

    Whole genome sequencing (previously a pipe-dream, recently becoming a cheap production-line process) has supplied a quantity of data outstripping scientists ability to interpret it. Perhaps Sal would like to chip in and explain how he goes about using the on-line comparison services he uses to produce his analyses.

  3. Alan Fox: I can’t find a version of that full paper that is free access but here is Niklas again in 2013.

    Darn. I didn’t notice it was behind a paywall. Andrew Knoll’s paper is as well. Sorry about that.

  4. Alan Fox,

    Why would you expect that? Genes can disappear from lineages analogously to species becoming extinct. If a gene becomes deleterious in a new niche, selection will tend to remove it.

    You have genes disappearing in one class at 10 times the rate of another. This does not make sense in either guided evolution or evolution by trial and error. You also have fish with 5% more common genes with humans then birds. This is counter to the nested hierarchy claim.

    The pattern looks like the result a gene tool box with a designer making choices;

    I think you are smart to question Sal’s data because it is devastating to the argument for evolution.

  5. Bill,

    Slow down. Show your work.

    Tell us:

    1) what the prediction is;
    2) why you think that common descent makes that prediction;
    3) how the evidence falsifies the prediction; and
    4) how ‘common design’ predicts the data better than common descent.

    Again: show your work. It’s hard for us to replicate your errors. You need to make them explicit by showing the steps in your reasoning.

  6. colewd: If there was descent based on inheritance I would expect genes to be inherited by different classes in a similar manner.

    And we would expect mutations too. Like deletions and duplications. As demonstrated like ten times now.

    From fish we have 2056 genes being inherited by mammals but not birds and 129 being inherited by birds but not mammals.

    When you write “fish” and “mammals” and “birds”, what you mean is Zebrafish, Human and Mouse, and Chicken, respectively. Those are not the same things, by a long shot.

    The gene loss in birds is 10% of the total. Where in world did 10% of those genes go?

    Those are not gene losses in birds compared to mammals and fish. The venn diagram does not represent the gene-contents of any clades.

    Those 2059 genes not present in chicken, many of them are probably present in birds. And by birds I mean the clade, not a particular taxon.

    Are you going to give even a HINT that you will one day come to understand what that diagram shows?

    There are also 892 genes present in Human, Mouse and Chicken, but not present in Zebrafish. Many of those could very well still exist in the fish CLADE, yet as we get closer to Zebrafish the number of losses will gradually increase.

    Again, gene duplications happen, and so do deletions. They are an observed fact. There isn’t anything going on in that venn diagram that in any way contradicts the nested hiearchy, or realistic rates of gene loss and gain.

  7. colewd:
    Alan Fox,

    You have genes disappearing in one class at 10 times the rate of another.

    Explain how you arrive at this. How do arrive at your calculation of “ten times” and what is ten times what?

    This does not make sense in either guided evolution or evolution by trial and error.

    You need to explain what “this” is and then you need to explain why “this” is evidence against evolutionary theory.

    You also have fish with 5% more common genes with humans then birds.

    Glancing at the zebrafish genome paper, I think you mean “homologous”, rather than “common”.

    This is counter to the nested hierarchy claim.

    So far, molecular phylogeny has largely confirmed earlier categorisations based only on morphology. Are the authors of the paper worried about their results? Seems not. They write;

    A core group of 10,660 genes is found in all four species and probably approximates an essential set of vertebrate protein-coding genes. This number is somewhat less than the core set of 11,809 vertebrate genes identified previously as being common to three fish genomes (Tetraodon, medaka, zebrafish) and three amniotes (human, mouse, chicken)16, but the discrepancy probably reflects the improved annotation of these genomes that often results in fusing fragmented gene structures. Each taxon has between 2,596 and 3,634 species-specific genes. The notable excess observed in zebrafish may be a consequence of the WGD [whole genome duplication*], because pairs of duplicated genes that arose from the WGD, but with no orthologue in amniotes, are counted as two specific genes. Furthermore, 2,059 genes are found in human, mouse and zebrafish but not in chicken, and this number is two times higher than the number of genes that are found in all amniotes but not in zebrafish (892). It is unclear whether these genes have been lost along the evolutionary branch leading to the chicken, or whether this is due to annotation or orthology assignation errors in the chicken genome.

    They allow the possibility of errors in assigning genes in the chicken listing as well as the probability of lost genes. Note too the gene duplication that occurred in the Zebrafish line.

    The pattern looks like the result a gene tool box with a designer making choices

    To you, maybe. The option of an unentailed, immaterial designer is not a persuasive idea to me.

    I think you are smart to question Sal’s data because it is devastating to the argument for evolution.

    Well, it might be. You seem to have forgotten about eyes and trilobites. If you’d rather we explored Sal’s “devastating” sequence comparison instead, that’s fine.

    ETA*

  8. Rumraket,

    Those 2059 genes not present in chicken, many of them are probably present in birds. And by birds I mean the clade, not a particular taxon.

    Why do you think this is true?

    There isn’t anything going on in that venn diagram that in any way contradicts the nested hiearchy, or realistic rates of gene loss and gain.

    Why the massive loss in chickens 2056 and the order of magnitude smaller loss in mice and men? Why greater genetic similarity in Zebra fish then chickens?

    Again, gene duplications happen, and so do deletions. They are an observed fact. There isn’t anything going on in that venn diagram that in any way contradicts the nested hiearchy, or realistic rates of gene loss and gain

    This does not explain the order of magnitude difference between chickens and mice/humans.

  9. colewd,

    Don’t ask Rumraket to do your work for you.

    You made the claims. Support them. Show your work, including the calculations.

    You’re badly misinterpreting Sal’s “flower”. Make your reasoning explicit so we can correct your mistakes.

  10. Alan, to Bill:

    You seem to have forgotten about eyes and trilobites.

    It’s just as well. The trilobite thing wasn’t going to accomplish anything. It would have been one long exercise in presenting evidence and arguments to Bill, which he would repeatedly deem as unsatisfactory.

    The only thing that will satisfy him is Jebus.

    Much better to have him attempting — and failing — to defend his conclusions regarding Sal’s “flower”.

  11. colewd: You have genes disappearing in one class at 10 times the rate of another. This does not make sense in either guided evolution or evolution by trial and error. You also have fish with 5% more common genes with humans then birds. This is counter to the nested hierarchy claim.

    No, not 10 times the rate, just 10 times the time. The chicken has been on a lineage separate from mammals for around 300 million years, while the mammals have been separate from each other for somewhere around 60 million, and the lost genes are distributed onto three branches (human lineage, mouse lineage, and combined mammal lineage). Similarly, you can’t compare the single bird to one of the two mammals, because there are three branches relevant to the mammals but only one relevant to the bird, and that explains why there are more genes uniquely shared between zebrafish and chicken than between zebrafish and human. You don’t understand the figure.

    The pattern looks like the result a gene tool box with a designer making choices;

    Then why do the designer’s choices follow a nested hierarchy so well? And why do the individual gene sequences follow that same hierarchy? I would expect independent insertions of the same gene to have the same sequence. You really haven’t thought this through.

    Nobody questions Sal’s data (it’s not his data, but never mind). It’s Sal’s silly misunderstanding of the data that we’re all questioning. And I think your understanding is even poorer than Sal’s.

  12. Alan Fox,

    Explain how you arrive at this. How do arrive at your calculation of “ten times” and what is ten times what?

    129 Genes move from the zebra fish to the chicken not mouse/human
    2059 Genes move from the zebra fish to the mouse/human but not to chickens this is almost 20x so 10x is conservative.

    So far, molecular phylogeny has largely confirmed earlier categorisations based only on morphology. Are the authors of the paper worried about their results? Seems not. They write;

    The authors don’t need to be worried because common descent is where all data is force fit in evolution. Their not being worried is a big red flag to me.

    They allow the possibility of errors in assigning genes in the chicken listing as well as the probability of lost genes. Note too the gene duplication that occurred in the Zebrafish line.

    This is speculation.

    To you, maybe. The option of an unentailed, immaterial designer is not a persuasive idea to me.

    I know but this is making you blind to evidence based on assuming your conclusion or circular reasoning. You caught the terrible cold from Dawkins 🙂

    Well, it might be. You seem to have forgotten about eyes and trilobites. If you’d rather we explored Sal’s “devastating” sequence comparison instead, that’s fine.

    I have an article I will soon post on this.

  13. 129 Genes move from the zebra fish to the chicken not mouse/human
    2059 Genes move from the zebra fish to the mouse/human but not to chickens

    In Bill’s description, zebrafish are running around promiscuously “moving” their genes to everything with a pulse. They are the sluts of the HGT world.

  14. John Harshman,

    No, not 10 times the rate, just 10 times the time. The chicken has been on a lineage separate from mammals for around 300 million years, while the mammals have been separate from each other for somewhere around 60 million, and the lost genes are distributed onto three branches (human lineage, mouse lineage, and combined mammal lineage). Similarly, you can’t compare the single bird to one of the two mammals, because there are three branches relevant to the mammals but only one relevant to the bird, and that explains why there are more genes uniquely shared between zebrafish and chicken than between zebrafish and human. You don’t understand the figure.

    The lost genes are present in both the human and mice.

    because there are three branches relevant to the mammals but only one relevant to the bird, and that explains why there are more genes uniquely shared between zebrafish and chicken than between zebrafish and human. You don’t understand the figure

    12897 shared genes between humans/mice and zebra fish
    10983 shared genes between chickens and zebra fish

    Not expected from a nested hierarchy. 17% end up more in the two mammals then the bird.

  15. keiths,

    In Bill’s description, zebrafish are running around promiscuously “moving” their genes to everything with a pulse. They are the sluts of the HGT world.

    Looks like they are more aroused by hair then feathers 🙂

  16. Alan Fox,

    Here is a UD article on the eye. We can assume Trilobites utilize the same biochemistry as a working assumption:

    William Bialek: More Perfect Than We Imagined – March 23, 2013
    Excerpt: photoreceptor cells that carpet the retinal tissue of the eye and respond to light, are not just good or great or phabulous at their job. They are not merely exceptionally impressive by the standards of biology, with whatever slop and wiggle room the animate category implies. Photoreceptors operate at the outermost boundary allowed by the laws of physics, which means they are as good as they can be, period. Each one is designed to detect and respond to single photons of light — the smallest possible packages in which light comes wrapped. “Light is quantized, and you can’t count half a photon,” said William Bialek, a professor of physics and integrative genomics at Princeton University. “This is as far as it goes.” … In each instance, biophysicists have calculated, the system couldn’t get faster, more sensitive or more efficient without first relocating to an alternate universe with alternate physical constants. 9

    From the book: Evolution of Visual and Non-visual Pigments, page 106
    Opsin—the protein that underlies all animal vision., has become a favorite research target, not only of vision scientists but of many researchers interested in the evolution of protein structure, function, and specialization. This level of focus has made the opsins canonical G-protein-coupled receptors (GPCRs) and arguably the most investigated protein group for its evolutionary radiations and diverse functional specializations. Still, opsin’s early evolution REMAINS PUZZLING, and there are many questions throughout its evolutionary history for which we have partial, but tantalizingly incomplete, answers. Obviously, the invertebrates, with their astonishing diversity and with evolutionary hints of the most ancient animals in their genomes, functions, and even body plans, offer the best hope of answering many of these fundamental questions.

    Rhodopsins and Cone opsins have two interdependent agents, namely 11 cis retinal chromophores, and opsins, to which they are attached. By absorbing a photon, 11 cis retinal isomerizes to trans retinal conformation, and that triggers a conformational change in opsins, which trigger the signal transduction cascade, which in the end, provokes the electrical signal, transmitted to the brain for processing.

    11-cis-Retinal is a unique molecule with a chemical design that allows optimal interaction with the opsin apoprotein in its binding pocket, and this is essential for the formation of the light-activated conformation of the receptor. 2

    There are many things that are functionally important, and must be JUST RIGHT, in order for these molecular mechanisms to work.

    The fact that rhodopsin has been intensely studied, provides a WEALTH of information on a molecular level, which permits to make INFORMED CONCLUSIONS of its origins.

    Now OBSERVE how many things must be JUST RIGHT and ESSENTIAL ( following is straightforward from the relevant scientific literature ) :

    Rhodopsin Structure and Activation

    Rhodopsin consists of an apoprotein opsin and an inverse agonist ( that’s like a mechanism which keeps a switch off ), the 11-cis-retinal chromophore, which is covalently bound through a Schiff base linkage to the side chain of Lys296 of opsin protein.

    The binding of the chromophore to the opsin is essential to trigger the conformational change. That means, there had to be

    – a Schiff base linkage
    – a Lys296 residue where chromophore retinal covalently binds
    – the side chain of the residue
    – an essential amino acid residue called “counter ion” key factor appears to be the protonation state of the Schiff-base counterion
    – a pivotal role of the covalent bond between the retinal chromophore and the lysine residue at position 296 in the activation pathway of rhodopsin
    – A key feature of this conformational change is a reorganization of water-mediated hydrogen-bond networks between the retinal-binding pocket and three of the most conserved GPCR sequence motifs. 2

    Residues important for stabilizing the tertiary structure

    – (e.g. disulphide bridge (S-S),
    – amino-terminal (N) glycosylation sites)
    – activation/deactivation of photopigments (e.g. carboxyl-terminal (C) phosphorylation sites)
    – membrane anchorage (e.g. palmitoylation sites)

    For visible light absorption, all opsins contain an essential amino acid residue called “counter ion”, in addition to a retinal-binding site, Lys296 (in the bovine rhodopsin numbering system), where chromophore retinal covalently binds through a protonated Schiff base linkage . The proton on the Schiff base is necessary for visible light absorption, but energetically unstable within the opsin molecule. In opsin pigments, a negatively charged amino acid residue, counterion, stabilizes the protonated Schiff base, and is an essential amino acid residue for opsin pigments to absorb visible light.

    Various types of opsin-based pigments with absorption maxima in the visible light region possess a “protonated” Schiff base linkage. In the protein moiety, the positive charge on the protonated Schiff base is unstable, and therefore a counterion, a negatively charged amino acid residue is needed to stabilize the positive charge. In vertebrate visual pigment, glutamic acid at position 113 serves as the counterion 11

    Furthermore: movement of the cytoplasmic end of the sixth transmembrane helix is essential for pigment activation.

    From the above information, it is clear that there is an evidently FINE- TUNED protein-protein interaction, that is, the 11 cis retinal chromophore physical constitution, and the opsin physical constitution, MUST BE JUST RIGHT from the beginning, and be able to interact PRECISELY to trigger the signal transduction chain.

    Let’s suppose, opsin is able to interact with TRANSDUCIN. So what ?? If the signal transduction pathway is not fully setup, and able to go all the way through – no signal – no vision. So having such a precise protein-protein arrangement will make only sense, if down down there, after many complex molecular interactions, a visual image is generated in the brain. After two amplification steps, the goal is achieved, and a signal is sent to the brain. To get that signal, is a REMARKABLE SIGNAL AMPLIFICATION mechanism:

    A single photoactivated rhodopsin catalyzes the activation of 500 transducin molecules. Each transducing can stimulate one cGMP phosphodiesterase molecule and each cGMP phosphodiesterase molecule can break down 1000 molecules of cGMP per second. Therefore, a single activated rhodopsin can cause the hydrolysis of more than 100.000 molecules of cGMP per second.

    Following enzymes, molecules, and proteins are ESSENTIAL in the signal transduction pathway:

    Rhodopsin Rhodopsin is an essential G-protein coupled receptor in phototransduction.
    Retinal Schiff base cofactor All-trans-retinal is also an essential component of type I, or microbial, opsins such as bacteriorhodopsin, channelrhodopsin, and halorhodopsin.
    Transducin Their function is to mediate the signal transduction from the photoreceptor proteins, the opsins, to the effector proteins, the phosphodiesterases 6
    Guanosine diphosphate ( GDP ) Transducin is tightly bound to a small organic molecule called Guanosine diphosphate ( GDP )
    Guanosine triphosphate GTP when it binds to rhodopsin the GDP dissociates itself from transducin and a molecule called GTP, which is closely related to, but critically different from, GDP, binds to transducin.
    G-nucleotide exchange factor (GEF) The exchange of GDP for GTP is done by a G-nucleotide exchange factor (GEF) 7
    Cyclic guanosine monophosphate (cGMP)
    phosphodiesterase (PDE) is necessary to transform cGMP to GMP. This closes the cGMP gated ion channel due to the decreasing amounts of cGMP in the cytoplasm 6
    cGMP-gated channel of rod photoreceptors
    Cyclic nucleotide-gated Na+ ion channels

    Once the signal goes through, a system is required to stop the signal that is generated and restore the opsin to its original state. For that task, other essential proteins are needed to restore the initial state of rhodopsin:

    Guanylate cyclase
    Rhodopsin kinase
    Arrestin

    The biosynthesis of 11 Cis retinal, essential in the first step of vertebrate vision, is also REMARKABLE.

    There is an INTRIGUING EVOLUTIONARY CONSERVATION of the key components involved in chromophore production and recycling, these genes also have adapted to the specific requirements of both insect and vertebrate vision. Visual GPCR signaling is unique with respect to its dependence on a diet-derived chromophore (retinal or 2-dehydro-retinal in vertebrates; retinal and 3-hydroxy-retinal in insects). The chromophore is naturally generated by oxidative cleavage of carotenoids (C40) to retinoids.(C20). Then the retinoid cleavage product must be metabolically converted to the respective 11-cis-retinal derivative in either the same carotenoid cleavage reaction or a separate reaction. 3

    All animals endowed with the ability to detect light through visual pigments need pathways in which dietary precursors for chromophore, such as carotenoids and retinoids, are first absorbed in the gut, and then transported, metabolized and stored within the body to establish and sustain vision.

    Two fundamental processes in chromophore metabolism defied molecular analysis for a long time: the conversion of the parent C40 carotenoid precursor into C20 retinoids and the all-trans to 11-cis isomerization and cleavage involved in continuous chromophore renewal. Following proteins are essential in the pathway to synthesize 11 cis retinals :

    retinal pigment epithelial (RPE) The retinal pigment epithelium (RPE), a single layer of cuboidal cells lying betweenBruch’s membrane and the photoreceptors, is an essential component of the visual system.
    Lecithin-retinol acyltransferase Is Essential for Accumulation of All-trans-Retinyl Esters in the Eye and in the Liver 4
    Retinyl ester hydrolase
    11-cis-retinol dehydrogenases
    Isomerohydrolase It performs the essential enzymatic isomerization step in the synthesis of 11-cis retinal. 5
    Retinoid-binding proteins
    RPE retinal G protein-coupled receptor (RGR)

    The absorption of light by rhodopsin results in the isomerization of the 11- cis -retinal chromophore to all- trans forming the enzymatically active intermediate, metarhodopsin II, which commences the visual transduction process.

    Continuous vision depends on recycling of the photoproduct all-trans-retinal back to visual chromophore 11-cis-retinal. This process is enabled by the visual (retinoid) cycle, a series of biochemical reactions in photoreceptor, adjacent RPE and Müller cells.

    Since the opsins lacking 11-cis-RAL lose light sensitivity, sustained vision requires continuous regeneration of 11-cis-RAL via the process called ‘visual cycle’. Protostomes and vertebrates use essentially different machinery of visual pigment regeneration, and the origin and early evolution of the vertebrate visual cycle is an UNSOLVED MYSTERY.

    Restoration of light sensitivity requires chemical reisomerization of trans-retinal via a multistep enzyme pathway, called the visual cycle, in cells of the retinal pigment epithelium (RPE).

    When a photon of light is absorbed, 11-cis retinal is transformed to all-trans retinal, and it moves to the exit site of rhodopsin. It will not leave the opsin protein until another fresh chromophore comes to replace it, except for in the ABCR pathway. Whilst still bound to the opsin, all-trans retinal is transformed into all-trans retinol by all-trans Retinol Dehydrogenase. It then proceeds to the cell membrane of the rod, where it is chaperoned to the Retinal Pigment Epithelium (RPE) by Interphotoreceptor Retinoid Binding Protein (IRBP). It then enters the RPE cells, and is transferred to the Cellular Retinol Binding Protein (CRBP) chaperone. 8

    The visual cycle fulfills an essential task of maintaining visual function and needs therefore to be adapted to different visual needs such as vision in darkness or lightness. For this, functional aspects come into play: the storage of retinal and the adaption of the reaction speed. Basically vision at low light intensities requires a lower turn-over rate of the visual cycle whereas during light the turn-over rate is much higher. In the transition from darkness to light suddenly, large amount of 11-cis retinal is required. This comes not directly from the visual cycle but from several retinal pools of retinal binding proteins which are connected to each other by the transportation and reaction steps of the visual cycle.

    This cycle is present only in vertebrates, as cephalochordates and tunicates do not possess the required enzymes. The isomerization of 11-cis retinal to all-trans retinal in photoreceptors is the first step in vision. For photoreceptors to function in constant light, the all-trans retinal must be converted back to 11-cis retinal via the enzymatic steps of the visual cycle. Within this cycle, all-trans retinal is reduced to all-trans retinol in photoreceptors and transported to the Retinal pigment epithelium (RPE). In the RPE, all-trans retinol is converted to 11-cis retinol, and in the final enzymatic step, 11-cis retinol is oxidized to 11-cis retinal. The first and last steps of the classical visual cycle are reduction and oxidation reactions, respectively, that utilize retinol dehydrogenase (RDH) enzymes.

    To make things even more intriguing, there are at least 4 different pathways for regeneration of 11 Cis retinal. Protostomes and vertebrates use essentially different machinery of visual pigment regeneration, and the origin and early evolution of the vertebrate visual cycle is an unsolved mystery. In the vertebrate cycle, following proteins are ESSENTIAL :

    Rhodopsin (also known as visual purple) is a light-sensitive receptor protein involved in visual phototransduction.
    Photoreceptor cells are specialized type of cell found in the retina that is capable of visual phototransduction.
    Retinal pigment epithelium (RPE) is the pigmented cell layer just outside the neurosensory retina that nourishes retinal visual cells
    Retinal G-protein-coupled receptor (RGR) is a non-visual opsin expressed in RPE. RGR bound to all-trans-RAL is capable of operating as a photoisomerase that generates 11-cis-RAL in the light-dependent manner
    Interphotoreceptor retinoid-binding protein (IRBP), an abundant 140 kDa glycoprotein secreted by photoreceptors . The binding of retinoids by IRBP protects them from oxidation and isomerization.
    β-Carotene 15,15′-monooxygenase (BCO) in RPE supplies all-trans-RAL to the visual cycle via central cleavage of β-carotene
    Cellular retinaldehyde-binding protein (CRALBP) binds 11-cis-ROL and 11-cis-RAL
    Retinoid isomerase RPE65 (or isomerohydrolase) in the RPE. RPE65 is involved in the all-trans to 11-cis isomerization.

    Retinoids need to be shuttled between different organelles and protected from isomerization, oxidation, and condensation. Thus, key retinoid-binding proteins are critical for maintaining proper retinoid isomeric and oxidation states. Cellular retinaldehyde–binding protein (CRALBP) in the RPE and Müller cells, and extracellular interphotoreceptor retinoid–binding protein (IRBP) are two major carriers involved. The structure of CRALBP—with its unanticipated isomerase activity—has been elucidated, whereas the structure of IRBP has only been partially characterized. Inactivating mutations in either one of these binding proteins can cause retinal degenerative disease.

  17. colewd,

    12897 shared genes between humans/mice and zebra fish
    10983 shared genes between chickens and zebra fish

    Not expected from a nested hierarchy. 17% end up more in the two mammals then the bird.

    Christ, Bill. You’re hopeless.

  18. colewd: The lost genes are present in both the human and mice.

    That makes no sense. Lost genes aren’t present; that’s what “lost” means.

    12897 shared genes between humans/mice and zebra fish
    10983 shared genes between chickens and zebra fish

    Not expected from a nested hierarchy. 17% end up more in the two mammals then the bird.

    Of course it’s expected from a nested hierarchy. What you are saying is that you expect there to be an exactly clocklike schedule of gene loss. There is no reason for that. Evolutionary rates of all sorts vary. Note also that you should also count the genes shared between human and zebrafish and mouse and zebrafish, since those were lost in chickens, and also consider those shared by mouse, chicken, and zebrafish as lost in humans, since the genes lost in chickens have had an extra 60 million years or so of loss compared to those lost in the mammals.

  19. John Harshman,

    Of course it’s expected from a nested hierarchy. What you are saying is that you expect there to be an exactly clocklike schedule of gene loss.

    Except were not comparing gene loss were comparing gene commonality. The data that zebra fish genes are closer to humans/mice then chicken genes to humans/mice violates the nested hierarchy claim.

    The only out is the common ancestor to zebra fish chickens and humans/mice had all the common genes and we are just dealing with loss with an erratic molecular clock. So erratic lost genes can have almost a 20 to 1 variation depending on the branching.

  20. John Harshman,

    Bill: The lost genes are present in both the human and mice.

    John: That makes no sense. Lost genes aren’t present; that’s what “lost” means.

    The genes lost in chickens are present in both humans and mice.

  21. Bill:

    Except were not comparing gene loss were comparing gene commonality. The data that zebra fish genes are closer to humans/mice then chicken genes to humans/mice violates the nested hierarchy claim.

    The only out is the common ancestor to zebra fish chickens and humans/mice had all the common genes and we are just dealing with loss with an erratic molecular clock. So erratic lost genes can have almost a 20 to 1 variation depending on the branching.

    It’s frikkin’ hopeless. Bill is simply incapable of grasping the science.

  22. keiths: 2) why you think that common descent makes that prediction

    Common descent doesn’t predict which genes will be gained. Common descent doesn’t predict which genes will be lost. Common descent doesn’t predict which genes will be shared. Common descent predicts nothing specific.

  23. Mung:

    Common descent doesn’t predict which genes will be gained. Common descent doesn’t predict which genes will be lost. Common descent doesn’t predict which genes will be shared. Common descent predicts nothing specific.

    Derp.

  24. A while back I proposed putting to the test the idea that the nested hierarchy is explained by (common) descent with modification. I’m willing to code an algo that does something like this (simple model of evolution):

    1. Define an initial LUCA sequence
    2. Mutate it at random for a while and then have it split in two branches
    3. Have each branch do (2), and so on
    4. At some point stop the program and publish the leaf (extant) sequences

    If the tree can be recreated by someone who didn’t run the algo, would our local creos be convinced that the nested hierarchy is explained by evolution?

  25. keiths:
    Cue the reflexive response:But if you code an algorithm, that’s Intelligent Design!

    My money is on “but your algo couldn’t evolve an eye”

  26. has supplied a quantity of data outstripping scientists ability to interpret it. Perhaps Sal would like to chip in and explain how he goes about using the on-line comparison services he uses to produce his analyses.

    It has become surprisingly easy now because the governments (US and European) have spent a lot of money on user friendliness and open access. The trick is just getting a couple days training here and there. I was fortunate to get some training at the NIH which serves as hub for a lot of this.

    By law gene sequences that were created by federal funds must be made publicly accessible. Obviously the private databases or databases with sensitive patient information is not available.

    As far as us not being able to interpret the data, that is correct. The is a lot of data that people haven’t figured out what it means. For example, the nylonase project that Dr. Sanford and I worked on is purely a search of publicly available databases and documents. It’s became readily apparent ideas that have existed for 30-40 were just plain wrong in light of a conceptually simple yet rather tedious database and literature search.

    The orphan gene issue and the diagram that Bill Cole and I have talked about is a well-known problem in scientific literature. If you think about it, doing that sort of data synthesis is more of a computational beast than some esoteric exercise.

    All you have to do is download human, chimp, zebrafish, chicken, whatever genome lists. Then just do a computational Venn Diagram. The trick is just navigating some of the not-so-well documented procedures for download.

    I have to credit Paul Nelson with his work on Orphan Genes. He was so adept at it that evolutionary biologists have published a work he co-authored with Richard Buggs. I extended Paul Nelson’s ideas to the phrase “Orphan Systems” or “Orphan Features.”

    https://www.researchgate.net/publication/304039133_Next-generation_apomorphy_the_ubiquity_of_taxonomically_restricted_genes?ev=prf_high

    Buggs also created a flower diagram in his specialty and published it in the prestigious scientific journal Nature.

    http://www.nature.com/nature/journal/v541/n7636/fig_tab/nature20786_F1.html

  27. colewd: Except were not comparing gene loss were comparing gene commonality. The data that zebra fish genes are closer to humans/mice then chicken genes to humans/mice violates the nested hierarchy claim.

    No it doesn’t. Can you explain why you think it does?

    The only out is the common ancestor to zebra fish chickens and humans/mice had all the common genes and we are just dealing with loss with an erratic molecular clock. So erratic lost genes can have almost a 20 to 1 variation depending on the branching.

    Ah, so we are talking about gene loss. Now, it does appear that there has been more gene loss in the chicken (=diapsid) lineage than in the mammal (=synapsid) lineage, and that’s quite an interesting question for further research. But it doesn’t violate any nested hierarchy. It might have something to do with the reduction in size of the dinosaur genome, previously well recognized in the literature.

  28. stcordova: The orphan gene issue and the diagram that Bill Cole and I have talked about is a well-known problem in scientific literature.

    Do you have a reference or two. I used a few combinations of keywords but didn’t find anything on a Google search.

  29. stcordova: All you have to do is download human, chimp, zebrafish, chicken, whatever genome lists. Then just do a computational Venn Diagram. The trick is just navigating some of the not-so-well documented procedures for download.

    At the BLAST site?

    ETA I see there has been a more recent sequencing of the chicken genome.
    Here! I guess this wasn’t used in the zebrafish paper. I wonder if the result would change.

  30. Yesterday I debunked DNA_Jock’s bizarre “You think we’re closet IDers!” claim. I also showed why some comments he proffered as evidence against my argument are actually perfectly compatible with it. Third, I corrected his misconstrual of the main ID argument.

    I’ll now move on to some other comments of his. Given his ill-advised flounce, I’ll refer to him in the third person for now. Of course he is welcome to be brave, deflounce, and re-engage the argument at any time. If that happens I’ll resume addressing him directly.

    In the meantime, let me point out a confusion of his that may explain the second error I mentioned above.

    DNA_Jock wrote:

    I have understood your argument from the get-go.
    You are arguing that, because there are many more ways for guided evolution to NOT produce an ONH than to produce an ONH, that therefore the ONH is evidence in favor of strictly unguided evolution, and that anyone who thinks that the ONH is compatible with (partially) guided evolution is making unwarranted assumptions about the goals, abilities, and preferred mode of operation of the guider.

    That’s not right. The problem lies here:

    …and that anyone who thinks that the ONH is compatible with (partially) guided evolution is making unwarranted assumptions about the goals, abilities, and preferred mode of operation of the guider.

    The ONH is compatible with guided evolution, in that the two aren’t mutually exclusive. My position is quite different. I hold that guided evolution doesn’t predict the ONH.

    Hence my disagreement with John’s statement…

    Guided evolution predicts a nested hierarchy as long as it occurs within a context of common descent.

    …and with DNA_Jock’s echo of it:

    …if this guiding occurs within the context of common descent, then we would expect it to produce an ONH.

    The interesting thing about Jock’s mistake is that it may explain his earlier error. If he thought I was arguing that the ONH couldn’t be reconciled with guided evolution, then it makes sense that he would look for cases in which guided evolution does produce an ONH, and then present them as a refutation.

    Unfortunately for him, they aren’t.

  31. keiths: I hold that guided evolution doesn’t predict the ONH.

    What do you mean by “guided”? Evolution is guided by the niche. If God created the universe, he created the niches. Such guidance produces a nested hierarchy.

  32. Keiths previously:

    We are using ‘guided evolution’ to refer to evolution that is guided by an intelligent agent.

    And this qualification makes what difference, exactly?

  33. Alan,

    And this qualification makes what difference, exactly?

    It maintains a useful and desired distinction, while your suggested usage erases that distinction.

  34. keiths:
    Alan,

    It maintains a useful and desired distinction, while your suggested usage erases that distinction.

    Can your support those assertions?

    Useful to whom?

    Desired by whom?

    What distinction?

    And how so?

  35. keiths,

    Oh, boy.
    keiths,

    I was happy to let you have the last word – it makes you so happy, after all – or “flounce”, as you so kindly put it, but your latest re-writing of history was a bit much .

    Nowhere did I claim that you claimed that the Four Horsemen (JH, DJ, R, and Z) were IDers, closet or otherwise. That was your addition, your failure at reading comprehension. Re-read the thread.
    You responded to JH’s statement by saying “To infer guided evolution from the ONH is as silly as inferring the Rain Fairy from the meteorological evidence” then later stated that you had never claimed that any of the 4H argued we should infer guided evolution. Given the context, yes you did make that claim.
    I was merely making fun of your inconsistency. The joke keeps going over your head. Almost as if you were unwilling to admit error.
    Moving on.
    My apologies for using the phrase “compatible with”; I had forgotten your somewhat esoteric use of this phrase. Try “isn’t compelling evidence against” instead:
    As I wrote earlier (ooo-er! quoting yourself is fun!):

    Yikes, keiths.
    The bit I am refuting is the bit where you state “Nowhere do I claim that John, or Zachriel, or Mikkel, or you have argued that we should infer guided evolution based on the available data”
    You accused me of using a fallacious argument to “support guided evolution”, noting “To infer guided evolution from the ONH is as silly as inferring the Rain Fairy from the meteorological evidence.”
    Why even bring it up? To any sane reader, you appear to be claiming that I am arguing that we should infer guided evolution.
    Now re-read my comment or, preferably, the entire thread. For comprehension.
    My point has always been: the ONH doesn’t support guided evolution, but isn’t compelling evidence against it either. You seem to think that it IS compelling evidence against (partially) guided evolution, and you are wrong.
    And you have completely and utterly failed to address the counter-points from four reality-based commenters here.

    Did I bracket your argument correctly?
    Would you care to try bracketing my argument?

  36. I have understood your argument from the get-go.
    You are arguing that, because there are many more ways for guided evolution to NOT produce an ONH than to produce an ONH, that therefore the ONH is evidence in favor of strictly unguided evolution, and that anyone who thinks that the ONH is compatible with <insert> isn’t compelling evidence against </insert> (partially) guided evolution is making unwarranted assumptions about the goals, abilities, and preferred mode of operation of the guider.

    There you go keiths. Care to return the favor?

  37. dazz: 1. Define an initial LUCA sequence
    2. Mutate it at random for a while and then have it split in two branches

    1.) What is going to decide the mutation rate?
    2.) What will be the basis for branching?

    I don’t think this algo of yours will show what you think it will show.

  38. keiths: Yesterday I debunked DNA_Jock’s bizarre “You think we’re closet IDers!” claim. I also showed why some comments he proffered as evidence against my argument are actually perfectly compatible with it. Third, I corrected his misconstrual of the main ID argument.

    LoL!

    First, you debunked a straw man.

    Second, you missed the point. Of course guided evolution is compatible with a nested hierarchy.

    And last but not least, you misrepresented ID. Go figure.

  39. John Harshman,

    No it doesn’t. Can you explain why you think it does?

    Human/mice are closer to chickens then zebra fish.

    https://evolution.berkeley.edu/evolibrary/images/evo/sixchars_phylo.gif

    I would expect the number of matching common genes to be higher with human/mice and chickens then humans/mice and zebra fish but it is not.

    Ah, so we are talking about gene loss. Now, it does appear that there has been more gene loss in the chicken (=diapsid) lineage than in the mammal (=synapsid) lineage, and that’s quite an interesting question for further research. But it doesn’t violate any nested hierarchy. It might have something to do with the reduction in size of the dinosaur genome, previously well recognized in the literature.

    Gene loss is a possible explanation. What you are explaining why the data does not follow what you expect based on your claim of nested hierarchy as a pattern of inheritance. The real issue is the data is not supporting your hypothesis.

  40. colewd:
    John Harshman,

    Human/mice are closer to chickens then zebra fish.

    What tells us that? Are you willing to accept the genetic evidence for them being closer? The morphologic evidence for them being closer?

    https://evolution.berkeley.edu/evolibrary/images/evo/sixchars_phylo.gif

    Yes, look at that, the evidence shows the nested hierarchy. Any reason why gene loss has to be in lockstep with that? Do gene duplications and reductions of genomes have an effect on the number of genes that survive?

    What about the much closer and much stronger signal of mice and humans? As expected, they share a huge number of genes that zebrafish and chickens lack.

    I would expect the number of matching common genes to be higher with human/mice and chickens then humans/mice and zebra fish but it is not.

    Why are you cherry-picking among the two distant relationships that have relatively few homologous genes? The total difference between 48 and 73, or whatever, isn’t all that much, you know. 25. You’re dealing with numbers that could be affected by a number of factors, or even just randomness.

    Gene loss is a possible explanation.What you are explaining why the data does not follow what you expect based on your claim of nested hierarchy as a pattern of inheritance.The real issue is the data is not supporting your hypothesis.

    The real issue is that you cherry-pick data that certainly needn’t have any absolute correlation with the nested hierarchy as shown by genes and morphology. While it’s not certain why we share fewer with chickens than with zebrafish that aren’t shared with the others, the fact is that they’re both rather distant relations, and the numbers happen to be at levels that can be substantially skewed by gene reductions, gene duplications, selection, and just random chance. You’re hanging onto your prejudices by trying to base them on a very thin cherry-picked number, while you ignore the much stronger and far more robust figure of genes shared by mice and humans and not the other two.

    It really won’t do for you to ignore the many factors affecting quite small numbers of genes, while you simply ignore what you don’t want to pay attention to, the huge number of homologous genes shared by the two mammals and not by the non-mammals–1602. That is the strong signal, not the few numbers of genes shared with humans by the fish and chicken and not by the other two.

    Glen Davidson

  41. Mung: 1.) What is going to decide the mutation rate?

    Low enough that the common descent signal is not lost

    Mung: 2.) What will be the basis for branching?

    I guess branching after a random number mutations should work.

    Mung: I don’t think this algo of yours will show what you think it will show.

    Why not?

  42. I would note, too, that in the diagram the chicken is depicted as having substantially fewer genes than the zebrafish. I didn’t double-check, but I added up 14,623 genes in the chicken, and 16,806 genes in the zebrafish. That in itself would account for some of the skew that Bill hangs onto desperately, but it also suggests the possibility that the chicken may have lost more genes than the zebrafish did, which would skew the difference even more.

    It’s worth noting as well that whatever factors did skew the number of homologous chicken genes shared with humans and not the other two, vs. the number of homologous zebrafish genes shared with humans and not the other two, seems to have affected all of the species on the diagram. The chicken and zebrafish share more genes with each other alone (129) than the chicken shares with humans alone (48) and with the mice alone (43). The mouse has 57 homologous genes with zebrafish alone, and, as noted previously, 43 with chickens alone. There seems to be something that skewed the loss of genes that left zebrafish with more genes homologous with the two mammal species alone than the chicken ended up sharing with the two mammal species alone.

    Anyway, by my calculations, 76.7% of zebrafish genes are “shared” with humans, while 80.0% of chicken genes are “shared” with humans. Going by the diagram’s numbers, of course. Certainly those figures accord well with the genetic and morphologic data showing chickens to be more closely related to us than to the zebrafish.

    Glen Davidson

  43. colewd: Gene loss is a possible explanation. What you are explaining why the data does not follow what you expect based on your claim of nested hierarchy as a pattern of inheritance. The real issue is the data is not supporting your hypothesis.

    That isn’t true. You are demanding an auxiliary and unnecessary hypothesis of clocklike gene loss, which is not connected to the common descent hypothesis. The data don’t support the auxiliary hypothesis, which nobody has advanced, but they do support the main hypothesis of common descent.

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