If ID is false, why can we detect human engineered virii?

There is a strong suspicion the coronavirus is an escaped specimen from a Chinese lab.

https://www.biorxiv.org/content/10.1101/2020.01.30.927871v1.full.pdf

An Indian scientist has purportedly discovered HIV inserted into the coronavirus. If true, this is pretty conclusive evidence the virus is humanly engineered, i.e. intelligently designed.

So, herein lies the conundrum. According to popular imagination, ID is both bad science and false (remember, good science is the falsifiable sort ;). If true, then it should not be possible to detect intelligent intervention in the genetic code.

Yet, this recent news item purports to be exactly that: identification of intelligent intervention in the genetic code.

Please explain this to me like I am 5: how can ID be both bad science and false, yet at the same time it is possible to identify intelligent intervention in the genetic code? If we can do so for the recent past, why can’t we do the same for the distant past?

Thanks!

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162 thoughts on “If ID is false, why can we detect human engineered virii?

  1. colewd: You appear to be ignoring neutral mutations and genetic drift.

    I am, because they are completely irrelevant to our discussion about whether simple (and complex) adaptations entail fitness variation and whether “function” is an acceptable substitute.

    colewd: Function can be made into specific biological claims. Fitness cannot.

    Remember that we are discussing adaptation. Please name an example where you can make specific biological claims using (simple or complex) adaptive function, but cannot do this using fitness.

    colewd: Fitness also appears to be reducing diversity as a mechanism of population genetics.

    No, that would be directional selection (acting on variation in fitness).

    Fun fact: selection can also preserve genetic variation, such as in the case of heterozygote advantage.

    colewd: The myh 7 discussion is showing this as we see divergence in sub populations which gets reduced in the overall population.

    I am not following PS that closely, so you’ll need to recap or add a link to that discussion, and explain why it is relevant. I am very curious how you are going to explain adaptive divergence in MYH7 function, without touching on fitness variation.

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  2. dazz: of course it never occurred to Bill that implies accepting fitness is real, even if only at a microevolutionary scale

    It sounds crazy, but it is true. In acknowledging that purifying selection and simple adaptations exist, Bill accepts fitness variation and natural selection, but he is the only person who doesn’t realize it.

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  3. Corneel,

    Remember that we are discussing adaptation. Please name an example where you can make specific biological claims using (simple or complex) adaptive function, but cannot do this using fitness.

    Any environmental change can make a fitness advantage go away. In the Lenski experiment the loss of citrate in the environment takes away the adaptive advantage. A real functional advantage can easily be applicable to various environments in the case of humans we can generate our own environment. Have you read Behe’s latest book?
    Corneel,

    I am not following PS that closely, so you’ll need to recap or add a link to that discussion, and explain why it is relevant. I am very curious how you are going to explain adaptive divergence in MYH7 function, without touching on fitness variation.

    Fitness appears here to be neutral or deleterious across all mammals with any functional variation.

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  4. Corneel,

    , Bill accepts fitness variation and natural selection, but he is the only person who doesn’t realize it.

    What does it mean to accept fitness variation and natural selection? Is this a religious commitment 🙂

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  5. colewd: What does it mean to accept fitness variation and natural selection?

    It means to accept that variation and selection happen in real life and in real time.

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  6. Let me quickly remind you how I defined adaptation: “A biological function becomes an adaptation only if it serves to increase an organisms ability to survive and reproduce in its environment”

    colewd: Any environmental change can make a fitness advantage go away. In the Lenski experiment the loss of citrate in the environment takes away the adaptive advantage.

    Yes, and the ability to grow aerobically on citrate ceases to be an adaptation in that environment. Fitness falls accordingly, but the function remains present.

    colewd: A real functional advantage can easily be applicable to various environments in the case of humans we can generate our own environment.

    And the “functional advantage” is only an adaptation if one or more of those “various environments” are encountered or generated. Fitness expresses that. Function does not.

    colewd: Have you read Behe’s latest book?

    Just the free chapter, but I remember him making a point that losing a molecular function often is adaptive. This is counter to your claim, in case you haven’t noticed.

    colewd: Fitness appears here to be neutral or deleterious across all mammals with any functional variation.

    That is a nonsensical statement. Perhaps you meant to say that certain allelic variants are neutral or deleterious. If a functional variant is neutral, then it is not an adaptation. If a functional variant is deleterious, then it is not an adaptation. In the latter case, this is correctly expressed by lower fitness of its carrier.

    colewd: What does it mean to accept fitness variation and natural selection? Is this a religious commitment 🙂

    Ab-so-lu-te-ly NOT. As I said, you have already accepted those concepts. You just need to bring some consistency to your arguments, and stop denying that fitness variation is a real thing.

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  7. Alan Fox,

    . However, blueprints of complex adaptations in molecular systems are pervasive, indicating that they can readily evolve.

    See it now?

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  8. colewd ro Alan Fox:

    . However, blueprints of complex adaptations in molecular systems are pervasive, indicating that they can readily evolve.

    See it now?

    Nothing circular there. It’s likely that you don’t understand what “blueprints” means in this context though.

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  9. colewd,

    I salute you for actually providing a definition.

    But I can’t help but notice that under that definition complex adaptations can evolve. The definition makes an adaptation complex relative to its context. To jump from a population in state A to a population in state D would require a complex adaptation. However, if the population goes from A to B to C and then to D, you have the same resulting population without any complex adaptation having occurred.
    So you need to go back to the drawing board for a new definition if you want complex adaptations to be unable to evolve.

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  10. Entropy,

    . It’s likely that you don’t understand what “blueprints” means in this context though.

    What do you think it means?

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  11. Walter Kloover,

    So you need to go back to the drawing board for a new definition if you want complex adaptations to be unable to evolve.

    I don’t think anyone should make the claim that complex sequences or adaptions can’t evolve. I think the right claim is that as they become more complex evolution by natural selection becomes a more unlikely hypothesis.

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  12. colewd:

    I don’t think anyone should make the claim that complex sequences or adaptions can’t evolve.I think the right claim is that as they become more complex evolution by natural selection becomes a more unlikely hypothesis.

    This confuses me. Near as I can tell, there’s no such thing as a complex adaptation – they are always small and incremental. What gives the illusion of a complex adaptation is viewing the current status of something that has been undergoing small changes for a very long time — generally through a long sequence of species branching events. I see no reason why a lineage that has been branching for a few hundred million years would encounter increasing difficulty experiencing selection.

    So “complex evolution” would only be an unlikely hypothesis if we could identify some reason why evolutionary forces might stop acting on any lineage as it increases in complexity. Do you have any candidates for this?

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  13. Flint,

    This confuses me. Near as I can tell, there’s no such thing as a complex adaptation – they are always small and incremental. What gives the illusion of a complex adaptation is viewing the current status of something that has been undergoing small changes for a very long time — generally through a long sequence of species branching events. I see no reason why a lineage that has been branching for a few hundred million years would encounter increasing difficulty experiencing selection.

    For the theory to work what you describe has to be the landscape. From my limited observation it is not. This is where Behe’s arguments come in.

    What has to happen for a bacteria to evolve rotary mobility? Are there small steps to this motor? It takes a DNA sequence of 100k nucleotides to build this motor. 4^100000 ways to arrange that DNA yet if I type 4^1000 into a exponent calculator the result I get is infinity. There are more than one flagellar sequence but to make a dent in this problem you need the number of flagellar sequences to be larger than the number of sub atomic particles in the universe. Time since the beginning of life does not put a small dent into this problem.

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  14. colewd: There are more than one flagellar sequence but to make a dent in this problem you need the number of flagellar sequences to be larger than the number of sub atomic particles in the universe.

    Fun fact, Bill. We know that the number of 80-mers that can bind ATP is greater than the number of subatomic particles in the universe.
    This has been explained to you multiple times, yet you remain imperviously.ignorant.

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  15. DNA_Jock,

    Fun fact, Bill. We know that the number of 80-mers that can bind ATP is greater than the number of subatomic particles in the universe.
    This has been explained to you multiple times, yet you remain imperviously.ignorant.

    Binding ATP is the same as a 40 protein rotary motor. Nice deflection through 🙂

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  16. colewd: What has to happen for a bacteria to evolve rotary mobility? Are there small steps to this motor?

    Yet the rotary motor evolved at least twice. At least once in bacteria and at least once in Archaea. Two completely different pathways to the same functional solution.

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  17. colewd: if I type 4^1000 into a exponent calculator the result I get is infinity.

    This is your standard response of “look-at-all-those-zeroes”, but that is not what Flint was asking. He asked how, given that an evolutionary path exists into a complex function, any of the small cumulative steps into it (simple adaptations) can be distinguished from the complex structure they inevitably become part of (complex adaptation).

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  18. In large populations, evolution can happen in parallel as well as in series. HGT in asexual procaryotes and recombination in sexual species and…

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  19. colewd: Time since the beginning of life does not put a small dent into this problem.

    Yet there are two independent solutions (at least)!

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  20. Alan Fox,

    Yet the rotary motor evolved at least twice. At least once in bacteria and at least once in Archaea. Two completely different pathways to the same functional solution.

    What could mechanistically account for this?

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  21. Corneel,

    This confuses me. Near as I can tell, there’s no such thing as a complex adaptation – they are always small and incremental.

    This is his assertion without condition. I showed him an exception in bacteria which makes his claim iffy.

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  22. colewd:
    Alan Fox,

    What could mechanistically account for this?

    One explanation is that evolutionary pathways are more abundant than some claim when they do the “one-needle-in-a-haystack” routine. Many more than one needle, and you only have to stumble on one, not exhaustively search the whole stack. And if you find a sharper needle, swap it with the one you had.

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  23. colewd: This is his assertion without condition. I showed him an exception in bacteria which makes his claim iffy.

    Er, nope. Series and parallel “simple” adaptations can accumulate and end up as “complex”.

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  24. colewd: This is his assertion without condition. I showed him an exception in bacteria which makes his claim iffy.

    I think he may have been aware of that “exception” already. Suit yourself, though.

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  25. colewd: Binding ATP is the same as a 40 protein rotary motor. Nice deflection through 🙂

    Well, that just makes the problem worse for you.
    Try to stay focused, Bill. You are claiming that the sequence space for the flagellar rotor is sooooooooo biiiiiiiiig that you would need to have 10^86 solutions [particles in the universe] in that space to “make a dent in this problem”.
    I am pointing out : “not a problem”, since, even in the relatively tiny sequence space of 80mers (a mere 10^104) there are still 10^93 different ways of binding ATP.
    In your hypothetical sequence space (4^100k = 10^60206, ROFL! do you even understand what you did there?) there’s gonna be at least 10^60000 flagellar rotors…
    You and gpuccio are sticking with the “we are off by a bit, but it doesn’t matter because the numbers are so big” argument, failing to realize that, as the denominator scales, so too does the numerator, more or less.
    This.has.been.explained.to.you.

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  26. colewd:
    Flint,

    For the theory to work what you describe has to be the landscape.From my limited observation it is not.This is where Behe’s arguments come in.

    What has to happen for a bacteria to evolve rotary mobility?Are there small steps to this motor?It takes a DNA sequence of 100k nucleotides to build this motor.4^100000 ways to arrange that DNA yet if I type 4^1000 into a exponent calculator the result I get is infinity.There are more than one flagellar sequence but to make a dent in this problem you need the number of flagellar sequences to be larger than the number of sub atomic particles in the universe.Time since the beginning of life does not put a small dent into this problem.

    I see some errors here.

    First, you assume there is only one pathway to rotary mobility. But there is actually almost an infinity of possible pathways, so that assumption fails.

    Second, you are again playing Texas sharpshooter, picking something that DID evolve (the target) while factoring out the infinity of things that might have evolved but did not. (I like to use the example of tossing a ball into the air, and noting the mind-boggling odds against it coming down to rest precisely where it did. Every ball toss becomes a statistical miracle!)

    Third, you simply ignore cumulative selection. You seem to forget that after each tiny step, the number of possible next steps is constrained. I’m guessing you ignore cumulative selection because it violates foregone presumptions.

    And fourth, what I asked for was what fact of nature would make tiny incremental changes MORE unlikely over time, or more unlikely depending on your assessment of the cumulative complexity of previous steps. Why would mutations be aware of a prior history of mutations? Why would that be necessary?

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  27. Flint: First, you assume there is only one pathway to rotary mobility.

    I keep telling him there at least two known completely unrelated rotary flagellar systems.

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  28. colewd: Binding ATP is the same as a 40 protein rotary motor. Nice deflection through

    Neither the flagellum, nor ATP synthase, evolved in one big jump. They are made of multiple proteins all of which have homologues with functions in other systems, and some even by themselves. The catalytic hexamer in ATP synthases is made of basically the same protein repeated six times(there are two different proteins, both deriving from a common ancestral protein). Even by itself, monomers of this hexameric oligomer have homologues that function by themselves. In other related hexameric molecular machines it is the very same protein oligomerized six times, for example in RNA helicases.

    I explained all of this and more to both you and Gilbert on peacefulscience. Specifically about ATP synthase 12 days ago here.

    Then later I basically have to repeat it all to Gilbert here.

    It is sad to have to repeat these things over and over again.

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  29. colewd: I think the right claim is that as they become more complex evolution by natural selection becomes a more unlikely hypothesis.

    That’s simply mistaken. As they become more complex their de novo evolution becomes less likely, but the evidence shows they evolved incrementally from simpler more likely systems, so there isn’t actually any problem here.

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  30. Rumraket: It is sad to have to repeat these things over and over again.

    Is there any doubt Bill’s religious blinders make it completely impossible for him to learn anything about the evolutionary sciences?

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  31. Flint,

    First, you assume there is only one pathway to rotary mobility. But there is actually almost an infinity of possible pathways, so that assumption fails.

    An infinite possible pathways. How would you support this claim. Infinite pathways to all biological solutions? How did flagellar and eyes evolve multiple times? What is the mechanistic explanation?

    Second, you are again playing Texas sharpshooter, picking something that DID evolve (the target) while factoring out the infinity of things that might have evolved but did not. (I like to use the example of tossing a ball into the air, and noting the mind-boggling odds against it coming down to rest precisely where it did. Every ball toss becomes a statistical miracle!)

    What infinite number of evolutionary solutions did the Lenski experiment produce?

    Third, you simply ignore cumulative selection. You seem to forget that after each tiny step, the number of possible next steps is constrained. I’m guessing you ignore cumulative selection because it violates foregone presumptions.

    I am interested in how you think this helps? Infinite possibilities takes infinite time.

    And fourth, what I asked for was what fact of nature would make tiny incremental changes MORE unlikely over time,

    Functional constraint. Alpha actin 1 humans mice rats 100% alignment.

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  32. colewd to DNA_Jock,
    Binding ATP is the same as a 40 protein rotary motor. Nice deflection through 🙂

    Is no deflection, it’s a demonstration that there’s more than one way to get to some function. It contrasts against your bare, implied, claim that the flagellum could have only been the exact one found in whatever bacteria you were talking about (your exponents are a mathematical statement of exactly that assumption).

    Another way to try and get the point across is the existence of other flagella, but no point going there until you understand where this is going and where you err.

    Do you understand the point yet? I’m going to try until you get it if not. So, please do answer with all honesty. If you don’t get the point yet, what’s unclear?

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  33. Rumraket,

    That’s simply mistaken. As they become more complex their de novo evolution becomes less likely, but the evidence shows they evolved incrementally from simpler more likely systems, so there isn’t actually any problem here.

    Circular reasoning.

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  34. colewd: Infinite possibilities takes infinite time.

    Well, lets say multiple possibilities. Evolution permits adaptations in parallel so different pathways can be stumbled upon by different individuals. Why would that take more time?

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  35. Alan Fox,

    Well, lets say multiple possibilities.

    Living in infinite mathematical space. The dog (mechanism) does not hunt 🙂

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  36. colewd: Living in infinite mathematical space. The dog (mechanism) does not hunt

    I can’t make sense of your remarks above.

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  37. colewd: Living in infinite mathematical space. The dog (mechanism) does not hunt 🙂

    As we have explained to you previously, the size of the space doesn’t matter. At all.
    The sparseness and connectivity of function do matter.
    Hunt away, Lassie!

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  38. colewd: An infinite possible pathways. How would you support this claim. Infinite pathways to all biological solutions?

    “If I type the number into my calculator the result I get is infinity”

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  39. colewd:
    Flint,

    An infinite possible pathways.How would you support this claim.Infinite pathways to all biological solutions?How did flagellar and eyes evolve multiple times?What is the mechanistic explanation?

    Not sure what you mean by “mechanistic” here. The mechanism seems the same in all cases. Start anywhere. Make a number of small changes. Preserve whatever works. Start there. Repeat endlessly. By “works” I mean “doesn’t kill the organism.”

    What infinite number of evolutionary solutions did the Lenski experiment produce?

    I thought my illustration wasn’t all that difficult to grasp, but I guess I was wrong. What infinite number of locations did the tossed ball land in? Again, you are assuming that what happens is the only thing that COULD happen. You keep confusing the probability of some particular result with the probability of ANY result at all. This is a concept nobody has been able to get through to you. But here in reality, everything that happens lies at the end of a long sequence of vanishingly unlikely prior conditions.

    I am interested in how you think this helps?Infinite possibilities takes infinite time.

    Not true at all. Infinite RESULTS take time. Infinite possibilities exist at all times.

    Functional constraint.Alpha actin 1 humans mice rats 100% alignment.

    ??? What I asked, once again, is why would any incremental change become more unlikely given any particular history of past changes. What mysterious force clamps the lid on mutations to complex systems but not on simple systems? Your response about mice is such a complete non-sequitur that I can only believe you can’t read.

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  40. Moved a comment to guano. Moderation is discussed only in the moderation issues thread.

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  41. Corneel: “If I type the number into my calculator the result I get is infinity”

    “Infinity, an imaginary number”
    -Bill Cole

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  42. Flint,
    .

    You keep confusing the probability of some particular result with the probability of ANY result at all. This is a concept nobody has been able to get through to you. But here in reality, everything that happens lies at the end of a long sequence of vanishingly unlikely prior conditions.

    I don’t think this concept has any grounding in reality. Life could have gone any direction is a high level flawed concept that is necessary because of the problems the cell causes for evolutionary stories. Proteins are interdependent on other proteins. Myosin the muscle protein depends on the other proteins actin and titin.

    I thought my illustration wasn’t all that difficult to grasp, but I guess I was wrong. What infinite number of locations did the tossed ball land in? Again, you are assuming that what happens is the only thing that COULD happen.

    The issue is you are proposing a probabilistic mechanism trying to find function in infinite mathematical space. This environment requires a deterministic mechanism. You’re breaking a lock by random trial is very difficult. If you know the combination it is much easier.

    Not true at all. Infinite RESULTS take time. Infinite possibilities exist at all times.

    You’re claiming infinite possibilities yet biology has finite possibilities. Once you have myosin the actin proteins sequence becomes defined as it needs to successfully interact with myosin.

    ??? What I asked, once again, is why would any incremental change become more unlikely given any particular history of past changes. What mysterious force clamps the lid on mutations to complex systems but not on simple systems? Your response about mice is such a complete non-sequitur that I can only believe you can’t read.

    Why do you think these changes are not happening. It’s because of deleterious mutations that are not getting fixed in the population. Many biological systems operate with high precision. This idea of almost infinite possibilities is a fairy tale.

    The mice response is something you don’t understand. It is showing 50 million years of evolution with hundreds of different populations and no fixed mutations. This is caused by functional constraint and is how biology really works. How does this protein evolve. It doesn’t and it is showing evolutions high level concepts are not supported by the data.

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  43. DNA_Jock,

    As we have explained to you previously, the size of the space doesn’t matter. At all.

    So a 2 digit lock is as hard to beak as a 10 digit lock. A lotto game with 5 balls is as easy to win as one with 20 balls. A protein binding ATP is as easy as a protein that interacts with 10 different proteins?

    Why in the world would someone with your intelligence and education make such claims? Where is the win here?

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  44. colewd: So a 2 digit lock is as hard to beak as a 10 digit lock.

    You’re both changing the size of the space AND the frequency of functions there, so your analogy simply begs the question.

    But for biological polymers, the frequency of function is not 1 in size of space.

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  45. colewd: A protein binding ATP is as easy as a protein that interacts with 10 different proteins?

    No, a protein that interacts with 10 different proteins is much easier.

    The natural tendency is for proteins to aggregate. They are inherently sticky entities. So much so that it is thought natural selection is generally against it as it can interfere with the normal functions of these proteins.

    Carija A, Pinheiro F, Iglesias V, Ventura S. Computational Assessment of Bacterial Protein Structures Indicates a Selection Against Aggregation. Cells.
    2019 Aug 8;8(8). pii: E856. doi: 10.3390/cells8080856. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6721704/

    The introduction to this article gives a nice overview:

    Proteins are central components of almost all biological processes, being involved in a variety of complex interactions in the crowded cellular environment [1]. The establishment of non-functional protein–protein interactions has a detrimental impact on cell fitness, both because these contacts sequester proteins into inactive complexes [2] and because it can lead to the aggregation or co-aggregation of proteins into toxic soluble and insoluble assemblies [3]. Importantly, it is increasingly evident that, instead of being an unusual feature of a reduced set of proteins, aggregation is a generic property of many polypeptides [4]. Accordingly, hundreds of unrelated proteins have been reported to aggregate under stress or during ageing [5,6,7]. It has been suggested that this intrinsic propensity to establish anomalous interactions and aggregate is encoded in the amino acid sequence [8,9,10] and, therefore, a variety of complementary methods have been developed to predict those propensities from the linear sequence [11]. Large-scale analysis using these algorithms has led to the hypothesis that proteins have evolved sequence adaptations to counteract their natural propensity to aggregate [12,13,14]. Because in these studies aggregation is analysed along sequences, they mostly measure the aggregation potential of the unfolded state; indeed, the aggregation-prone regions (APRs) that these algorithms identify and evaluate are blocked in properly folded proteins, either because they are buried inside the hydrophobic core or engaged in the series of cooperative non-covalent interactions that sustain the secondary and tertiary protein structure [15]. These sticky sequences might, however, become accessible in case the protein fails to fold due to translational errors. Accordingly, prevention of mistranslation-induced protein misfolding is thought to constraint the evolution of sequences [16,17]. However, it is worth to point out that protein aggregation is not always deleterious and different organisms have exploited the structural/mechanical properties of protein aggregates for functional purposes [18,19].

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  46. colewd:
    I don’t think this concept has any grounding in reality.

    It’s the other way around. We’re surrounded by options to the point where many people go nuts. It’s also the other way around in this discussion. if you think that the sequence you see is the one and only possible solution, then it’s on you to prove it so.

    colewd:
    Life could have gone any direction is a high level flawed concept that is necessary because of the problems the cell causes for evolutionary stories.

    You’re an artist condensing mistaken notions on top of one another in very short sentences. The issue is not whether life could have gone any direction, the issue is that you don’t understand that what you see today is not necessarily the one and only possible functional protein/system/etc.

    The concept comes from the way evolution works, not because of some “problem” you imagine that the cell gives to evolutionary “stories.”

    The “problem” you “propose” is flawed thinking in the first place. It’s ignoring that evolution is not about having each protein in a human coming about from a random soup of amino-acids in one go. We, humans, are newcomers. We don’t come from a soup of random amino-acids. We come from an exceedingly long lineage, with an exceedingly long chain of successful adaptations. That we have complex systems doesn’t come up as a surprise, let alone as a “problem” for any evolutionary biologist. It’s a natural outcome of the way evolution happens. Evolutionary biologists could not care less that you imagine problems where there are none. They actually have to think a lot in order to understand what you’re talking about. For biologists it’s a surprise that somebody would imagine that each function can only be performed by a single one protein. Thus they have no need to “invent” “flawed” concepts to rescue their scientific field.

    colewd:
    Proteins are interdependent on other proteins. Myosin the muscle protein depends on the other proteins actin and titin.

    So what? The state of some system doesn’t say anything about how the system got there. It just tells you what it’s like today, or, worse, just in those organisms you mention. Take the analysis a bit beyond that and presto, you see all kinds of variations in the theme and, worse, variations that betray potential routes to the one you’re so adamant to point.

    colewd:
    The issue is you are proposing a probabilistic mechanism trying to find function in infinite mathematical space.

    Nope. It’s you who’s proposing evolution as a random tossing of amino-acid “coins.” Evolutionary biologists propose a background of unplanned mutations, selection forces, and, very importantly, the cumulative effect of long lineages. This is why they try and find different versions of the proteins that so much worry you (and they do find them), of the systems that so much worry you (and they find them!). They don’t stop at “oh, actin and myosin are stuck from mice to humans!” They look around for clues. You’d rather have them staying with a particular version of actin, the one that has 100% identity with the mice one, and a particular version of myosin, again, the one that’s 100% identical to its counterpart in mice.

    It must be frustrating to you that they look around and find potential answers after potential answers, but scientists are just like that. They don’t stop looking because they really want to know, and because they know they’ll eventually find clues, and wow, they do find some pretty convincing clues. To a reasonable person that is.

    Good night.

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  47. Rumraket,

    No, a protein that interacts with 10 different proteins is much easier.

    Are you claiming this as a general rule :-). I think you need to cite papers of eukaryotic cells more often.

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