Over-egging the case for protein design

Recently, I was browsing through the latest posts over at Evolution News and Views, and an anonymous article titled, Imagine: 60 Million Proteins in One Cell Working Together, caught my eye. By now, most readers at TSZ will be aware that I consider it overwhelmingly likely that the first living thing was designed. However, I’m also highly critical of attempts to over-egg the case for intelligent design. The article I read was one such attempt: it contained some unfortunate errors and omissions.

The author tried to bolster his case by quoting from two articles in the same issues of Nature (volume 537, 15 September 2016): one by Aebersold & Mann, and the other by Huang, Boyken, and Baker. As it turned out, neither paper was about the origin of life: one was about the proteome (or the set of all the proteins in a cell), while the other discussed de novo protein design.

How many proteins are there in a single cell? And how many are needed?

The ENV article was titled, Imagine: 60 Million Proteins in One Cell Working Together. When I first saw that headline, I was a little puzzled. When I hear the phrase, “60 million proteins,” I automatically assume the speaker means different kinds of proteins. But what the author actually meant was: 60 million protein molecules inside a single cell.

“What kind of cell?” you may ask. Apparently the figure of 60 million is taken from a passage in the Nature article by Aebersold & Mann, where the authors are relating some astonishing facts about the proteins in a tiny yeast cell:

A proliferating Schizosaccharomyces pombe cell contains about 60 million protein molecules, which have abundances that range from a few copies to 1.1 million copies per expressed gene.

However, yeast cells are eukaryotic: they have a nucleus. The first living thing didn’t: it was prokaryotic, and it would have been much smaller than a yeast cell. How much smaller? We don’t know. But it turns out that the number of protein molecules in a tiny cell belonging to the bacterium Mycoplasma pneumoniae is only 0.05×106, or just 50,000. That’s three orders of magnitude less than the yeast cell described by Aebersold & Mann.

But the real question we need to ask is: how many different kinds of proteins are there in a simple bacterial cell? It turns out that a typical bacterium requires 4,000 proteins for growth and reproduction, while humans require more than 100,000 different kinds of proteins. Some bacteria, however, need far fewer than 4,000 proteins, according to MicrobeWiki:

In 1995, the entire genome of M. genitalium was sequenced in less than 6 months using the random shotgun sequencing technique. It was found to have the smallest known genome of any free-living organism at about 580 kilobase pairs long, with 479 coding sequences for proteins. For comparison M. pneumoniae has 677 protein coding sequences, H. influenzae has 1703, and E. coli K-12 has 4,288.

382 of the 482 protein-coding genes in Mycoplasma genitalium have since been identified as essential. Dr. Stephen Meyer, in his work, Signature in the Cell (New York: HarperOne, 2009), generously estimates (ibid., p. 213) that a minimally complex cell needs 250 different kinds of proteins. Dr. Michael W. W. Adams, in an article titled, The Influence of Environment and Metabolic Capacity on the Size of a Microrganism, makes a similar estimate: in a nutrient-rich environment, a life-form with a minimal biosynthetic capacity would require at least 250 genes.

So the first cellular life-form probably required 250 different kinds of proteins, in order to function. That’s still a pretty impressive number.

What proportion of amino acid sequences are functional?

The Evolution News and Views article refers to the recent article by Huang, Boyken, and Baker, before going on to cite the pioneering work of Intelligent Design researcher, Dr. Douglas Axe:

This paper is interesting because it relates to the work of Douglas Axe that resulted in a paper in the Journal of Molecular Biology in 2004. Axe answered questions about this paper earlier this year, and also mentioned it in his recent book Undeniable (p. 54). In the paper, Axe estimated the prevalence of sequences that could fold into a functional shape by random combinations. It was already known that the functional space was a small fraction of sequence space, but Axe put a number on it based on his experience with random changes to an enzyme. He estimated that one in 1074 sequences of 150 amino acids could fold and thereby perform some function — any function.

I’ll return to Dr. Axe’s estimate in a moment. The Evolution News and Views article went on to breathlessly declare that Axe’s figure of 1 in 1074 had actually been too generous, and that the true proportion of 150-aa sequences capable of performing a biological function was hundreds of orders of magnitude smaller (green bolding below is mine – VJT):

The new paper in Nature seems to point to a much smaller functional space. The authors say,

It is useful to begin by considering the fraction of protein sequence space that is occupied by naturally occurring proteins (Fig. 1a). The number of distinct sequences that are possible for a protein of typical length is 20200 sequences (because each of the protein’s 200 residues can be one of 20 amino acids), and the number of distinct proteins that are produced by extant organisms is on the order of 1012. Evidently, evolution has explored only a tiny region of the sequence space that is accessible to proteins.

Since 20200 is about 10260, and the space actually sampled by living organisms is 1012, the numbers differ by at least 240 orders of magnitude for proteins of length 200, or about 183 orders of magnitude the 150-amino-acid chains Axe used. No wonder the authors say that “the natural evolutionary process has sampled only an infinitesimal subset” of sequence space.

This, I have to say, is a complete misreading of the paper in Nature by Huang, Boyken, and Baker. The authors are not trying to answer the question explored by Axe – namely, what proportion of 200-amino acid sequences are capable of performing a useful biological function? Rather, what they are estimating is the proportion of possible 200-amino acid sequences which are found in nature. Their answer is: 1012 divided by 20200 (which is approximately 10260), or in other words, 1 in 10248. But instead of concluding that any amino acid sequences which are not found in nature are non-functional, as the writer of the Evolution News and Views article appears to do, they draw the opposite conclusion: “The huge space that is unlikely to be sampled during evolution is the arena for de novo protein design.” In other words, there are a whole lot of new proteins out there which nature hasn’t created yet, but which scientists can create.

Back to Dr. Axe’s estimate of the proportion of 150-amino acid sequences which are capable of performing a biological function: I have previously discussed his figure of 1 in 1074 in my online review of his latest book, Undeniable: How Biology Confirms Our Intuition That Life Is Designed (New York: HarperOne, 2016). I quoted from various professors, including an expert in protein structure who argued that the proteins in the first living things would have all contained considerably less than 100 amino acids:

So I think the counterargument to the ID folks is not that sequence populations of 10E80 needed to be searched to find a 100-mer with robust enzyme activity, but rather that random populations of a few million relatively small proteins could contain a few molecules from which to start the evolutionary process.

Another professor whom I cited regarded Dr. Axe’s work as highly biased, because he had based his studies and calculations on very large sequences of amino acids (150-amino acid chains), even though much shorter sequences (such as polypeptides) were known to have biological functions.

Additionally, I quoted from a third professor, who kindly pointed out to me that because a very large number of different amino acid sequences were capable of performing the same biological function, the actual number of attempts that would be required to make a molecule with the same function as one of these proteins was likely to be much lower than 1060 or 1080. This professor also estimated that the number of attempts that would have been available to evolution had been estimated at 1042 – far greater than the number of attempts that could be made by doing man-made experiments (no more than 1012, which means that any protein which is too difficult for human experiments to generate might still be created by natural processes). This professor added that that while he was very sympathetic towards arguments against the natural origins of the first cell, and while he thought Dr. Axe may well be correct in arguing that abiogenesis was astronomically unlikely, in his opinion, Dr. Axe seemed to be trying to calculate the probability of an unknown process, and was therefore overstating his case.

Bottom line: we don’t really know how rare functional 150-amino-acid proteins are in sequence space, and we don’t know that they couldn’t have been derived from shorter proteins.

How did life get to be left-handed?

The Evolution News and Views article went on to say that there were

Axe’s estimate of one in 1074, one must note, referred to mutations to existing proteins in the universal proteome of all organisms. When considering random chains of amino acids in a primordial soup, however, Steve Meyer noted in Signature in the Cell (pp. 210-212) two other requirements. The amino acids must be one-handed, and they must form only peptide bonds. Applying generous probabilities of 0.5 for handedness and 0.5 for peptide bonds, Meyer reduced the probability for a lucky functional protein chain of 150 amino acids to one in 10164, far beyond the universal probability bound (p. 212). [Green bolding mine – VJT.]

The problem of life’s one-handedness which Dr. Meyer raises in his book is a genuine one: without homochirality, life would not exist.

A recent article by Denise Henry in Phys.org, titled, Discovery demystifies origin of life chirality phenomenon (March 11, 2015) describes a promising breakthrough in the field:

University of Akron A. Schulman Professor of Polymer Science Tianbo Liu has discovered that Mother Nature’s clear bias toward certain amino acids and sugars and against others isn’t accidental.

Liu explains that all life molecules are paired as left-handed and right-handed structures. In scientific terms, the phenomenon is called chirality…

Liu found that any molecules, if large enough (several nanometers) and with an electrical charge, will seek their own type with which to form large assemblies. This “self-recognition” of left-handed and right-handed molecule pairs is featured in the March 10, 2015, issue of Nature Communications.

“We show that homochirality, or the manner in which molecules select other like molecules to form larger assemblies, may not be as mysterious as we imagined,” Liu says.

In their paper, Liu et al. summarized their results as follows:

In summary, chiral macroanions demonstrate chiral recognition behaviour by forming homogeneous blackberry structure via long-range electrostatic interactions between the individual enantiomers in their racemic mixture solutions. Adding chiral co-anions suppresses the self-assembly of one enantiomer while maintaining the assembly of the other one. This leads to a natural chiral selection and chiral amplification process, indicating that some environmental preferences can lead to a complete chiral selection. The fact that the relatively simple inorganic macroions exhibit chiral recognition and selection during their assembly process indicates that the related features of biomacromolecules might be due to their macroionic nature via long-range electrostatic interactions

Another, more recent paper in Chemistry World by Dr. Rachel Brazil, titled, The origin of homochirality provides an excellent overview of the work in the field done to date, and discusses new findings. Dr. Brazil puts forward her own hypothesis.

Readers may still be wondering: why are the amino acids in a protein linked by peptide bonds, instead of non-peptide bonds? I’d like to invite any biologists who may be reading this post to weigh in on this subject.

What the ENV article got right

The Evolution News and Views article redeems itself at the very end, when quoting from the paper by Huang, Boyken, and Baker. The authors state:

Despite the advances in technology of the past 100 years, human-made machines cannot compete with the precision of function of proteins at the nanoscale and they cannot be produced by self-assembly.

The authors go on to suggest that the extreme efficiency of these nanoscale proteins is the due to the fact that “selective pressure operated on randomly arising variants of primordial proteins, and there were also hundreds of millions of years in which to get it right.” But this is pure speculation. As the author of the ENV article aptly puts it:

Now ponder that. They are duly impressed by the intricate molecular machines that proteins make in the cell, yet their worldview does not allow them to consider this as evidence for design.

Indeed.

What I am arguing in this post is that while I see no reason in principle why nature cannot generate proteins capable of performing useful biological functions, and while the mathematical arguments against such proteins originating by natural processes strike me as inconclusive, it seems to me perfectly reasonable to ask why the proteins we observe in nature are capable of technical feats which even our best scientists cannot match. It is not enough to simply invoke “hundreds of millions of years”: this is lazy scientific thinking, which makes no testable predictions. In the absence of such predictions, intelligent design of these nano-machines by a super-intellect sounds like a plausible explanation which warrants consideration.

Here’s one questions I’d like to ask the biologists: do the most efficient nanoscale molecular machines tend to be relatively short (as we’d expect if they arose naturally) or relatively long?

Readers who would like to know more about the difficulties attending abiogenesis are welcome to view Dr. James Tour’s online talk, “The Origin of Life – An Inside Story,” here or here. The take-home message of Dr. Tour’s talk was that currently, scientists know nothing about how the ingredients of life originated, let alone life itself. Dr. Tour makes no attempt to “sell” intelligent design to his audience: indeed, he formulates his argument without even mentioning it. Readers will find it highly watchable.

232 thoughts on “Over-egging the case for protein design

  1. keiths, to Vincent:

    Have you read Andreas Wagner’s book Arrival of the Fittest?

    Erik:

    From your link: “Natural selection can preserve innovations, but it cannot create them. Nature’s many innovations—some uncannily perfect—call for natural principles that accelerate life’s ability to innovate.”

    So, nature has innovations even though it cannot create them. Where did the innovations come from then?

    You’re conflating “natural selection” with “nature”.

    Why would he say that? Is he an ID-ist?

    No, and his book is actually a bit of a nightmare for IDers, particularly those who cling to “islands of function”-style arguments.

    I highly recommend it.

  2. A few general comments – I haven’t time to debate, and feel this is an argument I have been round a few dozen times:

    – The rate of spontaneous protein hydrolysis in water is pretty irrelevant, other than to theories that see peptides forming long catalytic chains as a first step. These theories have far greater problems than the thermodynamics of the peptide bond. Not least, the problem of repeat specification, but also the difficulty of achieving alpha linkages consistently in (chemical) species that have more than one amino or carboxyl group. Not that a catalytic peptide is restricted to alpha linkages, of course, but that seems to be the kind of thing people are imagining. We have alpha chains (and L-isomerism) because of the ribosome. Which is RNA. Astute readers may see where I’m headed with that line of argumentation, and may be riffling through their papers as I speak to ‘prove’ that RNA molecules’ own thermodynamic issues close down that avenue too. I can see a post from Sal, complete with pretty picture at the end! Be that as it may, protein chemistry in solution is totally irrelevant in an RNA-first scenario.

    – whatever the thermodynamic difficulties of a non-ID version of life, the thermodynamic difficulties faced by a Designer should not be ignored. If one determines that a complex system of (say) 250 peptides needs to be manoeuvred in place, complete with a functional energy cascade, there is a problem of assembling the machine before allowing ‘current’ to flow through it. It is in the nature of these species to react whenever they come into proximity. These aren’t the components of a jumbo jet. These are molecules. So it bugs me somewhat to see people appeal to thermodynamics in their critiques, while then completely ignoring it. “Oh … it’s just Design, you know? Intelligence. And … er … stuff”.

    – In general, anti-evolutionists seem unable to think in evolutionary terms. That’s maybe part of why they are anti-evolutionists, of course. But it should be obvious that the remnants of a precursor system are not generally expected to be found in the simplest modern exemplar, in any system that has been churning away for a few billion years. Because – you know – evolution. Which includes Natural Selection. Simple evolutionary explanations should be considered by the critic. It should not always be the defender of evolution that brings them up. Why are there no RNA-only organisms? Extinct, mate. Why are there no short catalytic peptides? Improvements to basic function occupy bits, old bean. And so on …

  3. Tom English,

    Please, not that again.

    The Rules: We need a trusted third party for the holding of said bottom dollar. We also need sworn affidavits that said dollar is indeed the bottom one. Furthermore …

  4. keiths: You’re conflating “natural selection” with “nature”.

    So, nature can innovate by some other mechanism than natural selection. What is that other mechanism?

  5. Erik: So, nature can innovate by some other mechanism than natural selection. What is that other mechanism?

    Actually I think keiths is saying that natural selection CAN innovate (in the metaphorical sense). If he’s not, I have no idea what you two are arguing about.

  6. Rumraket: Actually I think keiths is saying that natural selection CAN innovate (in the metaphorical sense). If he’s not, I have no idea what you two are arguing about.

    “Natural selection can preserve innovations, but it cannot create them. Nature’s many innovations—some uncannily perfect—call for natural principles that accelerate life’s ability to innovate.” – Andreas Wagner, Arrival of the Fittest

    Natural selection, as stated, cannot create innovations. Nature and life apparently can. By what mechanism? And this is an evolutionist we are talking about, not an ID-ist.

  7. I can’t believe that our local ID crowd is so effing stupid that they can’t detetect a book jacket blurb designed to entice. In other words, to sell books.

    As they say in Star Wars, It’s a trap.

  8. Erik: Natural selection, as stated, cannot create innovations. Nature and life apparently can. By what mechanism? And this is an evolutionist we are talking about, not an ID-ist.

    Ahh okay I see what you’re asking.

    The answer is mutation (and in the case of sexual reproduction, genetic recombination). Natural selection if looked at in isolation obviously is not a creative process, since by definition selection is restrictive. Only some things make it. So to get something new, to get “innovation” you need a process of creation, something that creates new stuff that natural selection can select among. That creative process would be mutation and recombination.

  9. Vj,

    If I can show some reasons why I take estimates of the number of functional amino acids with a grain of salt, see the diagram below and reasons I would be saying that depending on the protein, Doug Axe’s estimates could be understated, especially for Eukaryotic proteins.

    Problematic in defining “function” is how we might tally the things that are important. An experiment can easily focus on only one aspect of a protein, and it could be decades before we realize the importance of other aspects. It may be fair to say many proteins, especially in Eukaryotes are poly functional in ways we are just learning. The approach of measuring protein functionality taken by some is like looking at a smart phone as purely a time keeping device!

    After several decades, we realized a class of proteins called histones had enormous function which we did not realize. Many of the amino acids on the tail of a histone can act as a memory device through chemical enhancements. Suffice to say also, the other amino acids on the tail of a histone are probably necessary as part of a road sign for the machines that dock on the histone and modify the random access memory of the histone.

    These class of proteins, histones, implement the histone code in Eukaryotes.
    https://en.wikipedia.org/wiki/Histone_code

    Unlike this simplified model, anaeal histone code has the potential to be massively complex; each of the four standard histones can be simultaneously modified at multiple different sites with multiple different modifications. To give an idea of this complexity, histone H3 contains nineteen lysines known to be methylated — each can be un-, mono-, di- or tri-methylated. If modifications are independent, this allows a potential 419 or 280 billion different lysine methylation patterns, far more than the maximum number of histones in a human genome (6.4 Gb / ~150 bp = ~44 million histones if they are very tightly packed). And this does not include lysine acetylation (known for H3 at nine residues), arginine methylation (known for H3 at three residues) or threonine/serine/tyrosine phosphorylation (known for H3 at eight residues), not to mention modifications of other histones.
    Every nucleosome in a cell can therefore have a different set of modifications, raising the question of whether common patterns of histone modifications exist. A recent study of about 40 histone modifications across human gene promoters found over 4000 different combinations used, over 3000 occurring at only a single promoter. However, patterns were discovered including a set of 17 histone modifications that are present together at over 3000 genes.[13] Therefore, patterns of histone modifications do occur but they are very intricate, and we currently have detailed biochemical understanding of the importance of a relatively small number of modifications.
    Structural determinants of histone recognition by readers, writers and erasers of the histone code are revealed by a growing body of experimental data.

    You can see a visual depiction of the memory unit below. It is becoming apparent that especially in Eukaryotes, where proteins are enhanced with sugars, that the sort of massive information processing for each histone may be the norm for many Eukaryotic proteins.

    I have to caution that some of the accounting of functionality of proteins is a bit simplistic in the evolutionary literature. You will see the amino acids individually labeled (with a number for he exact position of amino acid) along with the possible chemical modifications that enable a chemical “bit” to be flipped on and off. These bits are written and read to with a suite of molecular machines. The amino acids in those histones that aren’t modified are likely quite important to providing navigation road signs to help park the molecular machines on them.

    Bottom line: the numbers you’re seeing today in these debates could be a little premature, inaccurate, and likely understated in terms of actual complexity of the protein function. Histones are a good illustration of how a few decades of research will reveal heretofore unknown functionality.

  10. Tom English: “For my thoughts are not your thoughts, neither are your ways my ways,” declares the LORD.

    And boy did he ever get that one right!

    Great post, btw, probably deserving of an OP. I’m certainly going to save it. But no mention of cumulative selection making the highly improbable, probable.

  11. Allan Miller: In general, anti-evolutionists seem unable to think in evolutionary terms. That’s maybe part of why they are anti-evolutionists, of course. But it should be obvious that the remnants of a precursor system are not generally expected to be found in the simplest modern exemplar, in any system that has been churning away for a few billion years.

    Yup. Eukaryotes first!

  12. Vj,

    I mentioned proteins and sugars. In eukaryotes half the proteins are enhanced with sugars. There are terms like glycoproteins and proteoglycans, etc.

    Below is a proteoglycan. The protein is the little grey sliver in the middle of the diagram to which several blue chains of sugars are attached. It can be seen here the importance of individual amino acid residues on the protein. Also it may be fair to say the parts of protein that aren’t attached to sugars are probably pretty important as road signs and navigation aids to helping the molecular machines attach the right sugars to the right place on the protein!

    There is the emerging science to study the sugar code. The sugars are information processing and signaling molecules in the cell. The sugar proteins complexes are part of a massive information computational complex we are only beginning to figure out.

  13. petrushka: I can’t believe that our local ID crowd is so effing stupid that they can’t detetect a book jacket blurb designed to entice. In other words, to sell books. As they say in Star Wars, It’s a trap.

    … natural selection is not a creative force. It does not innovate, but merely selects what is already there. Darwin realized that natural selection allows innovations to spread, but he did not know where they came from in the first place.

    – Wagner, p. 14.

    Chapter 2 in the book is The Origin of Innovation. Just a book jacket blurb? Laughable.

  14. stcordova: There is the emerging science to study the sugar code. The sugars are information processing and signaling molecules in the cell. The sugar proteins complexes are part of a massive information computational complex we are only beginning to figure out.

    You’re just stringing words together, clawing terms and ideas out of your rectum as you go along.

    “sugar proteins complexes”
    “massive information computational complex”

    Can I throw up now? Seriously, what’s it like to just sit there and make shit up? Doesn’t it bother you that to defend your fundamentalist creationist doctrine if you feel a need to lie to do it?

  15. Hi Mung,

    Thank you for your comments. Re cumulative selection: this gets to the nub of the matter, as far as the biological case for intelligent design is concerned. But showing that cumulative selection occurred does not, of itself, discredit the design hypothesis. One also has to consider the possibility that the pathway leading to the product may have itself been designed.

  16. Hi Tom English,

    You wrote:

    Evolutionary biologists are not saying that evolution has some magical power for hitting prespecified targets. They’re saying that the vast majority of species that have existed are now extinct. They’re saying that there probably are vastly more folding proteins than evolution has “stumbled upon” (to use a term that Axe did in the video where he explained that evolutionary “search” doesn’t really search). I am saying that biological evolution is vastly more likely to stumble upon something that we regard as wondrous after the fact than to stumble upon something wondrous that we specify in advance.

    I very much agree with you here. I made a related observation in my review of Axe’s book, when I wrote:

    The point I want to make here is that even if we exclude possible life-forms with no plausible evolutionary predecessors (i.e. targets which will never be reached, no matter how much time is available) as well as life-forms whose emergence, on the most optimistic scenario, would require a fantastically long time (a “gazillion” years, as Axe puts it), we may still be left with a very large number of target life-forms which might be reached, over an interval of four billion years. Obviously, these reachable targets would comprise only a minuscule proportion (at best) of the set of all possible life-forms, but even a very small proportion of a fantastically large number of targets may turn out to be quite a large number of targets. All evolution has to do is hit some of these targets.

    Finally, even if Axe’s argument purporting to show that accidental inventions are fantastically improbable were valid, it would still only apply to accidental inventions in general. A much stronger argument is needed to show that each and every accidental invention is fantastically improbable. By definition, the inventions generated by a blind evolutionary process will tend to be the ones whose emergence is most likely: the creme de la creme, which make up only a tiny proportion of all evolutionary targets. For these targets, the likelihood of success may be very low, but not fantastically improbable.

    You also wrote:

    …What fraction of the possible sequences correspond to folding proteins is irrelevant to the adequacy of an evolutionary account. What’s relevant is the probabilities of individual transitions that actually have occurred (more accurately, the expected waiting times for the transitions to occur).

    I think this argument moves too quickly. Consider a sequence of 100 heads when tossing coins and you’ll see what I mean. Each step is reasonably probable, but we’d never believe someone who claimed to have tossed 100 heads in a row.

    You last point is an interesting one:

    …[W]hatever the thermodynamic difficulties of a non-ID version of life, the thermodynamic difficulties faced by a Designer should not be ignored. If one determines that a complex system of (say) 250 peptides needs to be manoeuvred in place, complete with a functional energy cascade, there is a problem of assembling the machine before allowing ‘current’ to flow through it. It is in the nature of these species to react whenever they come into proximity. These aren’t the components of a jumbo jet. These are molecules. So it bugs me somewhat to see people appeal to thermodynamics in their critiques, while then completely ignoring it. “Oh … it’s just Design, you know? Intelligence. And … er … stuff”.

    Near the end of my UD post on Dr. Tour’s talk on abiogenesis, I discussed the possibility that it might prove to be impossible to assemble a living cell step-by-step – in which case, I speculated, this would seem to indicate the existence of a transcendent Creator Who must have created life holus bolus. I emailed Dr. Tour about this and he agreed the idea was intriguing. Thoughts?

  17. Hi keiths,

    Thank you for your comment. You write:

    I think we should follow the evidence where it leads, and there’s no reason that science can’t handle supernatural hypotheses as long as they are testable.

    Have you read Andreas Wagner’s book Arrival of the Fittest?

    I agree with you that science is perfectly capable of handling the supernatural, should the need arise. Larry Moran and Jerry Coyne agree as well. There is a risk for believers that science may throw up evidence which discredits belief in the supernatural, but that’s a risk I think believers have to accept.

    I haven’t read Andreas Wagner’s latest book. I order about one book a year via Amazon. How I wish there were a cheap way of getting hold of books! Anyway, I should mention for the benefit of readers that Dr. Axe discusses Wagner’s book on pages 222-223 of Undeniable. To cut a long story short, he takes exception to the following statement by Wagner:

    With a limited number of building blocks connected in a limited number of ways, you can create an entire world. Out of such building blocks and standard links between them, nature has created a world of proteins, regulation circuits, and metabolisms that sustain life, that has brought forth simple viruses and complex humans, and ultimately, our culture and technology, from the Iliad to the iPad.

    Axe objects (p. 224) that this would be like saying that alphabet soup is capable of giving rise to oracles. But as I wrote in my review, this is a poor analogy:

    …[T]he number of ways in which parts can be arranged to perform a useful function is much, much larger than the number of ways in which letters can be arranged in order to convey a meaning. In other words, the emergence of a system of parts that can perform a function is a much more likely event than the emergence of a sequence that can convey a message…

    In order for an accidentally generated string of letters to convey a meaningful message, it needs to satisfy three very stringent conditions, each more difficult than the last: first, the letters need to be arranged into meaningful words; second, the sequence of words has to conform to the rules of syntax; and finally, the sequence of words has to make sense at the semantic level: in other words, it needs to express a meaningful proposition. For a string of letters generated at random to meet all of these conditions would indeed be fantastically improbable. But here’s the thing: living things don’t need to satisfy any of these conditions. Yes, it is true that all living things possess a genetic code. But it is quite impossible for this code to generate anything like nonsense words like “sdfuiop”, and additionally, there is nothing in the genome which is remotely comparable to the rules of syntax, let alone the semantics of a meaningful proposition. The sequence of amino acids in a protein needs to do just one thing: it needs to fold up into a shape that can perform a biologically useful task. And that’s it. Generating something useful by chance – especially something with enough useful functions to be called alive – is a pretty tall order, but because living things lack the extra dimensions of richness found in messages that carry a semantic meaning, they’re going to be a lot easier to generate by chance than (say) instruction manuals or cook books. Hence it may turn out that creating life by chance is extremely improbable, but not fantastically improbable. In practical terms, that means that given enough time, life just might arise.

    ID proponents need to drop the alphabet soup metaphor. It doesn’t help our case.

  18. Hi Sal,

    Thank you very much for your biological illustrations. I was very much impressed with the following passage:

    We can make several enzymes that catalyze the same reaction, but some can be made more excessively complex than needed. Just like we can build time keeping devices with a few parts, we can build them with hundreds of parts.

    I raise this issue because there is an unfortunate focus on trying to say one small enzyme (say a few hundred amino acids) can do the same job a big enzyme (a thousand amino acids). The insinuation being the big enzyme doesn’t need all its parts. But this is like saying a Swiss watch doesn’t need all its parts because a sundial can also keep time. Or that a 100-part Swiss watch can keep track of time, therefore a 200-part Swiss watch doesn’t need all 200 of its parts. There is some illogic here in the way some are estimating enzyme or protein complexity.

    …Sure, we can imagine simpler systems, but the real problem for OOL is why an extravagant one emerged. Why did an atomic clock emerge when a sundial would have sufficed?

    That is indeed a valid question. Why is it that life is so much more complex at the biochemical level than it needs to be, in order to metabolize, replicate and undergo Darwinian evolution? When one examines the world of proteins, life seems to exhibit a surfeit of riches. One explanatory hypothesis that comes to mind is that this surfeit was intended as a signal, pointing to the fact that life was designed. I’m inclined to agree.

    That said, how would you respond to Alan Miller’s point above? He writes: “Why are there no RNA-only organisms? Extinct, mate. Why are there no short catalytic peptides? Improvements to basic function occupy bits, old bean. And so on…” Of course, this presupposes (a) the existence of stepping stones to present-day life-forms, and (b) that said stepping stones are utterly unremarkable, from a chemical standpoint.

  19. Rumraket:

    You’re just stringing words together, clawing terms and ideas out of your rectum as you go along.

    “sugar proteins complexes”
    “massive information computational complex”

    Can I throw up now? Seriously, what’s it like to just sit there and make shit up? Doesn’t it bother you that to defend your fundamentalist creationist doctrine if you feel a need to lie to do it?

    Can I throw up now? Seriously, what’s it like to just sit there and make shit up?

    By all means please throw up. 🙂

    But I’m not make these terms up starting with the Sugar Code. Read and weep:

    https://www.ncbi.nlm.nih.gov/pubmed/10798195
    Biological information transfer beyond the genetic code: the sugar code.

    In the era of genetic engineering, cloning, and genome sequencing the focus of research on the genetic code has received an even further accentuation in the public eye. In attempting, however, to understand intra- and intercellular recognition processes comprehensively, the two biochemical dimensions established by nucleic acids and proteins are not sufficient to satisfactorily explain all molecular events in, for example, cell adhesion or routing. The consideration of further code systems is essential to bridge this gap. A third biochemical alphabet forming code words with an information storage capacity second to no other substance class in rather small units (words, sentences) is established by monosaccharides (letters). As hardware oligosaccharides surpass peptides by more than seven orders of magnitude in the theoretical ability to build isomers, when the total of conceivable hexamers is calculated.

    And Glycoproteome is a real term. See here:

    and the journal of Celluar and Molecular Proteomics:

    Mass Spectrometry Based Glycoproteomics—From a Proteomics Perspective

    Glycosylation is one of the most important and common forms of protein post-translational modification that is involved in many physiological functions and biological pathways….

    While glycomics is the study of glycome (repertoire of glycans), glycoproteomics focuses on studying the profile of glycosylated proteins, i.e. the glycoproteome, in a biological system.
    ….
    Most secretory and membrane-bound proteins produced by mammalian cells contain covalently linked glycans with diverse structures (2). The glycosylation form of a glycoprotein is highly specific at each glycosylation site and generally stable for a given cell type and physiological state. However, the glycosylation form of a protein can be altered significantly because of changes in cellular pathways and processes resulting from diseases, such as cancer, inflammation, and neurodegeneration.

    And from the proceedings of the National Academy of Science, 2012, there is even O-glycoproteomics:

    Moving the O-glycoproteome from form to function
    Life scientists who study carbohydrate structures are all too accustomed to hearing, “So, what things good for anyway?” In PNAS, Schjoldager et al. (1) provide an elegant comeback by using a unique strategy for mapping the location of O-GalNAc–linked carbohydrate structures to show how the addition of GalNAc to specific Ser and Thr residues by one of 20 polypeptide GalNAc-transferases (ppGalNAc-Ts) can modulate the biologic activity of the modified glycoprotein. The consequences can be dramatic, for example, altering cholesterol or triglyceride metabolism and thus exerting a significant effect on human health parameters.

    Carbohydrate structures O-glycosidically linked through N-acetylgalactosamine (i.e., GalNAc) to Ser or Thr residues were first described on mucins that contain tandem repeats of sequences rich in Ser, Thr, and Pro residues, resulting in glycoproteins with hundreds of O-GalNAc–type structures on a single glycoprotein. Clusters of O-GalNAc structures were then found on other secreted and membrane glycoproteins. With time, glycoproteins with single or limited numbers of O-GalNAc structures were identified, and it became apparent that modification of proteins with O-GalNAc structures is a highly abundant and a complex form of protein glycosylation. In most instances, the O-GalNAc–linked structures are relatively simple, containing a β1,3-linked galactose and one or two negatively charged moieties in the form of sialic acid. The presence of sialic acid on multiple closely spaced O-GalNAc structures has a dramatic effect on the secondary structure of proteins, forcing them to assume a very extended “bottle-brush” conformation. Although simple structures like those shown in Fig. 1 are typical, depending on the repertoire of glycosyltransferases being expressed, a vast array of distinct structures can be synthesized through the sequential addition of individual sugars. Thus, the presence or absence of O-GalNAc structures, the specific location of O-GalNAc structures in the protein sequence, and the structural features of the O-GalNAc structures each have the potential to profoundly affect the biologic properties of glycoproteins bearing this type of modification.

    See that? Serine, Proline, Threonine amino acids and their specific positions are pretty important if we extend protein function to include its role in the glycoproteome. Bwahaha!

    On the topic of glycomics generally (not just glyco-proteomics):

    https://en.wikipedia.org/wiki/Glycomics

    This area of research has to deal with an inherent level of complexity not seen in other areas of applied biology. 68 building blocks (molecules for DNA, RNA and proteins; categories for lipids; types of sugar linkages for saccharides) provide the structural basis for the molecular choreography that constitutes the entire life of a cell. DNA and RNA have four building blocks each (the nucleosides or nucleotides). Lipids are divided into eight categories based on ketoacyl and isoprene. Proteins have 20 (the amino acids). Saccharides have 32 types of sugar linkages.[4] While these building blocks can be attached only linearly for proteins and genes, they can be arranged in a branched array for saccharides, further increasing the degree of complexity.

    Add to this the complexity of the numerous proteins involved, not only as carriers of carbohydrate, the glycoproteins, but proteins specifically involved in binding and reacting with carbohydrate

    ….
    To answer this question one should know the different and important functions of glycans. The following are some of those functions:
    Glycoproteins found on the cell surface play a critical role in bacterial and viral recognition.
    They are involved in cellular signaling pathways and modulate cell function.
    They are important in innate immunity.
    They determine cancer development.
    They orchestrate the cellular fate, inhibit proliferation, regulate circulation and invasion.
    They affect the stability and folding of proteins.
    They affect the pathway and fate of glycoproteins.
    There are many glycan-specific diseases, often hereditary diseases.

    So no, I don’t make this stuff up. You apparently aren’t wanting to explore the latest cutting edge discoveries. It seems the amazing complexity of Eukaryotes is very bothersome to you.

  20. Truly he is the most intensely flabbergasted by fancy technical jargon of all.

    stcordova: Serine, Proline, Threonine amino acids and their specific positions are pretty important if we extend protein function to include its role in the glycoproteome. Bwahaha!

    “Bwahaha!”

    Did you seriously just write that? Aren’t you a grown man?

    : So no, I don’t make this stuff up.

    None of your quotes contain the terms I highlighted. Terms you DID make up.

    : You apparently aren’t wanting to explore the latest cutting edge discoveries.

    Sorry, that conclusion does not follow from me objecting to your ridiculous jargon and made-up to sound fancy technobabble about “massive information computational complexes”.

    And you always seem bent on trying to push this false narrative that “evolutionists resist the latest science”. Which is so ironic, considering it’s evolutionists who DO the science. Creationist morons like yourself have never set foot in a lab and done any actual experimental work. What kind of research have you actually contributed to? That’s right, not a fucking thing. You’re like the street-preachers standing outside with their placards. You’re just a particularly loud bullshitter and that is all you are.

    : It seems the amazing complexity of Eukaryotes is very bothersome to you.

    It does? How do you figure that? Please elaborate. I’m starting to understand how it is you’re a creationist, you see things that don’t exist everywhere.

    First you make shit up. Then you claim I’m against science out of fucking nowhere, and now you’re halluscinating that eukaryotic complexity is “bothersome” to me. This is almost Freudian to read.

  21. Rumraket: Ahh okay I see what you’re asking.

    The answer is mutation (and in the case of sexual reproduction, genetic recombination). Natural selection if looked at in isolation obviously is not a creative process, since by definition selection is restrictive. Only some things make it. So to get something new, to get “innovation” you need a process of creation, something that creates new stuff that natural selection can select among. That creative process would be mutation and recombination.

    Good, this is the right answer. But it’s the old inadequate answer.

  22. Erik: Good, this is the right answer. But it’s the old inadequate answer.

    Really? Please demonstrate that.

  23. Rumraket: Creationist morons like yourself have never set foot in a lab and done any actual experimental work.

    I did try to get into the Evolutionary Informatics Lab once, do I at least get credit for trying?

  24. Rumraket: Really? Please demonstrate that.

    Mutation cannot be too radical or it would not be advantageous for survival of the individual. But we are not talking about survival of the individual. We are talking about natural innovation so as to produce new species. So, a bunch of individuals should somehow develop the same mutation, the bunch of individuals should breed with each other to retain and reinforce the mutation, and the mutation should be advantageous for survival or at least good for some more limited purpose in the relevant environment.

    This is how you maybe get a different dog breed, but hardly a cat from a dog or any other relevantly new species. Moreover, the entire mechanism suggests a very gradual, practically unnoticeable transition between species, with constant intermediary forms between species. If it be true that humans evolved from apes (or ape-like ancestors) and we still have apes, then where are the current intermediary forms? If apes needed to evolve, then why are there still apes?

    It’s not clear at all why the original claim was that natural selection cannot innovate, but presumably mutation could.

  25. Where on earth did you get the idea that the same mutation must occur in more than one individual?

    Certainly not from reading biology.

  26. petrushka: Where on earth did you get the idea that the same mutation must occur in more than one individual?

    Certainly not from reading biology.

    Nonsense. What is the probability of loss of a new beneficial mutation? What is the probability of fixation of a new beneficial mutation?

  27. Erik: Mutation cannot be too radical or it would not be advantageous for survival of the individual.

    Why the hell not?

    Sorry, not going to take your word for it. You just sat there and made it up.

    Besides, what is a “too radical” mutation anyway? This is too vague to even mean anything.

    But we are not talking about survival of the individual. We are talking about natural innovation so as to produce new species.

    So what new “radical” innovations were required for chimpanzees and homo sapiens to evolve from their common ancestor?

    So, a bunch of individuals should somehow develop the same mutation

    Why? Why should multiple individuals develop the same mutation? What is the context here? What mutation specifically?

    The bunch of individuals should breed with each other to retain and reinforce the mutation

    Why? Why can’t the carrier of the mutation have lots of children, ~50% of which inherit it and who in turn do better on average (have higher reproductive success), than their siblings and the rest of the population?

    and the mutation should be advantageous for survival or at least good for some more limited purpose in the relevant environment.

    Why? The evolution of chloroquine resistance in Plasmodium Falciparum took several neutral mutations to evolve. Why MUST it be advantageous?

    This is how you maybe get a different dog breed, but hardly a cat from a dog or any other relevantly new species.

    Who in the world ever claimed cats evolved from dogs(or the other way around)? Cats and dogs share a common ancestor from which they both evolved.

    You have so far demonstrated you have at least five totally basic misconceptions about evolution.

    Moreover, the entire mechanism suggests a very gradual, practically unnoticeable transition between species

    If looked at from the standpoint of one organism giving birth to it’s direct offspring, yes.

    with constant intermediary forms between species.

    What does that mean, “constant intermediary forms between species”? What does “constant” mean in this context?

    If it be true that humans evolved from apes (or ape-like ancestors) and we still have apes, then where are the current intermediary forms?

    What do you mean by “current” intermediary forms? Where are our ancestors? Dead, that’s usually the fate of ancestors.

    If apes needed to evolve, then why are there still apes?

    There weren’t just one population of “apes” that lived in a single place on the globe and which suddenly “needed” to evolve. You get this, right? There are apes spread out basically on most continents. They are in Africa, Asia and America. The apes in one location can evolve and adapt in one direction, while the apes in another location can evolve and adapt to their local circumstances in another direction.

    You understand this, right? Your question is like asking “if polar bears evolved from Grizzlies, why are there still grizzlies?”. Some of them stayed behind in the forests, others moved to the arctic regions. It’s that simple.

    Or, if dogs evolved from wolves, why are there still wolves? Some stayed behind, others were caught and domesticated. It’s not like every wolf on the planet suddenly found itself caught and it’s offspring selected among by humans.

    It’s not clear at all why the original claim was that natural selection cannot innovate, but presumably mutation could.

    I actually agree and I was confused by that myself. I knew the answer but failed to think about it. It’s obvious to me why natural selection alone cannot be an “innovator” but combined with mutation, it can.

    As a demonstration that “the old answer” is inadequate, your reponse utterly fails. It seems more to constitute a chunk of unsupported claims based primarily on common creationist myths about evolutionary biology. The “old answer” might be inadequate, but it sure as heck isn’t for any of the reasons you erected.

  28. Mung: Nonsense. What is the probability of loss of a new beneficial mutation? What is the probability of fixation of a new beneficial mutation?

    The probability is relative to the selection coefficient and the population size. Would you care to give numbers for those?

  29. Rumraket: The probability is relative to the selection coefficient and the population size.

    So it has nothing to do with the initial frequency of the mutation in the population? Nothing at all? And we can’t find anything about that in biology books or papers?

  30. vjtorley:

    That is indeed a valid question. Why is it that life is so much more complex at the biochemical level than it needs to be, in order to metabolize, replicate and undergo Darwinian evolution?

    Who says it is? Except for Sal, of course, who really doesn’t bother with the evidence. That said, life probably is at least somewhat more complex than necessary, due to adaptation of pathways that aren’t exactly designed for the purpose, hence have “extra baggage.”

    When one examines the world of proteins, life seems to exhibit a surfeit of riches.

    There are a lot of proteins. How is there a surfeit of riches? Why are there so many proteins in protein families, except that more proteins of the same type were useful for greater possibilities than, say, yeast proteins would allow?

    One explanatory hypothesis that comes to mind is that this surfeit was intended as a signal, pointing to the fact that life was designed.

    Why? Is it because IDists claim that complexity is the sign of design? I haven’t seen that properly argued, only repeated without substance. Bird wings happen to be fused out of a number of bones that in their terrestrial ancestors were articulated, rather than just making single bones in the first place. That seems to be nothing but an evolutionary expedient, more complex than necessary from a design standpoint, but making do with what is bequeathed to birds from an evolutionary standpoint. Evolution seems to produce needless complexity, while I certainly see no good reason for supreme intelligence to do so.

    I’m inclined to agree.

    You may agree all you wish, but, unless you have an actual reason to agree with said claim, no one else has any reason to consider it.

    Glen Davidson

  31. GlenDavidson: Is it because IDists claim that complexity is the sign of design? I haven’t seen that properly argued…

    That’s a good thing, because the ID argument isn’t that complexity is the sign of design.

  32. How Cellular Enzymatic and Metabolic networks point to design

    http://reasonandscience.heavenforum.org/t2371-how-cellular-enzymatic-and-metabolic-networks-point-to-design

    The argument of a intelligent designer required to setup the Metabolic Networks for the origin of life

    Observation: The existence of metabolic pathways is crucial for molecular and cellular function. Although bacterial genomes differ vastly in their sizes and gene repertoires, no matter how small, they must contain all the information to allow the cell to perform many essential (housekeeping) functions that give the cell the ability to maintain metabolic homeostasis, reproduce, and evolve, the three main properties of living cells. Gil et al. (2004) In fact, metabolism is one of the most conserved cellular processes. By integrating data from comparative genomics and large-scale deletion studies, the paper “Structural analyses of a hypothetical minimal metabolism” proposes a minimal gene set comprising 206 protein-coding genes for a hypothetical minimal cell. The paper lists 50 enzymes/proteins required to create a metabolic network implemented by a hypothetical minimal genome for the hypothetical minimal cell. The 50 enzymes/proteins , and the metabolic network, must be fully implemented to permit a cell to keep its basic functions.
    Hypothesis (Prediction): The origin of biological irreducible metabolic pathways which also require regulation and and which are structured like a cascade, similar to electronic circuit boards, are best explained by the creative action of an intelligent agent.
    Experiment: Experimental investigations of metabolic networks indicate that they are full of nodes with enzymes/proteins, detectors, on/off switches, dimmer switches, relay switches, feedback loops etc. that require for their synthesis information rich, language-based codes stored in DNA . Hierarchical structures have been proved to be best suited for capturing most of the features of metabolic networks (Ravasz et al, 2002). It has been found that metabolites can only be synthesized if carbon, nitrogen, phosphor, and sulfur and the basic building blocks generated from them in central metabolism are available. This implies that regulatory networks gear metabolic activities to the availability of these basic resources. So one metabolic circuit depends on the product of other products, coming from other, central metabolic pathways, one depending from the other, like in a casacade. Further noteworthy is that Feedback loops have been found to be required to regulate metabolic flux, and the activities of many or all of the enzymes in a pathway. In many cases, metabolic pathways are highly branched, in which case it is often necessary to alter fluxes through part of the network while leaving them unaltered or decreasing them in other parts of the network (Curien et al., 2009). These are interconnected in a functional way, resulting in a living cell. The biological metabolic networks are exquisitely integrated, so the significant alterations in inevitably damage or destroys the funcion. Changes in flux often require changes in the activities of multiple enzymes in a metabolic sequence. Synthesis of one metabolite typically requires the operation of many pathways.
    Conclusion: Regardless of its initial complexity, self-maintaining chemical-based metabolic life could not have emerged in the absence of a genetic replicating mechanism insuring the maintenance, stability, and diversification of its components. In the absence of any hereditary mechanisms, autotrophic reaction chains would have come and gone without leaving any direct descendants able to resurrect the process. Life as we know it consists of both chemistry and information. If metabolic life ever did exist on the early Earth, to convert it to life as we know it would have required the emergence of some type of information system under conditions that are favorable for the survival and maintenance of genetic informational molecules. ( Ribas de Pouplana, Ph.D.)
    Intelligent agents have frequently end goals in mind, and use high levels of instructional complex information to met the goal. In our experience, systems storing large amounts of specified/instructional complex information through codes and languages — invariably originate from an intelligent source. Likewise, circuits or networks of coordinated interaction as for example of analog electronic devices can always be traced back to a intelligent causal agent. The operation of analog electronic devices maps very closely to the flow of information in chemical reactions of metabolic pathways (McAdams and Shapiro, 1995). A proposed mechanism to make metabolical networks must be capable of construct de novo, not merely modifying, a minimal set of 50 enzymes, and complex integrated metabolic circuits with the end goal to create life. A metabolic network that is not fully operational, will not permit life. We know in our experience that intelligence is able to setup circuit boards, like discrete electronic boards, and is the only known cause of irreducibly complex machines. Since evolution depends on metabolic circuits fully setup, its excluded as possible mechanism. The only two alternatives, chance/luck or physical necessity have never been observed to be able to setup circuit boards and irreducible complex systems. The origin of the basic metabolical network of the first cells is therefore best explained through the action of a intelligent agency.

  33. The irreducible, code-instructed process to make cell factories and machines points to intelligent design

    http://reasonandscience.heavenforum.org/t2364-the-irreducible-code-instructed-process-to-make-cell-factories-and-machines-points-to-intelligent-design

    To go from a bacterium to people is less of a step than to go from a mixture of amino acids to a bacterium. — Lynn Margulis

    Evolution has been a central point of the origins debate. Abiogenesis however provides far better elucidation of what mechanisms explain the origin of biological systems better: A intelligent designer, through power, information input, wisdom, will, or natural, non-guided, non-intelligent mechanisms, that is : random chance or physical necessity, long periods of time, mutation and natural selection, or self organisation of matter.

    Behes definition of Irreducible complexity can be expanded, and applied not only to biological systems, but also to systems , machines and factories created by man, that require a minimal number of parts to exercise a specific function, and this minimal number of parts cannot be reduced to keep the basic function. The term applies as well to processes, production methods and proceedings of various sorts. To reach a certain goal, a minimal number of manufacturing steps must be gone through. That applies in special to processes in living cells, where a minimal set of basic processes must be fully functional and operational, in order to maintain cells alive.

    Following irreducible processes and parts are required to keep cells alive, and illustrate mount improbable to get life a first go:
    Reproduction. Reproduction is essential for the survival of all living things.
    Metabolism. Enzymatic activity allows a cell to respond to changing environmental demands and regulate its metabolic pathways, both of which are essential to cell survival.
    Nutrition. This is closely related to metabolism. Seal up a living organism in a box for long enough and in due course it will cease to function and eventually die. Nutrients are essential for life.
    Complexity. All known forms of life are amazingly complex. Even single-celled organisms such as bacteria are veritable beehives of activity involving millions of components.
    Organization. Maybe it is not complexity per se that is significant, but organized complexity.
    Growth and development. Individual organisms grow and ecosystems tend to spread (if conditions are right).
    Information content. In recent years scientists have stressed the analogy between living organisms and computers. Crucially, the information needed to replicate an organism is passed on in the genes from parent to offspring.
    Hardware/software entanglement. All life of the sort found on Earth stems from a deal struck between two very different classes of molecules: nucleic acids and proteins.
    Permanence and change. A further paradox of life concerns the strange conjunction of permanence and change.
    Sensitivity. All organisms respond to stimuli— though not always to the same stimuli in the same ways.
    Regulation. All organisms have regulatory mechanisms that coordinate internal processes.

    chemist Wilhelm Huck, professor at Radboud University Nijmegen
    A working cell is more than the sum of its parts. “A functioning cell must be entirely correct at once, in all its complexity,”

    Following is the description of parts and processes in a theoretical protocell, which are essential and irreducible:

    What Might Be a Protocell’s minimal requirement of parts ?

    1. The Cell membrane
    2. DNA repair mechanisms
    3. Plasma membrane gates
    4. The Cytoplasm
    5. Glycolysis
    6. Left handed Amino Acids
    7. Membrane-enclosed vesicles
    8. Ribosomes
    9. tRNA
    10. right handed DNA
    11. Signal-Recognition Particles (SRP)
    12. Lysosomes
    13. A complete transcriptional machinery
    14. Protein-processing, -folding, secretion, and degradation functions and two proteases.
    15. FtsZ
    16. Cation, ABC transporters, a PTS for glucose transport, phosphate transporters
    17. Dihydroxyacetone phosphate
    18. ATP synthase

  34. Mung: So it has nothing to do with the initial frequency of the mutation in the population? Nothing at all? And we can’t find anything about that in biology books or papers?

    Of course that has a large impact, I was just assuming the initial frequency is a single individual in the population. It doesn’t HAVE to be larger than that, which is what you implied when you wrote “NONSENSE” in response to petrushka.

    Apparently Eric was working from the same misapprehension that mutations HAVE to occur in multiple individuals simultaneously. The implication of that belief is that you are apparently both completely sure that if a mutation does NOT happen in multiple individuals simultaneously, it gets lost by definition. Which is a really weird belief to have regarding a matter of probability.

    Mung: petrushka: Where on earth did you get the idea that the same mutation must occur in more than one individual?

    Certainly not from reading biology.

    Nonsense. What is the probability of loss of a new beneficial mutation? What is the probability of fixation of a new beneficial mutation?

    Yes, the probability of both loss and fixation is dependent on population size, initial frequency and selection coefficient.

  35. Oh look who came to spam the thread. Welcome Otangelo, did you get tired of being repeatedly humiliated about your volitional* ignorance on Sandwalk?

    * That means you chose it, that it was your choice to become and stay ignorant. I know you have a hard time with words so I’m just helping out.

  36. Mikkel wrote:

    “did you get tired of being repeatedly humiliated about your volitional* ignorance on Sandwalk? ”

    haha. Are you deflecting ? A confession of your own feelings…..??!!

    Yah, as said there : you are a intellectual masochist. Anyone is free to see :

    http://reasonandscience.heavenforum.org/t2384-some-fun-at-larrys-blog

    how your just so pseudo-scientific claims were exposed.

    Of course, since you were unable to refute the facts, you could not do else at the end than bitch about my religion and faith…..

    what a pity…. kkkk

  37. otangelo:
    . . .
    Yah, as said there : you are a intellectual masochist.
    . . . .

    The rules here are to address the ideas, not the person. Please read them and follow them.

  38. Patrick,

    But this post is Ok Patrick?

    Oh look who came to spam the thread. Welcome Otangelo, did you get tired of being repeatedly humiliated about your volitional* ignorance on Sandwalk?

    * That means you chose it, that it was your choice to become and stay ignorant. I know you have a hard time with words so I’m just helping out.

    Are you just angry because Trump had a bad week Patrick?

  39. phoodoo:
    Patrick,

    But this post is Ok Patrick?

    Nope, that’s a rule violation. I missed it while skimming to catch up.

    Are you just angry because Trump had a bad week Patrick?

    I’m not a Trump supporter. Those are mostly creationists like your good self.

  40. Patrick,

    You missed the exact post Otangelo was responding to, while you were criticizing him about responding?

    That’s a new one.

  41. Patrick,

    Patrick, what makes you think the thing that unites people who support Trump is creationism? Why isn’t it people who like guns (you)? People who don’t like to pay their share of taxes (you)?People who think Monsanto is great (skeptics)?

  42. phoodoo:

    Patrick, what makes you think the thing that unites people who support Trump is creationism?Why isn’t it people who like guns (you)?People who don’t like to pay their share of taxes (you)?People who think Monsanto is great (skeptics)?

    Trump can’t be trusted on second amendment rights and his economic plans would grow the government and increase taxes. Frankly, the only people foolish enough to vote for him are also foolish enough to believe that the Earth is less than 10,000 years old.

  43. phoodoo:

    Yea, he is just not right wing enough for you Patrick.

    Yeah, my support for drug legalization, reproductive rights, open borders, and non-interventionism is so right wing.

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