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What are the limits of Random Variation? A simple evaluation of the probabilistic resources of our biological world

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Coming from a long and detailed discussion about the limits of Natural Selection, here:

I realized that some attention could be given to the other great protagonist of the neo-darwinian algorithm: Random Variation (RV).

For the sake of clarity, as usual, I will try to give explicit definitions in advance.

Let’s call RV event any random event that, in the course of Natural History, acts on an existing organism at the genetic level, so that the genome of that individual organism changes in its descendants.

That’s more or less the same as the neo-darwinian concept of descent with modifications.

A few important clarifications:

a) I use the term variation instead of mutation because I want to include in the definition all possible kinds of variation, not only single point mutations.

b) Random here means essentially that the mechanisms that cause the variation are in no way related to function, whatever it is: IOWs, the function that may arise or not arise as a result of the variation is in no way related to the mechanism that effects the change, but only to the specific configuration which arises randomly from that mechanism.

In all the present discussion we will not consider how NS can change the RV scenario: I have discussed that in great detail in the quoted previous thread, and those who are interested in that aspect can refer to it. In brief, I will remind here that NS does not act on the sequences themselves (IOWs the functional information), but, if and when and in the measure that it can act, it acts by modifyng the probabilistic resources.

So, an important concept is that:

All new functional information that may arise by the neo-darwinian mechanism is the result of RV.

Examining the Summers paper about chloroquine resistance:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4035986/

I have argued in the old thread that the whole process of generation of the resistance in natural strains can be divided into two steps:

a) The appearance of an initial new state which confers the initial resistance. In our example, that corresponds to the appearance of one of two possible resistant states, both of which require two neutral mutations. IOWs, this initial step is the result of mere RV, and NS has no role in that. Of course, the initial resistant state, once reached, can be selected. We have also seen that the initial state of two mutations is probably the critical step in the whole process, in terms of time required.

b) From that point on, a few individual steps of one single mutation, each of them conferring greater resistance, can optimize the function rather easily.

Now, point a) is exactly what we are discussing in this new thread.

So, what are the realistic powers of mere RV in the biological world, in terms of functional information? What can it really achieve?

Another way to ask the same question is: how functionally complex can the initial state that for the first time implements a new function be, arising from mere RV?

And now, let’s define the probabilistic resources.

Let’s call probabilistic resources, in a system where random events take place, the total number of different states that can be reached by RV events in a certain window of time.

In a system where two dies are tossed each minute, and the numbers deriving from each toss are the states we are interested in, the probabilistic resources of the system in one day amount to  1440 states.

The greater the probabilstic resources, the easier it is to find some specific state, which has some specific probability to be found in one random attempt.

So, what are the states generated by RV? They are, very simply, all different genomes that arise in any individual of any species by RV events, or if you prefer by descent with modification.

Please note that we are referring here to heritable variation only, we are not interested to somatic genetic variation, which is not transmitted to descendants.

So, what are the probabilistic resources in our biological world? How can they be estimated?

I will use here a top-down method. So, I will not rely on empirical data like those from Summers or Behe or others, but only on what is known about the biological world and natural history.

The biological probabilstic resources derive from reproduction: each reproduction event is a new state reached, if its genetic information is different from the previous state. So, the total numbet of states reached in a system in a certain window of time is simply the total number of reproduction events where the genetic information changes. IOWs, where some RV event takes place.

Those resources depend essentially on three main components:

  1. The population size
  2. The number of reproductions of each individual (the reproduction rate) in a certain time
  3. The time window

So, I have tried to compute the total probabilistic resources (total number of different states) for some different biological populations, in different time windows, appropriate for the specific population (IOWs, for each population, from the approximate time of its appearance up to now). As usual, I have expressed the final results in bits (log2 of the total number).

Here are the results:

 

Population Size Reproduction rate (per day) Mutation rate Time window Time (in days) Number of states Bits + 5 sigma Specific AAs
Bacteria 5.00E+30 24 0.003 4 billion years 1.46E+12 5.26E+41 138.6 160.3 37
Fungi 1.00E+27 24 0.003 2 billion years 7.3E+11 5.26E+37 125.3 147.0 34
Insects 1.00E+19 0.2 0.06 500 million years 1.825E+11 2.19E+28 94.1 115.8 27
Fish 4E+12 0.1 5 400 million years 1.46E+11 2.92E+23 78.0 99.7 23
Hominidae 5.00E+09 0.000136986 100 15 million years 5.48E+09 3.75E+17 58.4 80.1 19

The mutation rate is expressed as mutations per genome per reproduction.

This is only a tentative estimate, and of course a gross one. I have tried to get the best reasonable values from the sources I could find, but of course many values could be somewhat different, and sometimes it was really difficult to find any good reference, and I just had to make an educated guess. Of course, I will be happy to acknowledge any suggestion or correction based on good sources.

But, even if we consider all those uncertainties, I would say that these numbers do tell us something very interesting.

First of all, the highest probabilistic resources are found in bacteria, as expected: this is due mainly to the huge population size and high reproduction rate. The number for fungi are almost comparable, although significantly lower.

So, the first important conclusion is that, in these two basic classes of organisms, the probabilistic resources, with this hugely optimistic estimate, are still under 140 bits.

The penultimate column just adds 21.7 bits (the margin for 5 sigma safety for inferences about fundamental issues in physics). What does that mean?

It means, for example, that any sequence with 160 bits of functional information is, by far, beyond any reasonable probability of being the result of RV in the system of all bacteria in 4 billion years of natural history, even with the most optimistic assumptions.

The last column gives the number of specific AAs that corrispond to the bit value in the penultimate column (based on a maximum information value of 4.32 bits per AA).

For bacteria, that corresponds to 37 specific AAs.

IOWs, a sequence of 37 specific AAs is already well beyond the probabilistic resources of the whole population of bacteria in the whole world reproducing for 4 billion years!

For fungi, 147 bits and 34 AAs are the upper limit.

Of course, values become lower for the other classes. Insects still perform reasonably well, with 116 bits and 27 AAs. Fish and Hominidae have even lower values.

We can notice that Hominidae gain something in the mutation rate, which as known is higher, and that I have considered here at 100 new mutations per genome per reproduction (a reasonable estimate for homo sapiens). Moreover, I have considered here a very generous population of 5 billion individuals, again taking a recent value for homo sapiens. These are  not realistic choices, but again generous ones, just to make my darwinist friends happy.

Another consideration: I have given here total populations (or at least generous estimates for them), and not effective population sizes. Again, the idea is to give the highest chances to the neo-darwinian algorithm.

So, these are very simple numbers, and they should give an idea of what I would call the upper threshold of what mere RV can do, estimated by a top down reasoning, and with extremely generous assumptions.

Another important conclusion is the following:

All the components of the probabilistic resources have a linear relationship with the total number of states.

That is true for population size, for reproduction rate, mutation rate and time.

For example, everyone can see that the different time windows, ranging from 4 billion years to 15 million years, which seems a very big difference, correspond to only 3 orders of magnitude in the total number of states. Indeed, the highest variations are probably in population size.

However, the complexity of a sequence, in terms of necessary AA sites, has an exponential relationship with the functional information in bits: a range from 19 to 37 AAs (only 18 AAs) corresponds to a range of 24 orders of magnitude in the distribution of probabilistic resources.

Can I remind here briefly, without any further comments, that in my OP here:

I have analyzed the informational jump in human conserved information at the apperance of vertebrates? One important result is that 10% of all human proteins (about 2000) have an information jump from pre-vertebrates to vertenrates of at least (about) 500 bits (corresponding to about 116 AAs)!

Now, some important final considerations:

  1. I am making no special inferences here, and I am drawing no special conclusions. I don’t think it is really necessary. The numbers speak for themselves.
  2. I will be happy of any suggestion, correction, or comment. Especially if based on facts or reasonable arguments. The discussion is open.
  3. Again, this is about mere RV. This is about the neutral case. NS has nothing to do with these numbers.
  4. For those interested in a discussion about the possible role of NS, I can suggest the thread linked at the beginning of this OP.
  5. I will be happy to answer any question about NS too, of course, but I would be even more happy if someone tried to answer my two questions challenge, given at post #103 of the other thread, and that nobody has answered yet. I paste it here for the convenience of all:

Will anyone on the other side answer the following two simple questions?

1) Is there any conceptual reason why we should believe that complex protein functions can be deconstructed into simpler, naturally selectable steps? That such a ladder exists, in general, or even in specific cases?

2) Is there any evidence from facts that supports the hypothesis that complex protein functions can be deconstructed into simpler, naturally selectable steps? That such a ladder exists, in general, or even in specific cases?

Comments
Dionisio: "The below link points to a relatively old* paper (it appeared 3 years ago) that seems like a game changer, because it explains in details the jump from prokaryotes to eukaryotes, doesn’t it?" :) :) :) Well, the 3 papers you quote are, in a sense, honest enough, because they clearly show how little we understand of the issue! :) They are all of the type: we understand practically nothing of how this happened, but let me suggest some new revealing idea! Of course, after the revealing idea is given, we still understand practically nothing. However, the transition to eukaryotes remains one of the big issues in biology, especially from an informational point of view. The amount of new information generated in that transition is simply staggering! Unfortunately, there is still a lot of uncertainty about the basics of the event: for example, when did it happen. These huge transitions (OOL, eukaryotes, metazoa, vertebrates, and certainly many others) are really beyond any hope of explanation, even vague, if design is not factored.gpuccio
November 9, 2017
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@153 follow-up The following papers seem to add supporting evidences for the paper referenced @153. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5557255/pdf/13062_2017_Article_190.pdf http://mmbr.asm.org/content/81/3/e00008-17Dionisio
November 9, 2017
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gpuccio, Perhaps you've seen this paper before. The below link points to a relatively old* paper (it appeared 3 years ago) that seems like a game changer, because it explains in details the jump from prokaryotes to eukaryotes, doesn't it? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4210606/pdf/12915_2014_Article_76.pdf (*) BTW, what would be considered 'old' for biology research papers?Dionisio
November 8, 2017
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jerry: By the way, I don't believe at all that transposons are evidence for an RNA world, as Brosius seems to suggest. Indeed, I don't believe at all in the RNA world theory. There is no evidence for it. It is only a necessary imaginary tool to try to answer questions about OOL that cannot be answered by neo-darwinism. And that cannot even be answered by the imaginary RNA world. However, I will not discuss in detail here the many irrational ideas in Brosius' paper, because this is not really the object of discussion in this thread. Be it enough to say that not only Brosius, as you say, is "not able to overcome the statistical boundaries and hurdles that gpuccio has listed in order to form complex new systems": in the paper I have read, he does not even try to address them in any way. A whole paper about how imaginary evolutionary events should have happened, at least according to him, and not even one simple attempt at analyzing if any of those events is even empirically credible, least of all probable!gpuccio
November 8, 2017
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jerry: "As I said he is a strident atheist." I am not interested in his world-view. I am only interested in his scientific ideas. Now, excuse me, but I have no special reasons to read everything he has written. I have already read that paper in Paleobiology you apparently referenced at #142. Frankly, I did not find it really interesting, except maybe for an early understanding (in 2004) of the important role of transposons in evolution, an idea that has been confirmed by the more recent literature, and that I will happily support, because as said many times I believe that transposons are a very good tool of design. Unfortunately, I found nothing in that paper regarding the point you mentioned:
It has been awhile since I have read about this but aren’t there lots of expressed sequences in the cell that may be due to just this, part of the junk DNA being expressed with no apparent function. Someone once said that these apparently useless proteins may be some of the so called Orphan proteins that have been discovered in the cell but which have no known function.
My answer was: "I think that a lot of non coding DNA is more or less transcribed, but not translated. Otherwise, cells should be packed of useless proteins, which would certainly be an extreme burden to cell life. Moreover, a sequence can be translated only if it has reached the state of ORF, with a starting codon and no stop codons. So, I believe that all the search that happens in non coding DNA cannot be helped by NS, at all. Only if and when an ORF is transcribed and translated it can be detected bt NS, and only if it confers some detectable reproductive advantage. IOWs, the walk to a new basic selectable function is a mere random walk. And therefore it can use only the probabilistic resources that I have highlighetd in my OP." Again, in all the citations you make of Brosius, or about him, I can find nothing about systematic translation of useless proteins. So, for the moment I will assume that there is no evidence about such an idea. I am interested in any argument about a different view, but please give me exact references for it, if you have them.gpuccio
November 8, 2017
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Gpuccio, Here is the full text of the previous article I mentioned The Persistent Contributions of RNA to Eukaryotic Gen(om)e Architecture and Cellular Function Brosius, J. 2014. The persistent contributions of RNA to eukaryotic gen(ome)e architecture and cellular function. Cold Spring Harb. Perspect. Biol. 2014. 6. pii: a016089. doi: 10.1101/cshperspect.a016089. http://cshperspectives.cshlp.org/content/6/12/a016089.full You might want to look at this too which references Brosius' paper
Life is physics and chemistry and communication Guenther Witzany Manfred Eigen extended Erwin Schroedinger’s concept of “life is physics and chemistry” through the introduction of information theory and cybernetic systems theory into “life is physics and chemistry and information.” Based on this assumption, Eigen developed the concepts of quasispecies and hypercycles, which have been dominant in molecular biology and virology ever since. He insisted that the genetic code is not just used metaphorically: it represents a real natural language. However, the basics of scientific knowledge changed dramatically within the second half of the 20th century. Unfortunately, Eigen ignored the results of the philosophy of science discourse on essential features of natural languages and codes: a natural language or code emerges from populations of living agents that communicate. This contribution will look at some of the highlights of this historical development and the results relevant for biological theories about life.
jerry
November 8, 2017
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Gpuccio, That is the first article I read and is in the journal article I referred to in Paleobiology. It gives you a flavor of the issues and how he thinks. As I said he is a strident atheist. He has a website for his group at the University of Muenster https://campus.uni-muenster.de/en/zmbe/the-institutes/inst-of-exp-pathology/staff/ https://campus.uni-muenster.de/en/zmbe/the-institutes/inst-of-exp-pathology/publications/ I believe some of these papers discuss the origin of specific proteins and their coding sequences. He has a wikipedia page https://en.wikipedia.org/wiki/Jürgen_Brosius
Jürgen Brosius (born 1948) in Saarbrücken) is a German molecular geneticist and evolutionary biologist. He is a professor at the University of Münster where he is the director of the Institute of Experimental Pathology. Some of his scientific contributions involve the first genetic sequencing of a ribosomal RNA operon, the design of plasmids for studying gene expression, expression vectors for high-level production of recombinant proteins and RNA, RNA biology, RNomics as well as the significance of retroposition for plasticity and evolution of genomes, genes and gene modules including regulatory sequences or elements.
Here is another article he wrote at the same time
Waste not, want not – transcript excess in multicellular eukaryotes There is growing evidence that mammalian genomes produce thousands of transcripts that do not encode proteins, and this RNA class might even rival the complexity of mRNAs. There is no doubt that a number of these non-protein-coding RNAs have important regulatory functions in the cell. However, do all transcripts have a function or are many of them products of fortuitous transcription with no function? The second scenario is mirrored by numerous alternative-splicing events that lead to truncated proteins. Nevertheless, analogous to ‘superfluous’ genomic DNA, aberrant transcripts or processing products embody evolutionary potential and provide novel RNAs that natural selection can act on.
Also more recently
The Persistent Contributions of RNA to Eukaryotic Gen(om)e Architecture and Cellular Function Jürgen Brosius Abstract Currently, the best scenario for earliest forms of life is based on RNA molecules as they have the proven ability to catalyze enzymatic reactions and harbor genetic information. Evolutionary principles valid today become apparent in such models already. Furthermore, many features of eukaryotic genome architecture might have their origins in an RNA or RNA/protein (RNP) world, including the onset of a further transition, when DNA replaced RNA as the genetic bookkeeper of the cell. Chromosome maintenance, splicing, and regulatory function via RNA may be deeply rooted in the RNA/RNP worlds. Mostly in eukaryotes, conversion from RNA to DNA is still ongoing, which greatly impacts the plasticity of extant genomes. Raw material for novel genes encoding protein or RNA, or parts of genes including regulatory elements that selection can act on, continues to enter the evolutionary lottery.
There are other more specific articles as these are review articles.jerry
November 8, 2017
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jerry: "But some day you should take on the specific claims of Brosius, that is post graduate work and appropriate for your time." Just to help, could you please confirn if this is the paper you refer to: "Disparity, adaptation, exaptation, bookkeeping, and contingency at the genome level" and, if possible, what is the part which makes the pertinent claims? Thank you. :)gpuccio
November 8, 2017
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Gpuccio,
I think that a lot of non coding DNA is more or less transcripted, but not translated. Otherwise, cells should be packed of useless proteins, which would certainly be an extreme burden to cell life. Moreover, a sequence can be translated only if it has reached the state of ORF, with a starting codon and no stop codons.
Thank you. But some day you should take on the specific claims of Brosius, that is post graduate work and appropriate for your time.jerry
November 8, 2017
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EugeneS: "With life, the situation is analogous: it may have started from something considerably simpler than the specific peptide sequences observed today (and consequently with much greater probabilities), which then gradually became more specific leading to what appears to be very low probabilities." Again, there are two problems: a) We know no independent form of life simpler than a prokaryote. All the rest is imagination. b) Whatever was simpler, must have been a starting point for the specific peptide sequences that we observe today. For example, ATP synthase beta chains, which is not simply something we observe today, but something thatwas already there, very similar to what we observe today, shortly after OOL. Now, how did the "simpler" (and never observed) thing serve as starting point to that specific sequence? Was it some partially homologous protein? Did it already have the function of synthesizing ATP from a proton gradient? Did it already contribute to the hexameric structure of F1, together with the alpha chain? How simple was it, then? IOWs we are again at the problem of the cart and the petrol engine, but thousands of times more complex. With the little problem that we have no cart! :) In the end, all leads again to my challenge, which nobody has answered yet. At the cost of being repetitive, I paste it again here:
Will anyone on the other side answer the following two simple questions? 1) Is there any conceptual reason why we should believe that complex protein functions can be deconstructed into simpler, naturally selectable steps? That such a ladder exists, in general, or even in specific cases? 2) Is there any evidence from facts that supports the hypothesis that complex protein functions can be deconstructed into simpler, naturally selectable steps? That such a ladder exists, in general, or even in specific cases?
gpuccio
November 7, 2017
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EugeneS: "An analogy is language: it may have started from very simple ideas (crude semantic islands in the ocean of possible sequences of letters of the same length). Then gradually the semantic islands were getting more specific and consequently relatively smaller in size." I am not sure I understand. Let's go back to our example of a 30 characters sequence. If we choose not form the 200000 words if English language, but from, say, 100 "crude semantic islands", always of about 5 letters, our target space is much smaller. It becomes "only": 1.1e+11 The search space remains the same. The probability of finding semantic islands goes down, a lot down. The probability goes up only if the functional islands are extremely big. For example, if in some language any word of five letters which contains two "a" can represent, say, a dog, than that result is easier to be found, because there are many words with two "a". IOWs, a very generic function is easy to find. But almost always useless in most realistic scenarios. The idea is: important functions require a lot of specific information, even in their basic form, which can then be optimized. A basic petrol engine requires a lot of specific configuration, much more than a cart. Even if it is a simple petrol engine. And it cannot be derived from a cart by extremely simple variations, each improving the original function of the cart. More in next post.gpuccio
November 7, 2017
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jerry: "I believe it relies on the concept that a lot of the junk DNA gets expressed but has no function but that some eventually will and the function will appear suddenly" I think that a lot of non coding DNA is more or less transcripted, but not translated. Otherwise, cells should be packed of useless proteins, which would certainly be an extreme burden to cell life. Moreover, a sequence can be translated only if it has reached the state of ORF, with a starting codon and no stop codons. So, I believe that all the search that happens in non coding DNA cannot be helped by NS, at all. Only if and when an ORF is transcripted and translated it can be detected bt NS, and only if it confers some detectable reproductive advantage. IOWs, the walk to a new basic selectable function is a mere random walk. And therefore it can use only the probabilistic resources that I have highlighetd in my OP.gpuccio
November 7, 2017
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EugeneS: Let's see. "The probability of something complex and specific is very low, but we must consider an ensemble, not a given individual. The probability of Mr X being born (with all his distinctive traits such as hair color, stature, weight, size of liver etc) is vanishingly small, but Mr X’s do get born." This seems just the classical wrong argument about unlikely things happening. One of the most senseless aguments ever made! It goes like that: let's say we have a total number of possible random states of one sequence. For example a sequence made of the 25 letters in the English alphabet, plus space and 4 puntuaction marks. Each sequence has a probability of about 2E-44 to be found. Then we generate a sequence of letters of that length, and of course one of the "unlikely" sequences has been found! Miracle, miracle... Of course this is only bad reasoning about probabilites. The probability of finding one specific sequence among all is, correctly, 2E-44. Therefore, if we specify in advance one of the possible sequences, and then we get that same sequence from a random event, we can really call that a miracle! But the probability of getting one generic sequence out of those 2x10^44 with one random event is exactly 1. Therefore, we have to find one of them by our random search. In functional specification, or other types of specification, the definition of the target space is not made by some arbitrary pre-specification, like in the above example, but rather by some objective property that implicitly defines a subset of the search space, and therefore generates a binary partition. Then the probability of finding the target space can be computed. For example, let's say that we generate by one random event a sequence of the 25 letters in correct alphabetical order, followed by space and the 4 punctuation marks in some specific order: that would really be astounding. But we are not pre-defining the target space, because the alphabetical order exists independently from our little experiment. So would any sequence made of 30 identical letters be extremely unlikely, and here again because of a specification which is independent and which is a form of intrinsic order. Finally, if we get a phrase which has good meaning in English, like: It is easy to understand that. again we touch an amazingly small target space. Now, one objection could be: but what if we get one result which is in one of the possible target spaces which have some good objective definition? OK, we must sum those target spaces. For example, just in our little example, the target space of the first case (ordered sequence, assuming that space and punctuation marks have some alphabetical order) is: 2 sequences (considering both possible orderings). The target space for sequences made of one symbol is: 30 sequences (because we have 30 symbols) The target space for "a phrase which has good meaning in English" is more difficult to compute. However, here: https://uncommondescent.com/intelligent-design/an-attempt-at-computing-dfsci-for-english-language/ I have given a simple way to appoximate the target space for the function "A phrase made of English words", which certainly includes the subset of "a phrase which has good meaning in English". Using my computations given in that OP, for a 30 characters phrase, the set of phrases made of English words is about: 3.2e+26 Now, let's say that the subset of phrases having good meaning in English is 3 orders of magnitude smaller (IOWs that 1:1000 of the phrases made of English words has good meaning in English, which is probably a very optimistic assumption). So, the target space for out function of "having good meaning in English" would be of about: 3.2e+23 Now, let's imagine that we have 1000 main languages on our planet, and that we want the target space for all of them together. It will be: 3.2e+26 If we add the 32 sequences corresponding to thw first two functions, we have practically the same number. With a search space of 2e+44, the probability of finding one sequence which has one of the three functions we have defined: a) Being fully ordered b) Being made of only one symbol c) Having good meaning in one of the 1000 main languages on earth remains about 1:10^18. This, for a very short sequence of 30 letters. In my OP cited above I have also demonstrated that, for language, the ratio between target space and search space is bound to increase with the length of the string. So, what can we learn from this example? a) Even in very simple digital sequences, complex functions are only a small part of the search space, even if large functional islands are defined. b) The longer the sequence, the smaller is the ratio between target space and search space. c) Considering many different functional islands usually does not increase much the target space, because functional islands are simply summed. In this kind of computations, it's mainly the effect of exponential components that can really change things. d) In particular, functional islands which have great specificity contribute very little to a general target space, as we have seen for the "ordered" and "same character" functions. e) So, if we find a very specific result, like a sequence completely ordered, that result remains absolutely unlikely, even if other functions, like "having good meaning in English", have a bigger target space. IOWs, we have to consider the functional information in our specific result, and not just a generic target space that can include many types of other functions. In particular, in the case of proteins and evolution, the only target space we can consider is the function: "any variation that, in this specific biological context, confers a detectable reproductive advantage". Because that is the only function that can be "offered" to NS. More in next post.gpuccio
November 7, 2017
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at the moment a functional sequence is formed in junk-dna, somehow, this particular sequence (and not any other) is activated and translated into proteins. Why or how this is done, no one knows.
It has been awhile since I have read about this but aren't there lots of expressed sequences in the cell that may be due to just this, part of the junk DNA being expressed with no apparent function. Someone once said that these apparently useless proteins may be some of the so called Orphan proteins that have been discovered in the cell but which have no known function. This is part of the punctuated equilibrium hypothesis, that sequences mutate away due to various means of random variaton until they become functional. I believe it relies on the concept that a lot of the junk DNA gets expressed but has no function but that some eventually will and the function will appear suddenly. This seems to be part of the ideas that Jurgen Brosius has written about. Brosius is a very strident atheist who attacks anybody suggesting something looking like design. Brosius wrote the key article in the issue of Paleobiology (31(sp5):1-16. 2005) dedicated to Stephen Gould. I have mentioned this several times before and gpuccio has looked at his work. This issue was republished as a book by Vrbra called Macroevolution. So novel new proteins can arise according to these ideas and Brosius and his colleague's publications discuss some of them. However, it seems they are not able to overcome the statistical boundaries and hurdles that gpuccio has listed in order to form complex new systems.jerry
November 7, 2017
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Gpuccio, Great reading and discussions once again. Thank you for your time and effort in answering questions and flushing out details. Origenes, your statement about graciously accepting JUNK DNA and Gpuccio's response should not be lost on readers...
Origenes: “Note that we graciously assume that, at the moment a functional sequence is formed in junk-dna, somehow, this particular sequence (and not any other) is activated and translated into proteins. Why or how this is done, no one knows.” Yes, we graciously assume a lot of things. We are definitely very kind to our darwinist interlocutors! ????
This is important. It brings to memory Dan Graur's angry rant against ENCODE and function found in JUNK DNA. His last paper insisting the Genome must be at least 75% Junk. Is 75% JUNK DNA enough to solve the problem for neo-Darwinist? And save materialist assumptions? Don't think so.DATCG
November 7, 2017
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gpuccio:
Well, the record gets better: after 1600+ views and 135 comments, not one single intervention from the other side.
Patience grasshopper. We are in the waiting time. The random mutations are accumulating but not yet selectable. You will see the results and it will be a wonderfully engineered design. By accident. Just you wait and see.Mung
November 7, 2017
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Forexhr 135 Yes, of course. I understand this.EugeneS
November 7, 2017
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GP Usually Darwinists prefer this argument. At least, I have seen or heard this more than once.
The probability of something complex and specific is very low, but we must consider an ensemble, not a given individual. The probability of Mr X being born (with all his distinctive traits such as hair color, stature, weight, size of liver etc) is vanishingly small, but Mr X's do get born. An analogy is language: it may have started from very simple ideas (crude semantic islands in the ocean of possible sequences of letters of the same length). Then gradually the semantic islands were getting more specific and consequently relatively smaller in size. With life, the situation is analogous: it may have started from something considerably simpler than the specific peptide sequences observed today (and consequently with much greater probabilities), which then gradually became more specific leading to what appears to be very low probabilities.
The most important observations that in my opinion invalidate this claim are: 1. complex function is/cannot be not a (re)combination of relatively simple function. We have discussed it at length about it in the other thread. 2. the language analogy is flawed because it does not take into account the physical/chemical constraints protein molecules must satisfy in order to be functional. Words can be added to words without constraints, to specify meaning; whereas physical constraints do not permit arbitrary functional adjustments in the protein world. GP, I wonder if you have any more comments on this. Thanks.EugeneS
November 7, 2017
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Larry Moran, wd400, CR, MatSpirit, Seversky, Goodusername, rvb8, Gordon Davidson and many others, Where Art Thou?
Maybe this time one of them will answer ;)Origenes
November 7, 2017
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To all: Well, the record gets better: after 1600+ views and 135 comments, not one single intervention from the other side. ;)gpuccio
November 7, 2017
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EugeneS: I was speaking strictly from a numerical perspective. Higher life forms are composed of more particles that lower life forms and as the number of particles increases the ratio between non-functional and functional states for any given specifier increases also. The higher the ratio, the more resources are required to find functional states. Of course, from a physicochemical perspective, life cannot originate from non-living matter due to one simple fact: processes of non-living matter are heading towards physicochemical equilibrium or a state of minimum total potential energy and not towards a state where some physicochemical system can use surrounding matter to reproduce and maintain its structure. In that regard, any isolated and momentary instances of self-reproduction would instantly be destroyed by equilibrium flows of matter and energy.forexhr
November 6, 2017
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Gpuccio,
Is that simple enough?
Too simple. My observation of discussions of complicated topics is that the discussion nearly always starts out at the kindergarten level and just a few paragraphs later is at discussions appropriate for graduate school. Your discussions are rightly at the graduate school level but what is needed is a discussion that is somewhat at the high school level in order to make it clear to the average educated person who is not schooled in the technological terms used here but would understand the logic when presented at that level. I am not asking you to do this because your time is obviously needed at these graduate level discussions and what you have produced is extremely valuable. But it would be a great service if someone would do this. 10 years ago I would have tried to do it but I am not aware of all the technical arguments you are using and don't have the time to think them all through. Keep up the great work. But somewhere there is a 100 page or less discussion of this at the "RV for Dummies" level.jerry
November 6, 2017
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EugeneS: "I may be wrong but I do not think that drift can do anything substantial statistically." It can't. It's easy to understand that if we reason very simply as follows: a) If the total number of states that can be generated in natural history is n, can drift change that number? The answer of course is no. Drift does not act on the number of states that can be generated: that depends only on the population size, reproduction rate, mutation rate and timw window. b) Drift can certainly modify the distribution of states at various times. That said, the only pertinent question is: can drift in some way favor the target space vs the rest of the search space? IOWs, can it favor functional states? And the answer, of course, is no. For neutral drift, all states are equivalent. Functional states are not recognized. Therefore, the probabilties of reaching a functional state remain absolutely the same. c) Only NS can recognize functional states, and therefore change the probabilistic distribution. But we have seen its severe limits, and its negative aspects too. However, NS can certainly contribute to optimize existing functions a lttle bit. That it can do, and that we can observe. Nothing else. Indeed, for the generation of new functional sequences, unrelated to existing sequences and functions, NS is a game stopper. Only neutral walks have any hope. And we know how likely that hope really is! (see the table in the OP) :)gpuccio
November 6, 2017
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GP I totally agree on the strong ID. It is not correct to attribute all biological information to what is basically noise. Natural selection in practice is not really a magic wand but rather a magic hammer ;) NS can only reduce information (not produce). Consequently, all Darwinism can rely on in terms of information production is RV + drift. I may be wrong but I do not think that drift can do anything substantial statistically. They have nothing else. forexhr An interesting observation indeed! However, this may be more difficult than it looks. In order to confidently say that the origin of higher life forms is a greater problem than the origin of life, we need to demonstrate that the additional constraints do not make the problem easier (because they can in theory). In combinatorial search, constraints can provide valuable information to narrow down the feasibility space. If you have a set of instances of graph coloring problems that you generate by varying the ratio of the number of edges to the number of vertices, you will get a spectrum of problems with different solubility: - no edges (too few constraints or none at all) easily soluble; - phase transition; the hardest problems to solve in practice; - too many edges (constraints) easily insoluble.EugeneS
November 6, 2017
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J-Mac: Thank you! :) Lonnig's paper seems very interesting indeed.gpuccio
November 5, 2017
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Origenes: "My point was not about fixation, but, instead, about the time necessary for restoring the population size to 7 billion. Is there a term for this period?" I am not sure. My impression is that it is a special form of time to fixation by NS. But I could be wrong. It also reminds me, even if it's not exactly the same, ot the idea of the "cost of Natural Selection", according to Haldane. That is more an effect of the competition between different selectable genes, but there too the problem is mainly the loss of reproductive resources because of the intervention of NS. Indeed, those are two ways in which NS can be an obstacle to evolution, because of its intrinsic behaviour as a destructive principle: both the antagonistic effect against what is new, effected by negative NS, and the reduction of reproductive resources in the course of fixation and explansion, effected by positive NS (see for example Haldane's dilemma and your Japanese example).gpuccio
November 5, 2017
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Good stuff gpuccio! Are you familiar with the origin of carnivorous plants by WE. Lonnig? http://onlinelibrary.wiley.com/doi/10.1002/9780470015902.a0003818.pub2/abstract Mind boggling evidence that Dawinists have access to and yet still refuse to accept it... I pity them...Maybe I shouldn't? Duno...J-Mac
November 5, 2017
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@122
GPuccio: Of course the waiting time is a critical factor. And it depends strictly on the population size.
Thank you for taking the time to answer my question. It seems that we agree. Or do we not?
GPuccio: Of course, NS will be more efficient, and its time to fixation will be shorter, according to the selection coefficient.
I agree. When we have a global deadly virus outbreak and only the Japanese survive, then, obviously, fixation time is very short — the frequency of the ‘Japan-allele’ is at 100% in a matter of days.
GPuccio: However, NS too has the problem of time to fixation, and that can be a real stopper in many situations, as you correctly say.
But, that's not what I was saying. My point was not about fixation, but, instead, about the time necessary for restoring the population size to 7 billion. Is there a term for this period? My point is that during that period, evolution is performing worse than without NS — worse than a blind search. Only when the 'pre-deadly-virus-outbreak' population size is restored are probabilities for an evolutionary search back to normal — a blind search. Just to be clear: fixation does not take into account the original population size before NS intervention.Origenes
November 5, 2017
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jerry: " the person got Kenneth Miller to support him" What a help, really! :)gpuccio
November 5, 2017
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jerry: Thank you for your questions. 1) Of course, my point of view is essentially similar to Behe's. My approach is probably a little different in the details. However, the general idea is the same. As I have said, my approach here is top down, and is aimed essentially to give some higher threshold of what RV, even in an extremely optimistic scenario, can really do. Bottom up approaches, like Behe's and Axe's, try to establish a lower threshold based on empirical observations or actual experiments. Those data are very interesting, but again I don't think that the problem is really to establish if the edge is at 2, 3, 5, or 10 AAs. Even 10 AAs are simply ridiculous, when we consider what is necessary to build up functional proteins. Even the 37 that I have given for a completely unrealistic bacterial system are completely useless. A few examples: ATP synthase beta chain: 334 identities between E. coli and humans. Dynein: 1137 identities between saccharomices cerevisiae and humans. SMC3: 1133 identities (93%) between shark and humans. And so on, and so on. 1.7 million specific functional bits generated in 30 million years from pre-vertebrates to vertebrates. All that with probabilistic resources that could be enough, at most , for 10 - 20 specific AAs! And no way that NS can help explain all that! (see my challenge). 2) I don't know much of Madascar. In general, I never discuss phenotypic differences unless the molecular basis is well known (which is really rare). There are many adaptational mechanisms that can explain much. Only if we know the functional information that separates species or organisms can we discuss what can be attributed to design with reasonable certainty. The relationship between genotype and phenotype is often mysterious and not well understood. 3) RV for dummies? Let's try: a) Our planet, with all its biological resources, cannot generate enough different genomic states to find anything that has a functional information higher than 19 - 37 specific AAs at most by RV (with an hyper-optimistic estimate) b) Almost all proteins have higher functional information, ranging often in the hundreds, or even thousands, of specific AAs per protein, as proved by absolute conservation throughout hundred million years of natural history. c) The role of NS is absolutely negligible in those scenarios. Is that simple enough? :) By the way, if anyone on the other side doubts these numbers, please invite them here to explain why.gpuccio
November 5, 2017
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