Uncommon Descent Serving The Intelligent Design Community

Sequences Probability Calculator

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You can find here an utility to calculate the probabilities of random sequences of symbols.

It tries to answer questions like this: “a random process generating sequences of length L from an alphabet of S symbols in T trials of t seconds each, involving c chemical reactions, does exceed the resources of the universe (age, max number of chemical reactions, universal probability bound)?”.

The user interface is meant to be self-explanatory. The “Demo” button has the function to preset an example of input values. After the “Demo” you can eventually change some or all inputs and click the “Calculate” button to obtain your new output results. Otherwise if you want to start from entirely different inputs you may click the “Reset” button that zeroes inputs and outputs.

Disclaimer: this is a mathematical tool dealing with processes considered purely random. It doesn’t pretend to simulate the physical, chemical, biological, functional constraints specific of the processes. For example, about proteins and biopolymers, it doesn’t include the deterministic effect of amino acids forcing other amino acids to come with them, which could make the sequence more probable. Besides it doesn’t deal with all the specialized cases where functional issues somehow dominate the sequence structure. However the tool may give an idea of the orders of magnitude of the numbers involved in scenarios as origin of life, production of biopolymers, binary and character text generation, and so on.

Note about notation: almost all numbers are in “exponential E” notation, which is used in informatics as equivalent to the “scientific 10^” notation. Example: 4.4E+17 = 4.4×10^17 (scientific notation) = 440,000,000,000,000,000 (integer notation). The decimal dot moves rightward as many places as the exponent/power of ten (in this case 17).

According to Mike Elzinga over at TSZ:
In real physical/chemical processes – including those kinds of processes suspected to be involved in the origins of life – complicated mixtures of atoms and molecules are brought together in a heat bath of sufficient energy that unlikely reactions can occur.
How much energy is required to bring about unlikely reactions? We;re left to wonder. Then Mike says:
Take the negative logarithm of the probability calculation and call it “information.” What does that tell us?
What does "entropy" tells us? Boltzmann's entropy formula Mung
Joseph Felsenstein:
The thermodynamics-and-evolution stuff is OT for this thread. So is the essence-of-a-protein stuff. The exception to that is the issue of which parts of a protein can change and still have it do the same job.
Apparently we can assume that a protein has parts without bothering to engage the essence of a protein. Mung
'BBC News - Leprosy bacteria use biological alchemy' ('No Intelligent Design to be seen here. Move along!') http://www.bbc.co.uk/news/health-21056644 Axel
Of related note: Belgian Waffle - Douglas Axe - January 18, 2013 Excerpt:,, an article from Ghent University in Belgium claims a recent scientific paper has rescued evolutionary theory by solving the problem of evolutionary innovation.,,, Here's the concession: "An important unanswered question in Darwin's theory of evolution is how new characteristics seem to appear out of nowhere." Hmmm. Yes, I can see how this could be a problem for a theory of biological origins.,, ,,,here's the plain statement: "The preduplication [i.e., ancestral] ancMalS enzyme was multifunctional and already contained the different activities found in the postduplication [i.e., evolved] enzymes, albeit at a lower level." So, all we have here is a demonstration of what we already knew -- that evolution can adjust somewhat the relative preferences enzymes show for the molecules they already work on. Those aren't new activities, though, and this isn't a new result either. What would be really new and welcome would be for evolutionary biologists to begin taking the word new seriously. http://www.evolutionnews.org/2013/01/belgian_waffle068421.html bornagain77
Alan Fox:
Is the doubt that the process of evolution happens by a process involving the selection of competing alleles in a gene pool (having passed through a succession of antecedents who were successful enough to have descendants) or that evolution happens at all?
Are you admitting that you are ignorant as to what is being debated? Intelligent design argues against unguided, ie blind watchmaker, evolution. That is accumulations of genetic accidents accounting for the diversity of living organisms. The premise isn't even testable.
Well, IC is merely a formalism of the doubt you are expressing. Rather than surrender to doubt, we can keep looking for answers.
So archaeology and forensic science are merely formalisms of doubt? And that if we keep looking all artifacts and crimes would really come down to nature, operating freely? Joe
What evidence do you have, if any, that LIFE does not require specific sequences or that BIOLOGICAL EVOLUTION itself does not require the presence of specific sequences in order to occur?
You appear to think that there is only ever one solution to a problem! Alan Fox
I doubt that “proteins evolution proceeds by small changes from a previous viable antecedent”.
Is the doubt that the process of evolution happens by a process involving the selection of competing alleles in a gene pool (having passed through a succession of antecedents who were successful enough to have descendants) or that evolution happens at all?
We should consider that countless cellular systems made of proteins are irreducibly complex (IC).
Well, IC is merely a formalism of the doubt you are expressing. Rather than surrender to doubt, we can keep looking for answers. Alan Fox
Yeah, functionality is wide spread and any functioning proteins will do. So there. Joe
Alan claims:
"Insurmountable? Alleles exist. Alleles arise. Alleles get selected."
That's the claim, and yet reality reveals that what is taken for granted by evolutionists about 'alleles 'randomly' arising' is anything but easy for Darwinists to account for:
Revisiting the Central Dogma in the 21st Century - James A. Shapiro - 2009 Excerpt (Page 12): Underlying the central dogma and conventional views of genome evolution was the idea that the genome is a stable structure that changes rarely and accidentally by chemical fluctuations (106) or replication errors. This view has had to change with the realization that maintenance of genome stability is an active cellular function and the discovery of numerous dedicated biochemical systems for restructuring DNA molecules.(107–110) Genetic change is almost always the result of cellular action on the genome. These natural processes are analogous to human genetic engineering,,, (Page 14) Genome change arises as a consequence of natural genetic engineering, not from accidents. Replication errors and DNA damage are subject to cell surveillance and correction. When DNA damage correction does produce novel genetic structures, natural genetic engineering functions, such as mutator polymerases and nonhomologous end-joining complexes, are involved. Realizing that DNA change is a biochemical process means that it is subject to regulation like other cellular activities. Thus, we expect to see genome change occurring in response to different stimuli (Table 1) and operating nonrandomly throughout the genome, guided by various types of intermolecular contacts (Table 1 of Ref. 112). http://shapiro.bsd.uchicago.edu/Shapiro2009.AnnNYAcadSciMS.RevisitingCentral%20Dogma.pdf
Also of interest from the preceding paper, on page 22, is a simplified list of the ‘epigentic’ information flow in the cell that directly contradicts what was expected from the central dogma (Genetic Reductionism/modern synthesis model) of neo-Darwinism. as well:
Shapiro on Random Mutation: "What I ask others interested in evolution to give up is the notion of random accidental mutation." http://www.huffingtonpost.com/james-a-shapiro/jerry-coyne-fails-to-unde_b_1411144.html New Research Elucidates Directed Mutation Mechanisms - Cornelius Hunter - January 7, 2013 Excerpt: mutations don’t occur randomly in the genome, but rather in the genes where they can help to address the challenge. But there is more. The gene’s single stranded DNA has certain coils and loops which expose only some of the gene’s nucleotides to mutation. So not only are certain genes targeted for mutation, but certain nucleotides within those genes are targeted in what is referred to as directed mutations.,,, These findings contradict evolution’s prediction that mutations are random with respect to need and sometimes just happen to occur in the right place at the right time.,,, http://darwins-god.blogspot.com/2013/01/news-research-elucidates-directed.html
Now Alan, that is just plain embarrassing for Darwinists! All this time Darwinists have been claiming that mutations are arising 'randomly' yet the fact of the matter turns out to be that higher levels of information in the genome are 'directing' the mutations! As to fixing unambiguously 'random' mutations, well the evidence does not get better for you Alan:
Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) - October 2010 Excerpt: "Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, "This research really upends the dominant paradigm about how species evolve," said ecology and evolutionary biology professor Anthony Long, the primary investigator. http://www.arn.org/blogs/index.php/literature/2010/10/07/experimental_evolution_in_fruit_flies Mutations : when benefits level off - June 2011 - (Lenski's e-coli after 50,000 generations which is roughly equal to 1 million years of human evolution) Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually. http://www2.cnrs.fr/en/1867.htm?theme1=7 Epistasis between Beneficial Mutations - July 2011 Excerpt: We found that epistatic interactions between beneficial mutations were all antagonistic—the effects of the double mutations were less than the sums of the effects of their component single mutations. We found a number of cases of decompensatory interactions, an extreme form of antagonistic epistasis in which the second mutation is actually deleterious in the presence of the first. In the vast majority of cases, recombination uniting two beneficial mutations into the same genome would not be favored by selection, as the recombinant could not outcompete its constituent single mutations. https://uncommondesc.wpengine.com/epigenetics/darwins-beneficial-mutations-do-not-benefit-each-other/
What really needs to be said Alan??? It is interesting to point out (once again) that Darwinists are barking up the wrong tree in the first place:
Stephen Meyer - Functional Proteins And Information For Body Plans - video http://www.metacafe.com/watch/4050681 Dr. Stephen Meyer comments at the end of the preceding video,,, ‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’ - Stephen Meyer - (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate - 2009)
etc.. etc.. bornagain77
You appear to be referring to the origin of life
No, I'm not. I'm talking about life as we know it, the only life we know of. It's you who keep insisting on appealing to the unknowable unknown. What evidence do you have, if any, that LIFE does not require specific sequences or that BIOLOGICAL EVOLUTION itself does not require the presence of specific sequences in order to occur? Heck, even evolutionary algorithms use sequences of symbols, but let's just ignore that minor difficulty. Mung
Alan Fox #14 Thank you for your reference and invitation to the interesting Prof. Felsenstein's blog I will read. Yes, you are right, in a sense the SPC is a “tornado in a junkyard” simulator. For this reason – in my opinion – it could be used to do some raw computations about some aspects of the origin of life problem (some have indeed compared the supposed naturalistic solution to this problem as a “tornado in a junkyard generating a Boeing 747”). I doubt that "proteins evolution proceeds by small changes from a previous viable antecedent". We should consider that countless cellular systems made of proteins are irreducibly complex (IC). In this case, their creation should somehow happen "in a single trial", so to speak, with the probabilities the SPS could help to imagine. The SPC is a general tool. You could even compute what is the probability of arise by chance of Shakespeare's works. As I wrote in the disclaimer, of course to really focus all the complex issues about the biological sequences, one should refer to the researches of the specialists on the topic (as those linked by bornagain77 – come to my mind, from the ID side, the works of Douglas Axe, Ann Gauger, Kirk Durston, who in addition consider the related functional information content of the biopolymers). niwrad
Alan, what evidence do you have, if any, that life does not require specific sequences or that biological evolution itself does not require the presence of specific sequences in order to occur?
You appear to be referring to the origin of life, about which nobody knows anything apart from the fact it happened on Earth between four and three billion years ago. Evolution is the only reasonable attempt to explain the subsequent diversity and why it only needed to happen once.
Feel free to say that you have none.
Thanks for the permission. Alan Fox
...as to the insurmountable difficulties of evolving new functional proteins from pre-existing sequences:...
Insurmountable? Alleles exist. Alleles arise. Alleles get selected. Alan Fox
Alan, what evidence do you have, if any, that life does not require specific sequences or that biological evolution itself does not require the presence of specific sequences in order to occur? Feel free to say that you have none. Mung
To single out all major sequence codes and trace them in action may be viewed as the major challenge of modern molecular biology, sequence biology. - Edward N. Trifonov
as to the insurmountable difficulties of evolving new functional proteins from preexisting sequences:
The Case Against a Darwinian Origin of Protein Folds - Douglas Axe - 2010 Excerpt Pg. 11: "Based on analysis of the genomes of 447 bacterial species, the projected number of different domain structures per species averages 991. Comparing this to the number of pathways by which metabolic processes are carried out, which is around 263 for E. coli, provides a rough figure of three or four new domain folds being needed, on average, for every new metabolic pathway. In order to accomplish this successfully, an evolutionary search would need to be capable of locating sequences that amount to anything from one in 10^159 to one in 10^308 possibilities, something the neo-Darwinian model falls short of by a very wide margin." http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2010.1 Stability effects of mutations and protein evolvability. October 2009 Excerpt: The accepted paradigm that proteins can tolerate nearly any amino acid substitution has been replaced by the view that the deleterious effects of mutations, and especially their tendency to undermine the thermodynamic and kinetic stability of protein, is a major constraint on protein evolvability,, http://www.ncbi.nlm.nih.gov/pubmed/19765975 “Mutations are rare phenomena, and a simultaneous change of even two amino acid residues in one protein is totally unlikely. One could think, for instance, that by constantly changing amino acids one by one, it will eventually be possible to change the entire sequence substantially… These minor changes, however, are bound to eventually result in a situation in which the enzyme has ceased to perform its previous function but has not yet begun its ‘new duties’. It is at this point it will be destroyed” Maxim D. Frank-Kamenetski, Unraveling DNA, 1997, p. 72. (Professor at Brown U. Center for Advanced Biotechnology and Biomedical Engineering) Nature Paper,, Finds Darwinian Processes Lacking – Michael Behe – Oct. 2009 Excerpt: Now, thanks to the work of Bridgham et al (2009), even such apparently minor switches in structure and function (of a protein to its supposed ancestral form) are shown to be quite problematic. It seems Darwinian processes can’t manage to do even as much as I had thought. http://www.evolutionnews.org/2009/10/nature_paper_finally_reaches_t026281.html Wheel of Fortune: New Work by Thornton’s Group Supports Time-Asymmetric Dollo’s Law – Michael Behe – October 5, 2011 Excerpt: Darwinian selection will fit a protein to its current task as tightly as it can. In the process, it makes it extremely difficult to adapt to a new task or revert to an old task by random mutation plus selection. http://www.evolutionnews.org/2011/10/wheel_of_fortune_new_work_by_t051621.html When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied. http://www.biologicinstitute.org/post/18022460402/when-theory-and-experiment-collide Corticosteroid Receptors in Vertebrates: Luck or Design? – Ann Gauger – October 11, 2011 Excerpt: if merely changing binding preferences is hard, even when you start with the right ancestral form, then converting an enzyme to a new function is completely beyond the reach of unguided evolution, no matter where you start. http://www.evolutionnews.org/2011/10/luck_or_design051801.html
In fact the Ribosome, which makes the myriad of different, yet specific, types of proteins found in life, is found to be severely intolerant to any random mutations occurring to the proteins it manufactures.
The Ribosome: Perfectionist Protein-maker Trashes Errors Excerpt: The enzyme machine that translates a cell’s DNA code into the proteins of life is nothing if not an editorial perfectionist…the ribosome exerts far tighter quality control than anyone ever suspected over its precious protein products… To their further surprise, the ribosome lets go of error-laden proteins 10,000 times faster than it would normally release error-free proteins, a rate of destruction that Green says is “shocking” and reveals just how much of a stickler the ribosome is about high-fidelity protein synthesis. http://www.sciencedaily.com/releases/2009/01/090107134529.htm
And exactly how is the evolution of new forms of life suppose to ‘randomly’ occur if it is prevented from ‘randomly’ occurring at the base level of proteins in the first place? On top of the lack of ability of proteins to evolve into new shapes and functions, what does the recent hard evidence say about novel protein-protein binding site generation? i.e. about the ability of protein with novel functions to combine with other proteins in a meaningful way to do something useful for the cell?
“The likelihood of developing two binding sites in a protein complex would be the square of the probability of developing one: a double CCC (chloroquine complexity cluster), 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the entire world in the past 4 billion years, so the odds are against a single event of this variety (just 2 binding sites being generated by accident) in the history of life. It is biologically unreasonable.” Michael J. Behe PhD. (from page 146 of his book “Edge of Evolution”) Waiting Longer for Two Mutations – Michael J. Behe Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that ‘for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years’ (1 quadrillion years)(Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘is 5 million times larger than the calculation we have just given’ using their model (which nonetheless “using their model” gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model. Generally, when the results of a simple model disagree with observational data, it is an indication that the model is inadequate. http://www.discovery.org/a/9461
Please note that Dr. Behe, even though the numbers from their model still supported his overall conclusion for the rarity of spontaneous binding site formation, was indignant with the weight they were giving to their ‘hypothetical’ model over what the evidence actually said (good for him, a true scientist to the core!!) Dr. Behe’s research of empirical evidence agrees with the extreme difficulty that was found for scientists trying to ‘purposely design’ a protein-protein binding site:
Viral-Binding Protein Design Makes the Case for Intelligent Design Sick! (as in cool) – Fazale Rana – June 2011 Excerpt: When considering this study, it is remarkable to note how much effort it took to design a protein that binds to a specific location on the hemagglutinin molecule. As biochemists Bryan Der and Brian Kuhlman point out while commenting on this work, the design of these proteins required: “…cutting-edge software developed by ~20 groups worldwide and 100,000 hours of highly parallel computing time. It also involved using a technique known as yeast display to screen candidate proteins and select those with high binding affinities, as well as x-ray crystallography to validate designs.2? If it takes this much work and intellectual input to create a single protein from scratch, is it really reasonable to think that undirected evolutionary processes could accomplish this task routinely? In other words, the researchers from the University of Washington and The Scripps Institute have unwittingly provided empirical evidence that the high-precision interactions required for PPIs requires intelligent agency to arise.,,, Computer-designed proteins programmed to disarm variety of flu viruses – June 1, 2012 Excerpt: The research efforts, akin to docking a space station but on a molecular level, are made possible by computers that can describe the landscapes of forces involved on the submicroscopic scale.,, These maps were used to reprogram the design to achieve a more precise interaction between the inhibitor protein and the virus molecule. It also enabled the scientists, they said, “to leapfrog over bottlenecks” to improve the activity of the binder. http://phys.org/news/2012-06-computer-designed-proteins-variety-flu-viruses.html
etc.. etc.. etc.. bornagain77
PS @ Niwrad There is also the issue of whether there is only one sequence that will have a particular function in the whole of search space. All research so far suggests functionality is widespread in novel proteins. Alan Fox
Do you mean evolutionary processes don’t involve sequences of symbols? In this case, for you, biological evolution would have nothing to do with biology, given that molecular biology has a lot to do with sequences of symbols.
As timothya may no longer be able to post here, let me point out that your calculator is a "tornado in a junkyard" simulator. Nobody suggests proteins arise in one random event. That problem is reserved for origin-of-life hypotheses. Evolution proceeds by small changes from a previous viable antecedent. Environmental design then picks out any improved protein mutants and the process can recur ad infinitum. Professor Joe Felsenstein writes here about the problem. You are very welcome to engage there with him. Alan Fox
If all that was not crushing enough for the 'bottom up' reductive materialistism of neo-Darwinism, it is now found, though at first thought to be impossible, that 'non-local' (i.e. beyond space and time) quantum entanglement drives protein folding:
Coherent Intrachain energy migration at room temperature - Elisabetta Collini and Gregory Scholes - University of Toronto - Science, 323, (2009), pp. 369-73 Excerpt: The authors conducted an experiment to observe quantum coherence dynamics in relation to energy transfer. The experiment, conducted at room temperature, examined chain conformations, such as those found in the proteins of living cells. Neighbouring molecules along the backbone of a protein chain were seen to have coherent energy transfer. Where this happens quantum decoherence (the underlying tendency to loss of coherence due to interaction with the environment) is able to be resisted, and the evolution of the system remains entangled as a single quantum state. http://www.scimednet.org/quantum-coherence-living-cells-and-protein/ Testing quantum entanglement in protein Excerpt: The authors remark that this reverses the previous orthodoxy, which held that quantum effects could not exist in biological systems because of the amount of noise in these systems.,,, Environmental noise here drives a persistent and cyclic generation of new entanglement.,,, In summary, the authors say that they have demonstrated that entanglement can recur even in a hot noisy environment. In biological systems this can be related to changes in the conformation of macromolecules. http://www.quantum-mind.co.uk/testing-quantum-entanglement-in-protein-c288.html Physicists Discover Quantum Law of Protein Folding – February 22, 2011 Quantum mechanics finally explains why protein folding depends on temperature in such a strange way. Excerpt: First, a little background on protein folding. Proteins are long chains of amino acids that become biologically active only when they fold into specific, highly complex shapes. The puzzle is how proteins do this so quickly when they have so many possible configurations to choose from. To put this in perspective, a relatively small protein of only 100 amino acids can take some 10^100 different configurations. If it tried these shapes at the rate of 100 billion a second, it would take longer than the age of the universe to find the correct one. Just how these molecules do the job in nanoseconds, nobody knows.,,, Their astonishing result is that this quantum transition model fits the folding curves of 15 different proteins and even explains the difference in folding and unfolding rates of the same proteins. That's a significant breakthrough. Luo and Lo's equations amount to the first universal laws of protein folding. That’s the equivalent in biology to something like the thermodynamic laws in physics. http://www.technologyreview.com/view/423087/physicists-discover-quantum-law-of-protein/
Non-Local Quantum entanglement on such a massive scale in proteins (and DNA) is simply so far beyond anything man has even dreamed of accomplishing in quantum computing that this finding, by itself, should have made the biologists/mathematicians/physicists who discovered it drop to their knees in reverence to God upon their realization of what they were actually dealing with. And as if all this was not enough to show that proteins are far, far, more complex than just linear sequences of amino acids, it is now also found that proteins communicate with other proteins in the rest of the cell, and with other cells, using 'biophoton' light:
Cellular Communication through Light Excerpt: Information transfer is a life principle. On a cellular level we generally assume that molecules are carriers of information, yet there is evidence for non-molecular information transfer due to endogenous coherent light. This light is ultra-weak, is emitted by many organisms, including humans and is conventionally described as biophoton emission. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0005086 The mechanism and properties of bio-photon emission and absorption in protein molecules in living systems - May 2012 Excerpt: From the energy spectra, it was determined that the protein molecules could both radiate and absorb bio-photons with wavelengths of less than 3??m and 5–7??m, consistent with the energy level transitions of the excitons.,,, http://jap.aip.org/resource/1/japiau/v111/i9/p093519_s1?isAuthorized=no Proteins Conduct Electricity - November 25, 2012 Excerpt: "The team showed that the protein could carry large currents, equivalent to a human hair carrying one amp. The team also discovered that current flow could be regulated in much the same way as transistors, the tiny devices driving computers and smartphones, work but on a smaller scale: the proteins are only a quarter of the size of current silicon based transistors." The finding represents a leap forward in measurement at the nano scale. “Prior to this work, measurement of millions, if not billions of proteins was only possible, so losing crucial details of how an individual molecule functions.” The team used scanning tunneling microscopy (STM) to read the electronics of a single molecule of cytochrome b562, a protein just 5 nanometers (billions of a meter) long. http://crev.info/2012/11/proteins-conduct-electricity/
Also of note: It is also of interest to note that photonic communication has much greater fidelity, and quality, of communication than molecular communication does:
Photonics Excerpt: Unlike electrons, the driving force behind electronics, photons do not require any copper wires or other barriers to keep them from interacting with one another crossing and mingling photons have no adverse interactions whatsoever, where clashing electronics results in signal confusion and noise.,,, Photonic systems greatly expand the amount of bandwidth available; photonic transmissions are measured in trillion hertz (terahertz), compared with less than 10 billion hertz (gigahertz) used to measure electronics. http://ecommerce.hostip.info/pages/853/Photonics.html
Kari Jobe - Revelation Song – http://www.youtube.com/watch?v=FObjd5wrgZ8
Niwrad as to:
There are other aspects of biopolymers that are more difficult to simulate (e.g. their tridimensional shape). Instead, to compute the probability of the mere symbolic sequence is easier because is a combinatorial problem and is what this tool tries to do somehow.
Yes, it is so easy to overlook the fact that proteins are far more complicated than just linear sequences of amino acids. Francis Collins gives us a glimpse here:
Francis Collins on Making Life Excerpt: 'We are so woefully ignorant about how biology really works. We still don't understand how a particular DNA sequence—when we just stare at it—codes for a protein that has a particular function. We can't even figure out how that protein would fold—into what kind of three-dimensional shape. And I would defy anybody who is going to tell me that they could, from first principles, predict not only the shape of the protein but also what it does.' - Francis Collins - Former Director of the Human Genome Project
In fact, in many cases, the same protein is found to be 'context dependent' (dependent on what overall situation the protein is in), instead of just sequence dependent:
Now Evolution Must Have Evolved Different Functions Simultaneously in the Same Protein - Cornelius Hunter - December 1, 2012 Excerpt: LysRS has two different structural and functional states. When not phosphorylated LysRS is a crucial part of the translation process, supplying lysine amino acids to tRNA molecules. When phosphorylated it regulates gene expression. This is a major problem for evolutionary theory. http://darwins-god.blogspot.com/2012/12/now-evolution-must-have-evolved.html Explaining how a protein can perform multiple roles - Cell Biology - December 18, 2009 Excerpt: It’s been known for more than a decade that some cell proteins can carry out multiple functions. For example, it was discovered in 1999 that the protein TyrRS (explained shortly) participated not only in the building of enzymes, but also could function to stimulate the growth of blood vessels. Discovering that the same protein could perform very different roles opened one of the great new chapters in molecular biology http://scitechstory.com/2009/12/18/explaining-how-a-protein-can-perform-multiple-roles/
Moreover, much contrary to the genetic reductionism model of the central dogma, (i.e. DNA makes RNA makes Protein), external factors (i.e. what cell is being built, where the protein is in the cell) are now strongly implicated in determining exactly how any specific protein is put together from exons:
Astonishing DNA complexity demolishes neo-Darwinism - Alex Williams Excerpt: Exons are not gene-specific but are modules that can be joined to many different RNA transcripts. One exon (i.e. a protein-making portion of one gene) can be used in combination with up to 33 different genes located on as many as 14 different chromosomes. This means that one exon can specify one part shared in common by many different proteins. http://creation.com/images/pdfs/tj/j21_3/j21_3_111-117.pdf Demise of the Gene - September 19, 2012 Excerpt: Although the gene has conventionally been viewed as the fundamental unit of genomic organization, on the basis of ENCODE data it is now compellingly argued that this unit is not the gene but rather the transcript (Washietl et al. 2007; Djebali et al. 2012a). On this view, genes represent a higher-order framework around which individual transcripts coalesce, creating a poly-functional entity that assumes different forms under different cellular states, guided by differential utilization of regulatory DNA. (What does our genome encode? John A. Stamatoyannopoulos Genome Res. 2012 22: 1602-1611.) http://www.evolutionnews.org/2012/09/demise_of_the_g064371.html The Extreme Complexity Of Genes – Dr. Raymond G. Bohlin – video http://www.metacafe.com/watch/8593991/ Multidimensional Genome – Dr. Robert Carter – video (Notes in video description) http://www.metacafe.com/w/8905048
bornagain77 #8: The particular specific sequence does indeed matter towards functionality.
Exactly. Most biopolymers must have specific sequence of symbols to work. So their generation by random evolution has unavoidably something to do with the probability of generating those specific sequences of symbols by chance. There are other aspects of biopolymers that are more difficult to simulate (e.g. their tridimensional shape). Instead, to compute the probability of the mere symbolic sequence is easier because is a combinatorial problem and is what this tool tries to do somehow. niwrad
of note: Nanomachines in the Powerhouse of the Cell: Architecture of the Largest Protein Complex of Cellular Respiration Elucidated - July 2010 Excerpt: In biological oxidation, the energy will be released by the membrane bound protein complexes of the respiratory chain in a controlled manner in small packages. Comparable to a fuel cell, this process generates an electrical membrane potential, which is the driving force of ATP synthesis. The total surface of all mitochondrial membranes in a human body covers about 14.000 square meter. This accounts for a daily production of about 65 kg of ATP. (A little over 143 pounds). The now presented structural model provides important and unexpected insights for the function of complex I. A special type of “transmission element,” which is not known from any other protein, appears to be responsible for the energy transduction within the complex by mechanical nanoscale coupling. Transferred to the technical world, this could be described as a power transmission by a coupling rod, which connects for instance the wheels of a steam train. This new nano-mechanical principle will now be analysed by additional functional studies and a refined structural analysis. http://www.sciencedaily.com/releases/2010/07/100702100414.htm bornagain77
Here is a brand new molecular animation of the ATP molecular machine Miniature Molecular Power Plant: ATP Synthase - video http://www.youtube.com/watch?v=XI8m6o0gXDY bornagain77
Tim, contrary to what you would like to think, the particular specific sequence does indeed matter towards functionality: Common Design in Bat and Whale Echolocation Genes? - January 2011 Excerpt: two new studies in the January 26th issue of Current Biology, a Cell Press publication, show that bats' and whales' remarkable ability and the high-frequency hearing it depends on are shared at a much deeper level than anyone would have anticipated -- all the way down to the molecular level. http://www.evolutionnews.org/2011/01/common_design_in_bat_and_whale042291.html Convergent sequence evolution between echolocating bats and dolphins - Liu et al (2010) Excerpt: We previously reported that the Prestin gene has undergone sequence convergence among unrelated lineages of echolocating bat [3]. Here we report that this gene has also undergone convergent amino acid substitutions in echolocating dolphins, http://www.cell.com/current-biology/abstract/S0960-9822%2809%2902073-9 Bat and Whale Echolocation Genes Point to Common Design - February 2011 - Podcast http://intelligentdesign.podomatic.com/entry/2011-02-21T10_59_16-08_00 Here's a figure showing bats and dolphins group together on the same tree based on Prestin sequence comparisons. http://sphotos.xx.fbcdn.net/hphotos-ash3/580955_215152708593734_182588468516825_355811_30197372_n.jpg Common Design in Bat and Whale Echolocation Genes? - January 2011 Excerpt: two new studies in the January 26th issue of Current Biology, a Cell Press publication, show that bats' and whales' remarkable ability and the high-frequency hearing it depends on are shared at a much deeper level than anyone would have anticipated -- all the way down to the molecular level. http://www.evolutionnews.org/2011/01/common_design_in_bat_and_whale042291.html Convergent sequence evolution between echolocating bats and dolphins - Liu et al (2010) Excerpt: We previously reported that the Prestin gene has undergone sequence convergence among unrelated lineages of echolocating bat [3]. Here we report that this gene has also undergone convergent amino acid substitutions in echolocating dolphins, http://www.cell.com/current-biology/abstract/S0960-9822%2809%2902073-9 Bothersome Bats and Other Pests Disturb the "Tree of Life" - Casey Luskin - December 5, 2012 Excerpt: But this is hardly the only known example of molecular convergent evolution. In his book The Cell's Design, chemist and Darwin-skeptic Fazale Rana reviewed the technical literature and documented over 100 reported cases of convergent genetic evolution. Each case shows an example where biological similarity -- even at the genetic level -- is not the result of inheritance from a common ancestor. http://www.evolutionnews.org/2012/12/bothersome_bats067121.html And,,, Bernard d'Abrera on Butterfly Mimicry and the Faith of the Evolutionist - October 5, 2011 Excerpt: For it to happen in a single species once through chance, is mathematically highly improbable. But when it occurs so often, in so many species, and we are expected to apply mathematical probability yet again, then either mathematics is a useless tool, or we are being criminally blind.,,, Evolutionism (with its two eldest daughters, phylogenetics and cladistics) is the only systematic synthesis in the history of the universe that proposes an Effect without a Final Cause. It is a great fraud, and cannot be taken seriously because it outrageously attempts to defend the philosophically indefensible. http://www.evolutionnews.org/2011/10/in_this_excerpt_from_the051571.html bornagain77
timothya #6 Do you mean evolutionary processes don't involve sequences of symbols? In this case, for you, biological evolution would have nothing to do with biology, given that molecular biology has a lot to do with sequences of symbols. niwrad
Niwrad posted this:
Thanks. I just wanted to confirm that the simulator has nothing to do with evolutionary processes. timothya
timothya #2 Yes. niwrad
Nice! Notes:
The Universal Plausibility Metric (UPM) & Principle (UPP) - Abel - Dec. 2009 Excerpt: Mere possibility is not an adequate basis for asserting scientific plausibility. A precisely defined universal bound is needed beyond which the assertion of plausibility, particularly in life-origin models, can be considered operationally falsified. But can something so seemingly relative and subjective as plausibility ever be quantified? Amazingly, the answer is, "Yes.",,, c?u = Universe = 10^13 reactions/sec X 10^17 secs X 10^78 atoms = 10^108 c?g = Galaxy = 10^13 X 10^17 X 10^66 atoms = 10^96 c?s = Solar System = 10^13 X 10^17 X 10^55 atoms = 10^85 c?e = Earth = 10^13 X 10^17 X 10^40 atoms = 10^70 http://www.tbiomed.com/content/6/1/27 Book Review - Meyer, Stephen C. Signature in the Cell. New York: HarperCollins, 2009. Excerpt: As early as the 1960s, those who approached the problem of the origin of life from the standpoint of information theory and combinatorics observed that something was terribly amiss. Even if you grant the most generous assumptions: that every elementary particle in the observable universe is a chemical laboratory randomly splicing amino acids into proteins every Planck time for the entire history of the universe, there is a vanishingly small probability that even a single functionally folded protein of 150 amino acids would have been created. Now of course, elementary particles aren't chemical laboratories, nor does peptide synthesis take place where most of the baryonic mass of the universe resides: in stars or interstellar and intergalactic clouds. If you look at the chemistry, it gets even worse—almost indescribably so: the precursor molecules of many of these macromolecular structures cannot form under the same prebiotic conditions—they must be catalysed by enzymes created only by preexisting living cells, and the reactions required to assemble them into the molecules of biology will only go when mediated by other enzymes, assembled in the cell by precisely specified information in the genome. So, it comes down to this: Where did that information come from? The simplest known free living organism (although you may quibble about this, given that it's a parasite) has a genome of 582,970 base pairs, or about one megabit (assuming two bits of information for each nucleotide, of which there are four possibilities). Now, if you go back to the universe of elementary particle Planck time chemical labs and work the numbers, you find that in the finite time our universe has existed, you could have produced about 500 bits of structured, functional information by random search. Yet here we have a minimal information string which is (if you understand combinatorics) so indescribably improbable to have originated by chance that adjectives fail. http://www.fourmilab.ch/documents/reading_list/indices/book_726.html
To clarify as to how the 500 bit universal limit is found for 'structured, functional information':
Dembski's original value for the universal probability bound is 1 in 10^150, 10^80, the number of elementary particles in the observable universe. 10^45, the maximum rate per second at which transitions in physical states can occur. 10^25, a billion times longer than the typical estimated age of the universe in seconds. Thus, 10^150 = 10^80 × 10^45 × 10^25. Hence, this value corresponds to an upper limit on the number of physical events that could possibly have occurred since the big bang. How many bits would that be: Pu = 10-150, so, -log2 Pu = 498.29 bits Call it 500 bits (The 500 bits is further specified as a specific type of information. It is specified as Complex Specified Information by Dembski or as Functional Information by Abel to separate it from merely Ordered Sequence Complexity or Random Sequence Complexity; See Three subsets of sequence complexity) Three subsets of sequence complexity and their relevance to biopolymeric information - Abel, Trevors http://www.tbiomed.com/content/2/1/29
Of note:
The story of the Monkey Shakespeare Simulator Project Excerpt: Starting with 100 virtual monkeys typing, and doubling the population every few days, it put together random strings of characters. It then checked them against the archived works of Shakespeare. Before it was scrapped, the site came up with 10^35 number of pages, all typed up. Any matches? Not many. It matched two words, “now faire,” and a partial name from A Midsummer Night’s Dream, and three words and a comma, “Let fame, that,” from Love’s Labour’s Lost. The record, achieved suitably randomly at the beginning of the site’s run in 2004, was 23 characters long, including breaks and spaces. http://io9.com/5809583/the-story-of-the-monkey-shakespeare-simulator-project "Monkeys Typing Shakespeare" Simulation Illustrates Combinatorial Inflation Problem - October 2011 Excerpt: In other words, Darwinian evolution isn't going to be able to produce fundamentally new protein folds. In fact, it probably wouldn't even be able to produce a single 9-character string of nucleotides in DNA, if that string would not be retained by selection until all 9 nucleotides were in place. http://www.evolutionnews.org/2011/10/monkeys_typing_shakespeare_sim051561.html “a one-celled bacterium, e. coli, is estimated (from a thermodynamic perspective) to contain the equivalent of 100 million pages of Encyclopedia Britannica. Expressed in information in science jargon, this would be the same as 10^12 bits of information. In comparison, the total writings from classical Greek Civilization is only 10^9 bits, and the largest libraries in the world – The British Museum, Oxford Bodleian Library, New York Public Library, Harvard Widenier Library, and the Moscow Lenin Library – have about 10 million volumes or 10^12 bits.” – R. C. Wysong
Let's see, 10^80 atoms, at 10^45 per sec for 10^25 s = 10^150 trials. Where, the UPB looks at odds of 1 in 10^150 as defining a search challenge that is insurmountable. To guarantee that, we routinely use a limit of 1,000 bits for the observed cosmos, so that the 1.07*10^301 possibilities swamp the 10^150 possibilities for 10^80 atoms for 10^25 s, 50 mn times the estimated lifespan of the observed cosmos to date. That looks like one trial per atom per 10^-45 sec for the thermodynamic lifespan of the observable cosmos to me. That would be ridiculously generous to any onlooker, save for the determined Darwinist hoping to find an out from the sampling space challenge he faces. And the predictable onward claim is that there is a sampling from a reduced space, but that omits that what that means -- on blind choice of subset -- is a selection from the set of all subsets, the power set of the original set. That is exponentially worse. Blind search for an advantageous search only makes the matter worse. kairosfocus
Does the model require the random trials to be run sequentially? timothya
Quite interesting device from the Progretto Cosmo folks. kairosfocus

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