Universal Common Descent Dilemma

  1. Despite lack of observational basis, Darwin proposed Universal Common Descent (UCD) saying:Therefore I should infer from analogy that probably all the organic beings which have ever lived on this earth have descended from some one primordial form, into which life was first breathed“. He also said elsewhere (referring to UCD): “…the littlest creature (or four or five of them)…” With his remarks, Darwin left the door open to creation (“life was first breathed”), but since then, Neo-Darwinists have rejected creation and replaced it with belief in undirected abiogenesis while maintaining belief in UCD.
  2. UCD is incompatible with the current view of Earth as just an ordinary planet circling an ordinary star located nowhere special inside an ordinary galaxy. If Earth is “nothing special” and abiogenesis is an ordinary “arising” of life from non-living matter, spontaneous abiogenesis would be a trivial common occurrence here on Earth as well as throughout the Universe, and we would have many “trees of life” instead of one. However, until now, all abiogenesis experiments have failed to produce life, spontaneous generation has been rejected, and the Fermi paradox stands, all these keeping the single “tree of life” and UCD hypothesis still alive and still inexplicable.
  3. Conditions for starting life should be similar to those required for sustaining it. The Big Bang model mandates a beginning of life. Furthermore, once started life must be sustained by the same or very similar environment. And since life is being sustained now on Earth, abiogenesis should be ongoing contrary to all observations to date. Tidal pools, deep sea hydrothermal vents, and the undersurface of ice caps have been hypothesized to originate abiogenesis due to their persistent energy gradients, but no abiogenesis or its intermediate phases have been observed around these sites. Given these, the only methodological naturalistic alternative is ‘limited window of opportunity for abiogenesis which suggests primordial life substantially different than all known forms of life, and perhaps originating on another planet followed by panspermia. However, this alternative defies Occam’s razor and the absence of supporting evidence including the earliest ever known fossils (stromatolites) that are of commonly occurring cyanobacteria rather than of alien origin.
  4. Universal Common Descent requires an inexplicable biologic singularity. All known forms of life are based on the same fundamental biochemical organization, so either abiogenesis happened only once or it happened freely for a while but then it stopped when the ‘window of opportunity’ closed and only one organism survived to become the Last Universal Common Ancestor (LUCA) of all existing life on Earth. However, these two biologic singularities should be unacceptable given the lack of evidence and the assumption of continuity in nature. Furthermore, the second scenario requires two discontinuities: one for the cessation of abiogenesis and the second one for the bottleneck leading to LUCA.
  5. In conclusion, UCD hypothesis leads to a number of bad and very bad scenarios: a) Earth is “nothing special” should lead to a “forest of life” rather than a single “tree of life” and to ubiquitous abiogenesis (unobserved); b) Alien life plus panspermia is refuted by the Fermi paradox and oldest known stromatolites fossils; c) Single event abiogenesis is an unsupported and therefore unacceptable singularity; d) ‘Window of opportunity’ abiogenesis followed by LUCA bottleneck is even less acceptable double-singularity. And this brings us back to Darwin’s “open door” to creation, perhaps the most rational alternative that fits all biologic observations.

Pro-Con Notes

Con: Maybe abiogenesis is happening a lot. I think the already existing life would dispose of it quickly though.

Pro:  if so, 1. We should be able to duplicate abiogenesis in the lab; 2. We should see at least some of the intermediate abiogenesis steps in nature; 3. Existing life can only process what looks like food. Cellulose is a well known organic material that cannot be broken down by a lot of organisms and is known to last as very long time in dry conditions.

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1,101 thoughts on “Universal Common Descent Dilemma

  1. CharlieM: Good question. No I don’t.

    From Goethe […]

    Not sure why I should care what Goethe thinks though? The point was, your very analogy against assuming common descent has within it commonly descended cells.

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  2. Allan Miller: Not sure why I should care what Goethe thinks though?

    It is not so much about what Goethe thought but about what he perceived through thinking.

    The point was, your very analogy against assuming common descent has within it commonly descended cells.

    My analogy was not against common descent in general. It was against assuming that there is a linear descent from alpha proteobacteria to mitochondria.

    We can study life and organisms at many levels. With a buttercup that begins from a seed, a single cell divides and multiplies to form the growing plant. So I would never argue against common descent at this level. But looking at a higher level the leaves along the stem can be seen to form a series due to their similar morphology. But this is not due to linear descent one from the other, it is due to individual expression of a common plan.

    Alpha proteobacteria and mitochondria might be connected by a line of descent or they might equally be connected because they are individual expressions of a common plan. That is what I am saying.

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  3. John Harshman: I agree that the fault lies with you, but in both your analogy and the present case. Your arrogance is not helpful. Some kind of coherent argument would work better, if you are capable of such a thing.

    If he were capable of producing a coherent argument, he would have done so the first few dozen times he was asked. All you’re going to do is make yourself more frustrated if you continue to engage with him. There’s no point in trying to get to some mythical common ground of mutual understanding with people who can’t grasp basic reasoning. That’s why TSZ was doomed to fail from the start.

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  4. CharlieM,

    My analogy was not against common descent in general. It was against assuming that there is a linear descent from alpha proteobacteria to mitochondria.

    And hence fails on its own terms, since you haven’t established that ‘plan’, and not common descent, is responsible for the genetic relationship between parts of a buttercup. Clearly, the cells are commonly descended, so whatever other forces are at work, it’s a poor choice for an attempt to raise an alternative to common descent for the relationship discovered between mitochondria and bacteria. Furthermore, it ignores the hierarchical component of the relationship: where it sits on the tree of all bacteria, which accords with common descent and not hand-wavy ‘plan’. Invoking ‘common plan’ sheds no light on why a group as diverse as the alpha proteobacteria themselves should also include something as different from the rest as the mitochondrion.

    I’ve said it before: your analogies are unhelpful.

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  5. Allan Miller: Clearly, the cells are commonly descended

    If cells can pour their DNA into a pool, and then be incorporated as part of the genome of a totally different cell, how can we ever say “clearly” they are commonly descended?

    This is what you don’t get about the new revelations of genetic science, and why Darwinism is dead.

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  6. Allan Miller:

    CharlieM, My analogy was not against common descent in general. It was against assuming that there is a linear descent from alpha proteobacteria to mitochondria.

    And hence fails on its own terms, since you haven’t established that ‘plan’, and not common descent, is responsible for the genetic relationship between parts of a buttercup. Clearly, the cells are commonly descended, so whatever other forces are at work, it’s a poor choice for an attempt to raise an alternative to common descent for the relationship discovered between mitochondria and bacteria.

    What is the genetic relationship between all parts of a buttercup? It is that all the cell types found throughout the plant contain the same genome, so in what way does this explain the variation? We agree that all the cells are descended from one original cell. But that is an observation not an explanation as to what causes the genes to be expressed differently in the various cells. The “face of a frog” appears in a way reminiscent of iron filings marking out the magnetic field of a bar magnet. This is evidence that there are overarching field forces at work.
    The fact that the cells share a common source cannot be used as evidence for the variation.

    Furthermore, it ignores the hierarchical component of the relationship: where it sits on the tree of all bacteria, which accords with common descent and not hand-wavy ‘plan’. Invoking ‘common plan’ sheds no light on why a group as diverse as the alpha proteobacteria themselves should also include something as different from the rest as the mitochondrion..

    And exactly how is it determined where mitochondria sit on the tree of all bacteria? How do you know what is vertical descent and what is shared by horizontal gene transfer?

    I’ve said it before: your analogies are unhelpful.

    I would say they are at least helpful in that they have stimulated you to think about these things even if in the end you do reject them.

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  7. phoodoo to Allan Miller: If cells can pour their DNA into a pool, and then be incorporated as part of the genome of a totally different cell, how can we ever say “clearly” they are commonly descended?

    This is what you don’t get about the new revelations of genetic science, and why Darwinism is dead.

    Good point. Although division by binary fission means that both daughter cells are equal products of the parent

    What is it that is handed down through the generations of cells in the growth of a buttercup? It cannot be the material as the mature buttercup has much more material than the original cell. If it is the information in the form of the genetic code, why are the offspring not all clones. And genetic recombination cannot be the answer.

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  8. Kantian Naturalist: There’s no point in trying to get to some mythical common ground of mutual understanding with people who can’t grasp basic reasoning. That’s why TSZ was doomed to fail from the start.

    So Barry Arrington was right all along.

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  9. Mung: So Barry Arrington was right all along.

    Right, this is what they have been struggling their hardest to avoid saying. I think the thought alone gives Alan night tremors. “Dam that Barryyyy!!!”

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  10. Corneel:

    regulation of gene expression

    You’re welcome.

    From your link:

    Regulation of gene expression includes a wide range of mechanisms that are used by cells to increase or decrease the production of specific gene products (protein or RNA), and is informally termed gene regulation. Sophisticated programs of gene expression are widely observed in biology, for example to trigger developmental pathways, respond to environmental stimuli, or adapt to new food sources. Virtually any step of gene expression can be modulated, from transcriptional initiation, to RNA processing, and to the post-translational modification of a protein. Often, one gene regulator controls another, and so on, in a gene regulatory network.

    Notice the first sentence where it says that gene regulation is used by the cell. You will tie yourself in knots if you want to argue that gene networks are controlled by a master gene. They are controlled from above the level of the genes.

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  11. phoodoo

    Kantian Naturalist: There’s no point in trying to get to some mythical common ground of mutual understanding with people who can’t grasp basic reasoning. That’s why TSZ was doomed to fail from the start.

    So Barry Arrington was right all along.

    Right, this is what they have been struggling their hardest to avoid saying.I think the thought alone gives Alan night tremors.“Dam[n] that Barryyyy!!!”

    KN lives is the US: that’s his problem, not mine.

    I do have concerns for the future. I have friends and family spread through Europe and North America. I have about the same level of influence on World affairs as Barry. Whether I care, Barry cares, phoodoo cares (about more than the cost of his watch) matters little. The dice fall where they may.

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  12. CharlieM: You will tie yourself in knots if you want to argue that gene networks are controlled by a master gene.

    Then I won’t argue that. Instead I will tie myself in knots to try and make you concede that gene regulation neatly addresses your objection that daughter cells that have the same genome (not genetic code, that’s a different thing) should be phenotypic clones.

    The different celltypes develop as a result of the developmental program playing out, which depends on the interplay of genetic information and external feedback (e.g. positional information from morphogens). And of course, this is completely different from phylogenesis during evolution, so your analogy breaks down at this point.

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  13. phoodoo: If cells can pour their DNA into a pool, and then be incorporated as part of the genome of a totally different cell, how can we ever say “clearly” they are commonly descended?

    This is what you don’t get about the new revelations of genetic science, and why Darwinism is dead.

    It is only by standing out against the more general signal of common (vertical) descent that we can detect gene transfers at all. You seem to have nearly wet yourself with excitement over this discovery, but it is not the body blow to ‘Darwinism’ you imagine.

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  14. CharlieM,

    And exactly how is it determined where mitochondria sit on the tree of all bacteria?

    By phylogenetic analysis.

    How do you know what is vertical descent and what is shared by horizontal gene transfer?

    By phylogenetic analysis …

    Think: if there were no pattern against which to recognise it, gene transfer would never have been discovered.

    Me: I’ve said it before: your analogies are unhelpful.

    Charlie: I would say they are at least helpful in that they have stimulated you to think about these things even if in the end you do reject them.

    They haven’t though. I look at them and think “Jeez, this guy’s got the wrong end of the stick”. That’s as far as they take me; they illustrate your confusion.

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  15. If ‘it’s all gene transfer’, mitochondria are in the curious position of having had more genes transferred from alpha proteobacteria than any other bacterial group. Quite how that is supposed to work, mechanistically, I’m not quite sure, especially when there is a much simpler path to consider.

    The lengths some people will go to to avoid a conclusion of common descent!

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  16. CharlieM:
    Notice the first sentence where it says that gene regulation is used by the cell.

    So you think that means that they’re saying that the cell is consciously deciding what to express? Wow.

    CharlieM:
    You will tie yourself in knots if you want to argue that gene networks are controlled by a master gene.

    I don’t see why anybody would want to argue such a thing. Isn’t it better to study those networks and figure it out?

    The issue under discussion, that all cells in an organism and descendants of a single cell, is regulation of differentiation during embryo development, and that starts with regulation by the products of a couple “master” genes, cascading into other regulatory genes.

    CharlieM:
    They are controlled from above the level of the genes.

    The proteins involved are encoded by genes, and the things responding to the proteins are more genes, and the role of environmental/situational aspects in cell differentiation are sensed by proteins, which are also gene products, that then go on and bind to DNA, thus expressing more genes. So, I’d say that it’s not above, but concomitant to the genes, and I’d be talking about physical/chemical stuff (relative positions, chemical signals, concentration gradients), not some woo-woo.

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  17. Mung: So Barry Arrington was right all along.

    What he was wrong about all along was whether it still is worth trying.

    Look at you Mung, you are a moderator.Who could have foreseen that?

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  18. Allan Miller: The lengths some people will go to to avoid a conclusion of common descent!

    There’s several layers to their tactics. the first one is to call it all “Darwinism,” as if evolution was just about Darwin. The next one is to imagine that if Darwin had one thing wrong, then all of evolution is wrong. If we took the position that one thing wrong in Darwin’s proposals makes the whole of evolution false, then evolution would have died a very long time ago. But that’s not how things work, which is why I start by trying to get them to understand that Darwin didn’t propose just one thing, that we’ve known him to have been wrong about some things, that evolutionary theory has gone well beyond Darwin for many years already, and that they should be aware that horizontal gene transfer is one more mechanism in evolution.

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  19. CharlieM: Notice the first sentence where it says that gene regulation is used by the cell. You will tie yourself in knots if you want to argue that gene networks are controlled by a master gene. They are controlled from above the level of the genes.

    This idea can only be entertainted by someone who hasn’t had molecular biology of cells 101.

    I recommend you learn about the Lac-Operon. It is taught at the introductory level basically everywhere and there is a very good reason for that. Once you understand the Lac-Operon, a whole new world of how genes and their regulation actually works will become clear to you.

    Find the wikipedia article on the Lac-operon and read it. Find some youtube videos on it and watch them, then think a bit about it. I’m not saying this to mock you, but because it genuinely is a bit of an eye opener.

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  20. Entropy,

    Yep. I composed a post along similar lines, but binned it when I remembered who I was talking to!

    I recall the furore over the New Scientist cover: Was Darwin Wrong? Possibly, thought I, but you’ll have to be more specific …

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  21. Corneel: Then I won’t argue that. Instead I will tie myself in knots to try and make you concede that gene regulation neatly addresses your objection that daughter cells that have the same genome (not genetic code, that’s a different thing) should be phenotypic clones.

    Gene regulation ensures that the right proteins are produced in the right amount at the correct time and place. This does not account for form. The daughter cells would only be phenotipic clones if everything came from the genes, but I think we agree that everything does not come from the genes.

    Corneel: The different celltypes develop as a result of the developmental program playing out, which depends on the interplay of genetic information and external feedback (e.g. positional information from morphogens).

    The developmental program and environmental feedback are the means by which the form is achieved, they are not the cause.

    The distribution of morphogens can be quite complex in itself:

    See here for example:

    To understand how this is accomplished, several questions have to be addressed. How does the signal transduction pathway transmit graded information intracellularly to control concentration-dependent differential gene expression? How is a continuous gradient transformed into discrete changes in gene expression that ultimately determine the choice of cell fate from the available alternatives? And how does graded signalling accommodate fluctuations in biological conditions to achieve the necessary robustness required for accurate developmental patterning? By focusing on specific examples, we review recent work that addresses these questions and, where possible, we highlight some of the general principles that appear to be shared between different morphogen gradients…

    Although the standard view of a morphogen gradient is a continuous gradient, the embryonic Dpp gradient is unusual in that it contains a threshold, or step, in its distribution at the dorsal midline..

    Quantitative aspects of morphogen activity appear at odds with normal biological processes. Small changes in the concentration of an extracellular signalling molecule can have dramatic consequences on cell fate, yet embryonic development is able to cope with stochiometric fluctuations in gene expression and with changes in environmental and genetic conditions, such as changes in temperature and gene dose. Investigations of the mechanisms that underlie the precision and robustness of different signalling pathways have largely focused on morphogen distribution and the regulation of the signal transduction. Such studies have found that a number of mechanisms appear to operate to increase the reliability of graded signalling

    And here

    some biologists have raised questions about the theory, which contends that physical features are necessarily tied to absolute concentrations of proteins within the morphogen gradient.

    If a certain critical mass of protein is present, then a given physical feature—for example, cells that make the skin on your forehead—will appear. If less than that critical mass is present, a different structure—say, the skin that makes your eyebrows—will appear, and a boundary will be formed between the two structures.

    Alternative views have suggested physical features are not necessarily the result of a specified number of proteins, but, rather, come from more complex interactions between multiple gradients that work against one another.

    I find that the phrase, “more complex than thought”, appears quite frequently when I read any literature on the latest biological research.

    Corneel: And of course, this is completely different from phylogenesis during evolution, so your analogy breaks down at this point.

    The difference lies in the details. The overall pattern is strikingly similar.

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  22. Allan Miller:
    CharlieM,

    By phylogenetic analysis.

    By phylogenetic analysis …

    Think: if there were no pattern against which to recognise it, gene transfer would never have been discovered.

    How do you explain this

    “The natural world is full of examples of species that have evolved similar characteristics independently, such as the tusks of elephants and walruses,” said Stephen Rossiter of the University of London, an author on one of the studies. “However, it is generally assumed that most of these so-called convergent traits have arisen by different genes or different mutations. Our study shows that a complex trait — echolocation — has in fact evolved by identical genetic changes in bats and dolphins.”

    What choices do you have other than common descent or horizontal gene transfer? Coincidence I suppose.

    And then there is the question of identical sequences appearing in cone snails and orange tip butterflies. See here where I linked to the story, which is very hard to explain from an orthodox perspective.

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  23. Did you read the review (Ashe and Briscoe) that you quoted? It is rather old (2006) but seems pretty interesting:

    Altering the gene dose of dpp by decreasing the gene copy number to one or by increasing it to three or four has significant effects on the position at which target genes are expressed (Ashe et al., 2000). Consistent with this, the injection of dpp transcripts into Drosophila embryos is sufficient to promote the development of ectodermal cells with incremental two- to fourfold increases in the injected concentration eliciting progressively more-dorsal cell fates (Ferguson and Anderson, 1992).

    How do you explain these data in terms of the archetype? Looks like genes regulating genes to me.
    You might want to learn about sex determination in fungi, birds and mammals, too.

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  24. Allan Miller:
    If ‘it’s all gene transfer’, mitochondria are in the curious position of having had more genes transferred from alpha proteobacteria than any other bacterial group. Quite how that is supposed to work, mechanistically, I’m not quite sure, especially when there is a much simpler path to consider.

    The lengths some people will go to to avoid a conclusion of common descent!

    You have restricted yourself to the belief that organisms having the same or similar genes must be due either to common descent or horizontal gene transfer. I am not saying that these explanations are totally invalid, I am saying that there are other options.

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  25. CharlieM: The daughter cells would only be phenotipic clones if everything came from the genes, but I think we agree that everything does not come from the genes.

    Why no. The commitment to a specific cell fate involves epigenetic and cytoplasmic factors as well. But since these are largely orchestrated by genetic information it is fair to say that developmental control is, to borrow Entropy’s term, concomitant to genes. Your objection that cells with the same genome should have identical phenotypes simply doesn’t fly, and doesn’t require some mysterious “control” either.

    CharlieM: The developmental program and environmental feedback are the means by which the form is achieved, they are not the cause.

    Well, in a sense they are; They are the proximate causes. If you want to discuss the ultimate causes, we need to talk evolutionary biology.

    CharlieM: I find that the phrase, “more complex than thought”, appears quite frequently when I read any literature on the latest biological research.

    Not nearly as often as in discussions here at TSZ. 😀

    CharlieM: The difference lies in the details. The overall pattern is strikingly similar.

    Hey, have you seen the guy that typed this:

    Looking at life as a whole does not mean ignoring the detail. In fact the opposite is the case. In order to make the necessary connections the life processes should be studied in intimate details.

    ETA: nice review BTW. Did you read that?

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  26. Entropy: So you think that means that they’re saying that the cell is consciously deciding what to express? Wow.

    If I said that plants use carbon dioxide and sunlight to produce energy would you automatically assume that I was saying plants are conscious? They stated it accurately, “the cell uses its genes”. That is what happens.

    I don’t see why anybody would want to argue such a thing. Isn’t it better to study those networks and figure it out?

    The protein networks we see on the internet and in books are a vastly simplified model of reality, and even with them the obvious complexity of the pathways and interactions cannot be untangled to give a nice neat account of the processes involved. If you think you can easily figure out a typical network then I would say you are just scratching the surface.

    The issue under discussion, that all cells in an organism and descendants of a single cell, is regulation of differentiation during embryo development, and that starts with regulation by the products of a couple “master” genes, cascading into other regulatory genes.

    The proteins involved are encoded by genes, and the things responding to the proteins are more genes, and the role of environmental/situational aspects in cell differentiation are sensed by proteins, which are also gene products, that then go on and bind to DNA, thus expressing more genes. So, I’d say that it’s not above, but concomitant to the genes, and I’d be talking about physical/chemical stuff (relative positions, chemical signals, concentration gradients), not some woo-woo.

    You think that a couple of master genes suddenly spring into action and everything follows from there? I would say you are not even scratching the surface.

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  27. Rumraket: This idea can only be entertainted by someone who hasn’t had molecular biology of cells 101.

    We wouldn’t want anyone thinking outside the box!

    I recommend you learn about the Lac-Operon. It is taught at the introductory level basically everywhere and there is a very good reason for that. Once you understand the Lac-Operon, a whole new world of how genes and their regulation actually works will become clear to you.

    Find the wikipedia article on the Lac-operon and read it. Find some youtube videos on it and watch them, then think a bit about it. I’m not saying this to mock you, but because it genuinely is a bit of an eye opener.

    I first came across the lac operon when Behe discussed it a decade or two ago.

    And I just found a paper entitled, Rethinking the Hierarchy of Sugar Utilization in Bacteria

    Bacteria are known to consume some sugars over others, although recent work reported by Koirala and colleagues in this issue of the Journal of Bacteriology (S. Koirala, X. Wang, and C. V. Rao, J Bacteriol 198:386–393, 2016, http://dx.doi.org/10.1128/JB.00709-15) revealed that individual cells do not necessarily follow this hierarchy. By studying the preferential consumption of l-arabinose over d-xylose in Escherichia coli, those authors found that subpopulations consume one, the other, or both sugars through cross-repression between utilization pathways. Their findings challenge classic assertions about established hierarchies and can guide efforts to engineer the simultaneous utilization of multiple sugars…

    …the apparent cross-repression between the pathways and the ability of some cells to have both pathways induced suggested a more complex and nuanced hierarchy than previously envisioned.

    There we go, “more complex” than thought! I would say when dealing with processes such as these, more complexity should always be the default assumption.

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  28. Allan Miller:
    Entropy,

    Yep. I composed a post along similar lines, but binned it when I remembered who I was talking to!

    I recall the furore over the New Scientist cover: Was Darwin Wrong? Possibly, thought I, but you’ll have to be more specific …

    Did I participate in that ‘furore’? I don’t remember. Maybe you can remind me.

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  29. CharlieM: There we go, “more complex” than thought! I would say when dealing with processes such as these, more complexity should always be the default assumption.

    None of this has anything to do with what you first said and to which I responded. The genes are environmentally regulated. Go read about the Lac Operon.

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  30. CharlieM: We wouldn’t want anyone thinking outside the box!

    You’re not thinking outside the box, you’re blindly regurgitating other people’s work even though it’s irrelevant to the topic at hand. You’re not being this amazing independent thinker you like to imagine, you’re just being stubborn. But I’m sure it feels nice to think of yourself in those terms.

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  31. CharlieM:
    If I said that plants use carbon dioxide and sunlight to produce energy would you automatically assume that I was saying plants are conscious? They stated it accurately, “the cell uses its genes”. That is what happens.

    Nope. What happens is much harder to explain if explained properly, which is why they use those shortcuts. Plants don’t “use carbon dioxide to produce energy,” their chlorophyl reacts to photons in a way that cascades into several chemical reactions that result in CO2 reacting with water and thus forming some carbohydrate, etc, etc. See how much longer it takes to say that? Thus the teleologically-sounding shortcut.

    In what way you’d say “the cell uses its genes” other than consciously? In having those genes and the genes doing what they’re going to doregardless of whether the cell could even want them to do it or not?

    CharlieM:
    The protein networks we see on the internet and in books are a vastly simplified model of reality,

    Exactly right, which is why people use those teleologically-sounding shortcuts to try and explain what’s going on. That doesn’t mean that the writers really think that cells are consciously deciding to “use their genes.”

    CharlieM:
    You think that a couple of master genes suddenly spring into action and everything follows from there? I would say you are not even scratching the surface.

    Why would you think I’d think of it happening “suddenly”? The fact is: two master genes start the process of differentiation. The trigger is the fertilization. But even that’s not above the genes, but concomitant, since the way these “signals” are detected use gene products as well.

    Here’s where you should try and clarify, rather than try and obfuscate the issue further. So, you didn’t mean that the cell is conscious, then what do you mean when you say “the cell uses it’s genes”? Then for the second part you should clarify what you mean by: “above the genes.”

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  32. CharlieM: There we go, “more complex” than thought! I would say when dealing with processes such as these, more complexity should always be the default assumption.

    You missed the point. What Rum is advising is for you to understand how that works. Whether there’s more complications is not the issue. The issue is understanding how it works. The model produced from the classic, Nobel-winning, experiments, has a simple-yet-powerful explanatory logic, and would help you get a better grasp as to how gene regulation operates. Then you’d be able to judge what “more complex” actually means in that context. Then you’d realize that focusing on whether somebody said “more complex” doesn’t cut it. You have to actually understand what they’re talking about.

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  33. CharlieM,

    How do you explain this

    Oh, good grief! Yes, convergent evolution is a thing. However, it is vanishingly rare at the molecular level, the level I am struggling manfully to get you consider.

    As I said in regard to gene transfer: “Think: how do they know it’s anomalous?”.

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  34. CharlieM

    Did I participate in that ‘furore’? I don’t remember. Maybe you can remind me.

    Not as far as I’m aware, no. It’s not all about you, you know.

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  35. CharlieM: You have restricted yourself to the belief that organisms having the same or similar genes must be due either to common descent or horizontal gene transfer. I am not saying that these explanations are totally invalid, I am saying that there are other options.

    These other options are even more elaborate. There is a very simple mechanistic cause of common sequence: common descent. Not only that, but common descent explains why common absences (gene loss) and gains (gene transfers, retroviral inserts, transposons) themselves form into a hierarchic pattern. It’s not just mutations that act as phylogenetic markers; any heritable change has that capacity.

    Hand-wavy ‘other options’ appear not to cut the mustard. In order to think outside the box, it helps to know what’s in it.

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  36. DNA_Jock:
    Did you read the review (Ashe and Briscoe) that you quoted? It is rather old (2006) but seems pretty interesting:

    Altering the gene dose of dpp by decreasing the gene copy number to one or by increasing it to three or four has significant effects on the position at which target genes are expressed (Ashe et al., 2000). Consistent with this, the injection of dpp transcripts into Drosophila embryos is sufficient to promote the development of ectodermal cells with incremental two- to fourfold increases in the injected concentration eliciting progressively more-dorsal cell fates (Ferguson and Anderson, 1992).

    How do you explain these data in terms of the archetype? Looks like genes regulating genes to me.

    Genes regulating genes are a very large part of morphogenesis. But they are the physical means by which a form are expressed, not its root cause. If we think of the organism as a building, the genes are involved in construction. If the construction is interfered with say by adding an ingredient which prevents mortar from setting then it is going to seriously affect the construction, but the architects plans are not affected by this.

    Now returning to dpp.

    Dpp is a morphogene which, by forming an intracellular diffusion gradient, controls growth patterns. But how is it able to achieve and maintain a suitable concentration throughout the gradient’s domain. It just so happens there are other genes which control its concentration by active transport and other means.

    BMP/Dpp signaling and epithelial morphogenesis in Drosophila development

    Extracellular environment in Dpp diffusion
    Once emitted from cells, Dpp faces an complex extracellular environment. Many transmembrane receptors, secreted proteins and ECM components mediate Dpp diffusibility and activity (Kim et al., 2011).
    In addition to being the generic receptor for Dpp, Tkv can also serve as a trap, promoting degradation of abundant Dpp in an endocytosis-dependent manner (Gonzalez-Gaitan and Jackle, 1999). Interestingly, activation of Tkv enhances binding activity to Dpp as the exogenous expression of the constitutively-active form of Tkv blocks the ligand diffusion from LVs into PCV (Matsuda and Shimmi, 2012b). Besides, the biased expression of tkv promotes Dpp morphogen gradient formation in the wing imaginal disc of 3rd instar larvae (Lecuit and Cohen, 1998).

    Integrins are cell surface receptors mediating cell-ECM (extracellular matrix) communications (Brown, 2000). Previous studies suggested that they can positively regulate the activity of Sog (Araujo et al., 2003; Larrain et al., 2003), a secreted protein involved in the transport of Dpp in a variety of developmental processes in different species (Holley et al., 1995; Serpe et al., 2005). As one of the most abundant components of ECM, collagen IV was reported to bind Dpp, enhance Dpp signaling and promote the morphogen gradient formation during D-V patterning in the Drosophila embryo (Wang et al., 2008). Moreover, human type-IV collagen can also bind BMP4, suggesting strong mechanistic conservation between human and fly (Wang et al., 2008). Heparan sulfate proteoglycans (HSPGs), comprising a protein core and attached heparan sulfate (HS) glycosaminoglycan (GAG) chains, are ECM and cell surface macromolecules (Yan and Lin, 2009). Based on the protein core, HSPGs are classified into three families: glypican, perlecan and syndecan, and are highly structurally and functionally conserved in vertebrates and fly. In Drosophila, there are two glypicans (Dally and Dally-like protein (Dlp), one perlecan and one syndecan (Yan and Lin, 2009). During Dpp gradient formation in the wing imaginal disc, Dally and Dlp were reported to be partially redundant; loss of either enhances the defects of morphogen signaling (Belenkaya et al., 2004). The genetic and biochemical studies suggested that Dally positively regulates stability and mobility of Dpp (Akiyama et al., 2008; Fujise et al., 2003). In addition, Dally can regulate Dpp diffusion by interacting with Sog, a protein mediating its transport (Chen et al., 2012b). Besides Dpp and its ortholog in vertebrates, BMP2, HSPGs broadly modulate diffusion and activity of other growth factors, such as Wnt (Wingless (Wg) in fly), Fgf and Hedgehog (Hh) during development (Han et al., 2004; Han et al., 2005; Quarto and Amalric, 1994).

    These various molecules are working together to produce the form of the organism in a similar way to termites cooperating to build a nest. And just as there is no master termite controlling the operation there is no master gene regulating the process. All genes are dependent on other genes.

    You might want to learn about sex determination in fungi, birds and mammals, too.

    Thank you for the advice.

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  37. DNA_Jock:
    CharlieM: See here where I linked to the story, which is very hard to explain from an orthodox perspective.
    Not so hard as you seem to think, however.

    That all depends on your explanation as to how this coincidence occurred..

    Glacontryphan-M (GT) is a protein of 63 amino acids which is identical in both the butterfly and the cone snail.

    From this article

    Our laboratory is not only initiating investigation of GT protein chemistry in HG samples from across the world but also in samples from a series of other toxic animals to possibly bridge the large gap between the evolutionarily totally open question of why a butterfly and a sea snail share the identical toxin GT.

    If you think that the matching sequences were just a pure random coincidence then all the other cone snail toxin sequences are irrelevant. You still need to get the right amino acid in position 63 times in a row. What is your theory as to how it happened?

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  38. CharlieM: If you think that the matching sequences were just a pure random coincidence then all the other cone snail toxin sequences are irrelevant.

    No, they are not.
    As I wrote before

    If you really don’t understand why adding an extra thousand targets degrades the significance of the match, I’m not sure I can help you out.

    Maybe 80,000 targets.
    Now I don’t think that the match is pure random coincidence, but to humor you I ignored the effect of selection. You do not appear to understand even the simplest of concepts.

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  39. This juxtaposition made me laugh.

    CharlieM: And just as there is no master termite controlling the operation there is no master gene regulating the process. All genes are dependent on other genes.

    [quotes DNA_Jock]
    You might want to learn about sex determination in fungi, birds and mammals, too.

    Thank you for the advice.

    I am puzzled as to why you and Sal are determined to deny the hierarchical nature of the control of gene expression — is it in homage to a poorly-thought-through IC argument, or something else?

    I am seeing a pattern develop however [joke unintended]. When challenged regarding the role of decapentaplegic (Dpp) in setting up the dorsal-ventral axis in the embryo, Charlie responds with a cut&paste from a thesis discussing the role of Dpp in the imaginal wing disc . Huh?
    When challenged to learn about the lac operon, Charlie responds with a cut&paste about the bistable nature of Arabinose / Xylose catabolism switching. WTF? Research by Google, evidently.
    When you do this, you come across as ignorant.

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  40. Corneel:

    CharlieM: The daughter cells would only be phenotipic clones if everything came from the genes, but I think we agree that everything does not come from the genes.

    Why no. The commitment to a specific cell fate involves epigenetic and cytoplasmic factors as well.But since these are largely orchestrated by genetic information it is fair to say that developmental control is, to borrow Entropy’s term, concomitant to genes. Your objection that cells with the same genome should have identical phenotypes simply doesn’t fly, and doesn’t require some mysterious “control” either.

    I have not objected that cells with the same genome should have identical phenotypes. I said that if everything came from the genes they would be clones. But I suppose it depends on the definition of clone. Would you say that Dollie the sheep was a clone?

    CharlieM: The developmental program and environmental feedback are the means by which the form is achieved, they are not the cause.

    Well, in a sense they are; They are the proximate causes. If you want to discuss the ultimate causes, we need to talk evolutionary biology.

    No. If we are to discuss the ultimate causes, we need to talk philosophy.

    CharlieM: The difference (between ontogony and phylogeny) lies in the details. The overall pattern is strikingly similar.

    Hey, have you seen the guy that typed this:

    Looking at life as a whole does not mean ignoring the detail. In fact the opposite is the case. In order to make the necessary connections the life processes should be studied in intimate details.

    And what is wrong with that? In order to compare the differences and similarities between ontogony and phylogeny we need to study both.

    ETA: nice review BTW. Did you read that?

    Yes.

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  41. Rumraket: None of this has anything to do with what you first said and to which I responded. The genes are environmentally regulated. Go read about the Lac Operon.

    I have.

    And just as living organisms make the earthly environment what it is, the cells of a multicellular organism make the environment in which they live and die. Symbiosis is the rule by which life is maintained.

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  42. Rumraket: You’re not thinking outside the box, you’re blindly regurgitating other people’s work even though it’s irrelevant to the topic at hand. You’re not being this amazing independent thinker you like to imagine, you’re just being stubborn. But I’m sure it feels nice to think of yourself in those terms.

    Wise words:

    O wad some Power the giftie gie us. To see oursels as ithers see us!

    from Rabbie Burns 🙂

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  43. CharlieM: I have not objected that cells with the same genome should have identical phenotypes. I said that if everything came from the genes they would be clones. But I suppose it depends on the definition of clone. Would you say that Dollie the sheep was a clone?

    In that case, this statement of yours makes no sense:

    What is it that is handed down through the generations of cells in the growth of a buttercup? […] If it is the information in the form of the genetic code, why are the offspring not all clones.

    Ehrm, barring somatic mutations*, all the cells in an individual buttercup ARE genetic clones. Are you sure that is what you meant?

    CharlieM: No. If we are to discuss the ultimate causes, we need to talk philosophy.

    Have it your way. Good luck finding the philosophical cause for cell differentiation.

    CharlieM: And what is wrong with that? In order to compare the differences and similarities between ontogony and phylogeny we need to study both.

    The issue is that you are NOT studying the differences, you are dismissing them as “details” in order to salvage your analogy.

    ETA: * and the gametes

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  44. Rumraket: You’re not thinking outside the box, you’re blindly regurgitating other people’s work even though it’s irrelevant to the topic at hand. You’re not being this amazing independent thinker you like to imagine, you’re just being stubborn. But I’m sure it feels nice to think of yourself in those terms.

    Content rich! Just ask Jock.

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  45. Allan Miller: There is a very simple mechanistic cause of common sequence: common descent. Not only that, but common descent explains why common absences (gene loss) and gains (gene transfers, retroviral inserts, transposons) themselves form into a hierarchic pattern. It’s not just mutations that act as phylogenetic markers; any heritable change has that capacity.

    Nicely said sir!

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