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ID Foundations 15(c) — A FAQ on Front-Loading, thanks to Genomicus

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Onlookers, Geno concludes for the moment with FAQ’s:

____________________

Geno: >>

A Testable ID Hypothesis: Front-loading, part C

In the last two articles on front-loading, I explained what the front-loading hypothesis is all about and some research questions we can ask from a front-loading perspective. This article will be an FAQ about the front-loading hypothesis. So, without further introduction, let’s begin (note: some of the content of this FAQ can be found in the previous two articles).

  1. What is front-loading?

Front-loading is the investment of a significant amount of information at the initial stage of evolution (the first life forms) whereby this information shapes and constrains subsequent evolution through its dissipation. This is not to say that every aspect of evolution is pre-programmed and determined. It merely means that life was built to evolve with tendencies as a consequence of carefully chosen initial states in combination with the way evolution works.” Mike Gene, The Design Matrix: A Consilience of Clues, page 147

In short, this ID hypothesis proposes that the earth was, at some point in its history, seeded with unicellular organisms that had the necessary genomic information to shape future evolution. Necessarily, this genomic information was designed into their genomes.

 

  1. How is front-loading different from directed panspermia?

 

In a paper published in the journal Icarus, Francis Crick and Leslie Orgel proposed the hypothesis of directed panspermia. According to this hypothesis, the earth was intentionally seeded with life forms by some intelligence. The front-loading hypothesis goes a step further and proposes that these life forms contained the necessary genomic information to shape the course of future evolution. For example, the origin of metazoan complexity would have been planned and anticipated by the genomic information in the first genomes. Thus, the front-loading hypothesis is inherently teleological and an ID hypothesis.

 

  1. Does front-loading propose that all the genes found in life were in the first life forms?

 

No, it does not. Front-loading does not suggest that all genes were there from the start. Indeed, many genes found in modern life forms are probably the result of purely unplanned mechanisms (gene duplication and subsequent divergence, for example). Nevertheless, genes essential for the origin and development of the metazoan body plan would be present in the first genomes (or have homologs in the first genomes).

 

  1. If genes necessary for the origin of metazoan life forms were placed, then random mutation would have destroyed them and they would decay, right?

 

This is a common objection to the front-loading hypothesis, but it can be easily answered. These genes would be given an important function in the first life forms, such that they would be preserved across deep time. Front-loading doesn’t involve much of simply turning genes (that were previously unexpressed) on at some given time.

 

  1. How could sophisticated molecular systems be front-loaded?

There are two basic solutions to the problem of front-loading sophisticated molecular systems, but more research is needed so that we can find out exactly how these solutions would work in practice. In theory, however, there’s the “bottom up” approach and the “top down” approach to front-loading molecular systems. In the “bottom up” approach, the original cells would contain the components of the molecular machine we want to front-load, but these components would be carrying out functions not related to the function of the molecular machine. Then, somehow (here’s where we need research), something causes them to associate such that they fit nicely with each other, forming a novel molecular machine.

The “top down” approach proposes that the first cells had a highly complex molecular machine, composed of, say, components A, B, C, D, E, F, G, H, and J. If we want to front-load a molecular machine composed of components A, B, C, and D, then this highly complex molecular machine contains a functional subset of A, B, C, and D. In other words, components E, F, G, H, and J would simply have to be deleted from the highly complex molecular machine, resulting in a molecular machine composed of A, B, C, and D. This model is actually testable. Under this model, we would tentatively predict that a homologous system of a molecular machine will be more complex if it is more ancient than the molecular machine.

  1. What testable predictions does the front-loading hypothesis make?

There are several testable predictions the front-loading hypothesis makes:

  1. Cytosine deamination. Of the three bases in DNA (adenine, guanine, and cytosine) that are prone to deamination, cytosine is the most likely to undergo deamination. This ultimately results in a C –> T transition. Cytosine deamination often causes severe genetic diseases in humans, so why would a front-loader choose cytosine as a base in DNA? It has been observed that C –> T transitions result in a pool of strongly hydrophobic amino acids, which leads to the following prediction from a front-loading perspective: a designer would have chosen cytosine because it would facilitate front-loading in that mutations could be channeled in the direction of increased hydrophobicity. This prediction would be confirmed if key protein sequences in metazoan life forms were the result of numerous C –> T transitions.
  2. The genetic code. The front-loading hypothesis proposes that the universal optimal genetic code was present at the dawn of life: in other words, we won’t find precursors of sub-optimal genetic codes, because the genetic code was optimal from the start. Further, the front-loading hypothesis predicts that all 20 amino acids would have been used in the first life forms, and that the transcription, translation, and proof-reading machinery would have all been present at the start of life on earth.
  3. Biological complexity. Front-loading predicts that the last universal common ancestor (LUCA) was quite complex, complete with genes necessary for the origin and development of metazoan life forms.
  4. Protein sequence conservation. In eukaryotes, there are certain proteins that are extremely important. For example, tubulin is an important component of cilia; actin plays a major role in the cytoskeleton and is also found in sarcomeres (along with myosin), a major structure in muscle cells; and the list could go on. How could such proteins be front-loaded? Of course, with some of these proteins they could be designed into the initial life forms, but some of them are specific to eukaryotes, and for a reason: they don’t function that well in a prokaryotic context. For these proteins, how would a designer front-load them? Let’s say X is the protein we want to front-load. How do we go about doing this? Well, firstly, we can design a protein, Y, that has a very similar fold to X, the future protein we want to front-load. Thus, a protein with similar properties to X can be designed into the initial life forms. But what is preventing random mutations from basically destroying the sequence identity of Y, over time, such that the original fold/sequence identity of Y is lost? To counter this, Y can also be given a very important function so that its sequence identity will be well conserved. Thus, we can make this prediction from a front-loading perspective: proteins that are very important to eukaryotes, and specific to them, will share deep homology (either structurally or in sequence similarity) with prokaryotic proteins, and importantly, that these prokaryotic proteins will be more conserved in sequence identity than the average prokaryotic protein. Darwinian evolution only predicts the first part of that: it doesn’t predict that part that is in bold text. This is a testable prediction made exclusively by the front-loading hypothesis.

 

  1. Does the front-loading hypothesis suggest that evolution was programmed?

 

No. Front-loading does not propose that all biological innovations were the result of planning and teleology.

 

Conclusion

 

The more I discuss front-loading with its opponents and proponents, the more I will add to this FAQ. Please add any questions, comments, etc., below.

 

About me

Over the years, I have become quite interested in the discussion over biological origins, and I think there is “something solid” behind the idea that teleology has played a role in the history of life on earth. When I’m not doing multiple sequence alignments, I’m thinking about ID and writing articles on the subject, which can be found on my website, The Genome’s Tale.

I am grateful to UD member kairosfocus for providing me with this opportunity to make a guest post on UD. Many thanks to kairosfocus.

Also see The Design Matrix, by Mike Gene.  >>

____________________

So, here we have one specific model for how ID could possibly have been done. Obviously, not the only possibility, but a significant one worthy of investigations. END

Comments
It seems to have happened a total of one (that is, 1) time in the billion years since the divergence of fungi from other eukaryotes. So there is at least one chain requiring a duplication and two specific mutations, and the complaint is that it is only known to have happened once. Considering that Behe would have proclaimed it impossible to have happened at all, that's quite a few times. I believe Behe's stock response to any demonstration that a three step bit of evolution has happened is, "that's cool, now do it again." I'm not sure what you mean to imply by the complete package being easy. What the paper says is, "These losses were complementary, so both copies became obligate components with restricted spatial roles in the complex." This is cutting edge research. I'm sure as the technology becomes available there will be more scenarios outlined.
Petrushka
February 1, 2012
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Front-loading predicts that the last universal common ancestor (LUCA) was quite complex, complete with genes necessary for the origin and development of metazoan life forms.
I'll repeat my question I asked in part (a) - how can you test this "testable prediction" without resort to a time machine?Heinrich
February 1, 2012
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well pet, you accuse me of contorted reasoning when the detrimental mutation rate is shown to be so exceedingly high??? You don't even contest the fact man! You just sluff it off??? I guess if my reasoning is contorted that must make you stark raving mad! Go figure!!! ,,,In reply to a personal e-mail from myself, Dr. Cano commented on the 'Fitness Test' I had asked him about: Dr. Cano stated: "We performed such a test, a long time ago, using a panel of substrates (the old gram positive biolog panel) on B. sphaericus. From the results we surmised that the putative "ancient" B. sphaericus isolate was capable of utilizing a broader scope of substrates. Additionally, we looked at the fatty acid profile and here, again, the profiles were similar but more diverse in the amber isolate.": Fitness test which compared ancient bacteria to its modern day descendants, RJ Cano and MK Borucki Thus, the most solid evidence available for the most ancient DNA scientists are able to find does not support evolution happening on the molecular level of bacteria. In fact, according to the fitness test of Dr. Cano, the change witnessed in bacteria conforms to the exact opposite, Genetic Entropy; a loss of functional information/complexity, since fewer substrates and fatty acids are utilized by the modern strains. Considering the intricate level of protein machinery it takes to utilize individual molecules within a substrate, we are talking an impressive loss of protein complexity, and thus loss of functional information, from the ancient amber sealed bacteria. Here is a revisit to the video of the 'Fitness Test' that evolutionary processes have NEVER passed as for a demonstration of the generation of functional complexity/information above what was already present in a parent species bacteria: Is Antibiotic Resistance evidence for evolution? - 'Fitness Test' - video http://www.metacafe.com/watch/3995248bornagain77
February 1, 2012
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you then state 'Current laboratory experiments — Lenski, Thornton — support a functional space that can be connected.' And the real world says: Mutations : when benefits level off - June 2011 - (Lenski's e-coli after 50,000 generations) 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 More from Lenski's Lab, Still Spinning Furiously - Behe - January 2012 Excerpt: So at the end of the day there was left the mutated bacteriophage lambda, still incompetent to invade most E. coli cells, plus mutated E. coli, now with broken genes which remove its ability to metabolize maltose and mannose. It seems Darwinian evolution took a little step sideways and two big steps backwards. http://www.evolutionnews.org/2012/01/more_from_lensk055751.html A Blind Man Carrying a Legless Man Can Safely Cross the Street - Michael J. Behe - January 2012 Excerpt: Finnegan et al’s (2012) work intersects with several other concepts. First, their work is a perfect example of Michael Lynch’s idea of “subfunctionalization”, where a gene with several functions duplicates, and each duplicate loses a separate function of the original. (Force et al, 1999) Again, however, the question of how the multiple functions arose in the first place is begged. Second, it intersects somewhat with the recent paper by Austin Hughes (2011) in which he proposes a non-selective mechanism of evolution abbreviated “PRM” (plasticity-relaxation-mutation), where a “plastic” organism able to survive in many environments settles down in one and loses by degradative mutation and drift the primordial plasticity. But again, where did those primordial functions come from? It seems like some notable workers are converging on the idea that the information for life was all present at the beginning, and life diversifies by losing pieces of that information. That concept is quite compatible with intelligent design. Not so much with Darwinism. Finally, Thornton and colleagues latest work points to strong limits on the sort of neutral evolution that their own work envisions. The steps needed for the scenario proposed by Finnegan et al (2012) are few and simple: 1) a gene duplication; 2) a point mutation; 3) a second point mutation. No event is deleterious. Each event spreads in the population by neutral drift. Notice that the two point mutations do not have to happen together. They are independent, and can happen in either order. Nonetheless, this scenario is apparently exceedingly rare. It seems to have happened a total of one (that is, 1) time in the billion years since the divergence of fungi from other eukaryotes. It happened only once in the fungi, and a total of zero times in the other eukaryotic branches of life. If the scenario were in fact as easy to achieve in nature as it is to describe in writing, we should expect it to have happened many times independently in fungi and also to have happened in all other branches of eukaryotes. http://behe.uncommondescent.com/2012/01/a-blind-man-carrying-a-legless-man-can-safely-cross-the-street/bornagain77
February 1, 2012
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The fact remains that bacteria do not go extinct, and rivers do flow uphill through evaporation and rainfall. All your contorted reasoning is trumped by simple observation of reality.Petrushka
February 1, 2012
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Sanford’s pro-ID thesis supported by PNAS paper, read it and weep, literally - September 2010 Excerpt: Unfortunately, it has become increasingly clear that most of the mutation load is associated with mutations with very small effects distributed at unpredictable locations over the entire genome, rendering the prospects for long-term management of the human gene pool by genetic counseling highly unlikely for all but perhaps a few hundred key loci underlying debilitating monogenic genetic disorders (such as those focused on in the present study). https://uncommondescent.com/darwinism/sanfords-pro-id-thesis-supported-by-pnas-paper-read-it-and-weep-literally/ Unexpectedly small effects of mutations in bacteria bring new perspectives - November 2010 Excerpt: Most mutations in the genes of the Salmonella bacterium have a surprisingly small negative impact on bacterial fitness. And this is the case regardless whether they lead to changes in the bacterial proteins or not.,,, using extremely sensitive growth measurements, doctoral candidate Peter Lind showed that most mutations reduced the rate of growth of bacteria by only 0.500 percent. No mutations completely disabled the function of the proteins, and very few had no impact at all. Even more surprising was the fact that mutations that do not change the protein sequence had negative effects similar to those of mutations that led to substitution of amino acids. A possible explanation is that most mutations may have their negative effect by altering mRNA structure, not proteins, as is commonly assumed. http://www.physorg.com/news/2010-11-unexpectedly-small-effects-mutations-bacteria.html
To get around the problem of slightly detrimental mutations, that are below the power of Natural Selection to remove from the genome, Darwinists have tried to relabel the slightly detrimental mutations as 'neutral', but the fact is that if a mutation is 'just sitting there', not doing anything, then it is in reality placing a energetic burden on the cell and is not truly 'neutral' but is in fact slightly detrimental. Dr. Berlinski comments on the ad hoc 'neutral theory' of evolution here:
Majestic Ascent: Berlinski on Darwin on Trial - David Berlinski - November 2011 Excerpt: The publication in 1983 of Motoo Kimura's The Neutral Theory of Molecular Evolution consolidated ideas that Kimura had introduced in the late 1960s. On the molecular level, evolution is entirely stochastic, and if it proceeds at all, it proceeds by drift along a leaves-and-current model. Kimura's theories left the emergence of complex biological structures an enigma, but they played an important role in the local economy of belief. They allowed biologists to affirm that they welcomed responsible criticism. "A critique of neo-Darwinism," the Dutch biologist Gert Korthof boasted, "can be incorporated into neo-Darwinism if there is evidence and a good theory, which contributes to the progress of science." By this standard, if the Archangel Gabriel were to accept personal responsibility for the Cambrian explosion, his views would be widely described as neo-Darwinian. http://www.evolutionnews.org/2011/11/berlinski_on_darwin_on_trial053171.html
As well, the slow accumulation of 'slightly detrimental mutations' in humans, that is 'slightly detrimental mutations' which are far below the power of natural selection to remove from our genomes, is revealed by these following facts:
“When first cousins marry, their children have a reduction of life expectancy of nearly 10 years. Why is this? It is because inbreeding exposes the genetic mistakes within the genome (slightly detrimental recessive mutations) that have not yet had time to “come to the surface”. Inbreeding is like a sneak preview, or foreshadowing, of where we are going to be genetically as a whole as a species in the future. The reduced life expectancy of inbred children reflects the overall aging of the genome that has accumulated thus far, and reveals the hidden reservoir of genetic damage that have been accumulating in our genomes." Sanford; Genetic Entropy; page 147 Children of incest - Journal of Pediatrics Abstract: Twenty-nine children of brother-sister or father-daughter matings were studied. Twenty-one were ascertained because of the history of incest, eight because of signs or symptoms in the child. In the first group of 21 children, 12 had abnormalities, which were severe in nine (43%). In one of these the disorder was autosomal recessive. All eight of the group referred with signs or symptoms had abnormalities, three from recessive disorders. The high empiric risk for severe problems in the children of such close consanguineous matings should be borne in mind, as most of these infants are relinquished for adoption. http://www.jpeds.com/article/S0022-3476%2882%2980347-8/abstract
Real world computer simulations are here
Using Computer Simulation to Understand Mutation Accumulation Dynamics and Genetic Load: Excerpt: We apply a biologically realistic forward-time population genetics program to study human mutation accumulation under a wide-range of circumstances.,, Our numerical simulations consistently show that deleterious mutations accumulate linearly across a large portion of the relevant parameter space. http://bioinformatics.cau.edu.cn/lecture/chinaproof.pdf MENDEL’S ACCOUNTANT: J. SANFORD†, J. BAUMGARDNER‡, W. BREWER§, P. GIBSON¶, AND W. REMINE http://mendelsaccount.sourceforge.net/ The GS (genetic selection) Principle - David L. Abel - 2009 Excerpt: Stunningly, information has been shown not to increase in the coding regions of DNA with evolution. Mutations do not produce increased information. Mira et al (65) showed that the amount of coding in DNA actually decreases with evolution of bacterial genomes, not increases. This paper parallels Petrov’s papers starting with (66) showing a net DNA loss with Drosophila evolution (67). Konopka (68) found strong evidence against the contention of Subba Rao et al (69, 70) that information increases with mutations. The information content of the coding regions in DNA does not tend to increase with evolution as hypothesized. Konopka also found Shannon complexity not to be a suitable indicator of evolutionary progress over a wide range of evolving genes. Konopka’s work applies Shannon theory to known functional text. Kok et al. (71) also found that information does not increase in DNA with evolution. As with Konopka, this finding is in the context of the change in mere Shannon uncertainty. The latter is a far more forgiving definition of information than that required for prescriptive information (PI) (21, 22, 33, 72). It is all the more significant that mutations do not program increased PI. Prescriptive information either instructs or directly produces formal function. No increase in Shannon or Prescriptive information occurs in duplication. What the above papers show is that not even variation of the duplication produces new information, not even Shannon “information.” http://www.bioscience.org/2009/v14/af/3426/fulltext.htm Experimental Evolution in Fruit Flies - October 2010 Excerpt: "This research really upends the dominant paradigm about how species evolve".,,, as stated in regards to the 35 year experimental failure to fixate a single beneficial mutation within fruit flies. http://www.arn.org/blogs/index.php/literature/2010/10/07/experimental_evolution_in_fruit_flies
Further notes on mutations
"I have seen estimates of the incidence of the ratio of deleterious-to-beneficial mutations which range from one in one thousand up to one in one million. The best estimates seem to be one in one million (Gerrish and Lenski, 1998). The actual rate of beneficial mutations is so extremely low as to thwart any actual measurement (Bataillon, 2000, Elena et al, 1998). Therefore, I cannot ...accurately represent how rare such beneficial mutations really are." (J.C. Sanford; Genetic Entropy page 24) - 2005 Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? (Thomas Bataillon) Abstract......It is argued that, although most if not all mutations detected in mutation accumulation experiments are deleterious, the question of the rate of favourable mutations (and their effects) is still a matter for debate. Distribution of fitness effects caused by random insertion mutations in Escherichia coli Excerpt: At least 80% of the mutations had a significant negative effect on fitness, whereas none of the mutations had a significant positive effect. “But in all the reading I’ve done in the life-sciences literature, I’ve never found a mutation that added information… All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it.” Lee Spetner - Ph.D. Physics - MIT - Not By Chance John Sanford writes in “Genetic Entropy & the Mystery of the Genome”: “Bergman (2004) has studied the topic of beneficial mutations. Among other things, he did a simple literature search via Biological Abstracts and Medline. He found 453,732 ‘mutation’ hits, but among these only 186 mentioned the word ‘beneficial’ (about 4 in 10,000). When those 186 references were reviewed, almost all the presumed ‘beneficial mutations’ were only beneficial in a very narrow sense–but each mutation consistently involved loss of function changes–hence loss of information. While it is almost universally accepted that beneficial (information creating) mutations must occur, this belief seems to be based upon uncritical acceptance of RM/NS, rather than upon any actual evidence. I do not doubt there are beneficial mutations as evidenced by rapid adaptation yet I contest the fact that they build meaningful information in the genome instead of degrade preexisting information in the genome.” (pp. 26-27) “Mutations, in summary, tend to induce sickness, death, or deficiencies. No evidence in the vast literature of heredity change shows unambiguous evidence that random mutation itself, even with geographical isolation of populations leads to speciation.” Lynn Margulis - Acquiring Genomes [2003], p. 29. “But there is no evidence that DNA mutations can provide the sorts of variation needed for evolution… There is no evidence for beneficial mutations at the level of macroevolution, but there is also no evidence at the level of what is commonly regarded as microevolution.” Jonathan Wells (PhD. - Molecular Biology) "Of carefully studied mutations, most have been found to be harmful to organisms, and most of the remainder seem to have neither positive nor negative effect. Mutations that are actually beneficial are extraordinarily rare and involve insignificant changes. Mutations seem to be much more degenerative than constructive…" Kurt Wise, paleontologist (2002, p.163) "The neo-Darwinians would like us to believe that large evolutionary changes can result from a series of small events if there are enough of them. But if these events all lose information they can’t be the steps in the kind of evolution the neo-Darwin theory is supposed to explain, no matter how many mutations there are. Whoever thinks macroevolution can be made by mutations that lose information is like the merchant who lost a little money on every sale but thought he could make it up on volume." Lee Spetner (Ph.D. Physics - MIT - Not By Chance) "The opportune appearance of mutations permitting animals and plants to meet their needs seems hard to believe. Yet the Darwinian theory is even more demanding: a single plant, a single animal would require thousands and thousands of lucky, appropriate events. Thus, miracles would become the rule: events with an infinitesimal probability could not fail to occur,,, There is no law against day dreaming, but science must not indulge in it." Pierre P. Grasse - past President of the French Academie des Sciences Mutations: evolution’s engine becomes evolution’s end! - Article Highlighting The Technical Points Of Genetic Entropy Excerpt: recent discoveries show that mutations interfere with all molecular machinery. Life’s error correction, avoidance and repair mechanisms themselves suffer the same damage and decay. The consequence is that all multicellular life on earth is undergoing inexorable genome decay. Darwin Was Wrong: A Study in Probabilities "To propose and argue that mutations even in tandem with 'natural selection' are the root-causes for 6,000,000 viable, enormously complex species, is to mock logic, deny the weight of evidence, and reject the fundamentals of mathematical probability." Cohen, I.L. (1984) - No Beneficial Mutations - Not By Chance - Evolution: Theory In Crisis - Lee Spetner - Michael Denton - video http://www.metacafe.com/watch/4036816 “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 - along with the organism carrying it.” Maxim D. Frank-Kamenetski, Unraveling DNA, 1997, p. 72. (Professor at Brown U. Center for Advanced Biotechnology and Biomedical Engineering) ...Advantageous anatomical mutations are never observed. The four-winged fruit fly is a case in point: The second set of wings lacks flight muscles, so the useless appendages interfere with flying and mating, and the mutant fly cannot survive long outside the laboratory. Similar mutations in other genes also produce various anatomical deformations, but they are harmful, too. In 1963, Harvard evolutionary biologist Ernst Mayr wrote that the resulting mutants “are such evident freaks that these monsters can be designated only as ‘hopeless.’ They are so utterly unbalanced that they would not have the slightest chance of escaping elimination through natural selection." - Jonathan Wells "A Dutch zoologist, J.J. Duyvene de Wit, clearly demonstrated that the process of speciation (such as the appearance of many varieties of dogs and cats) is inevitably bound up with genetic depletion as a result of natural selection. When this scientifically established fact is applied to the question of whether man could have evolved from ape-like animals,'.. the transformist concept of progressive evolution is pierced in its very vitals.' The reason for this, J.J. Duyvene de Wit went on to explain, is that the whole process of evolution from animal to man " ' . . would have to run against the gradient of genetic depletion. That is to say, . . man )should possess] a smaller gene-potential than his animal ancestors! [I] Here, the impressive absurdity becomes clear in which the transformist doctrine [the theory of evolution] entangles itself when, in flat contradiction to the factual scientific evidence, it dogmatically asserts that man has evolved from the animal kingdom!" —Op. cit., pp. 129-130. [Italics his; quotations from *J.J. Duyvene de Wit, A New Critique of the Transformist Principle in Evolutionary Biology (1965), p. 56,57.]
bornagain77
February 1, 2012
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you state; 'If genetic entropy were actually a problem, the fastest replicators — viruses, bacteria — would go extinct. Doesn’t happen.' Pretty simplistic reasoning pet, given the multiple layers of DNA repair mechanisms now being found in the cell (a VERY anti Darwinian discovery!), unfortunately for you many more lines of 'real world' evidence completely supports GE:
Genetic Entropy - Dr. John Sanford - Evolution vs. Reality http://vimeo.com/35088933 Mutations Prove Creation with Dr. Jerry Bergman Part 1 - video http://www.youtube.com/watch?v=i9ue1P50L48 See Part 2 here: http://www.youtube.com/watch?v=Pvjsy_p6eSs
The evidence for the detrimental nature of mutations in humans is overwhelming for scientists have already cited over 100,000 mutational disorders.
Inside the Human Genome: A Case for Non-Intelligent Design - Pg. 57 By John C. Avise Excerpt: "Another compilation of gene lesions responsible for inherited diseases is the web-based Human Gene Mutation Database (HGMD). Recent versions of HGMD describe more than 75,000 different disease causing mutations identified to date in Homo-sapiens."
I went to the mutation database website cited by John Avise and found this stated in 2009:
HGMD®: Now celebrating our 100,000 mutation milestone!
I really question their use of the word 'celebrating'. (Of note, apparently someone with a sense of decency has now removed the word 'celebrating')
"Mutations" by Dr. Gary Parker Excerpt: human beings are now subject to over 3500 mutational disorders. (of note: this 3500 figure is cited from the late 1980's) http://www.answersingenesis.org/home/area/cfol/ch2-mutations.asp
This following study confirmed the detrimental mutation rate for humans, of 100 to 300 per generation, estimated by John Sanford in his book 'Genetic Entropy' in 2005:
Human mutation rate revealed: August 2009 Every time human DNA is passed from one generation to the next it accumulates 100–200 new mutations, according to a DNA-sequencing analysis of the Y chromosome. (Of note: this number is derived after "compensatory mutations") http://www.nature.com/news/2009/090827/full/news.2009.864.html
This more recent study found a slightly lower figure:
We Are All Mutants: First Direct Whole-Genome Measure of Human Mutation Predicts 60 New Mutations in Each of Us - June 2011 http://www.sciencedaily.com/releases/2011/06/110613012758.htm
This 'slightly detrimental' mutation rate of 100 to 200, or even 60, per generation is far greater than even what evolutionists agree is an acceptable mutation rate for an organism:
Beyond A 'Speed Limit' On Mutations, Species Risk Extinction Excerpt: Shakhnovich's group found that for most organisms, including viruses and bacteria, an organism's rate of genome mutation must stay below 6 mutations per genome per generation to prevent the accumulation of too many potentially lethal changes in genetic material. http://www.sciencedaily.com/releases/2007/10/071001172753.htm Contamination of the genome by very slightly deleterious mutations: why have we not died 100 times over? Kondrashov A.S. http://www.ingentaconnect.com/content/ap/jt/1995/00000175/00000004/art00167 The Frailty of the Darwinian Hypothesis "The net effect of genetic drift in such (vertebrate) populations is “to encourage the fixation of mildly deleterious mutations and discourage the promotion of beneficial mutations,” http://www.evolutionnews.org/2009/07/the_frailty_of_the_darwinian_h.html#more
bornagain77
February 1, 2012
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Petrushka, love you man, but you are completely wrong, as usual; You state that second law principles are not violated by 'work', perhaps not violated by 'work', I never said work did violate it, but OOL and neo-Darwinian evolution is certainly a flagrant violation of the second law.
"The laws of probability apply to open as well as closed systems." Granville Sewell - Professor Of Mathematics - University Of Texas El Paso Can “ANYTHING” Happen in an Open System? - Granville Sewell PhD. Math Excerpt: If we found evidence that DNA, auto parts, computer chips, and books entered through the Earth’s atmosphere at some time in the past, then perhaps the appearance of humans, cars, computers, and encyclopedias on a previously barren planet could be explained without postulating a violation of the second law here (it would have been violated somewhere else!). http://www.math.utep.edu/Faculty/sewell/articles/appendixd.pdf Granville Sewell - Mathematics Dept. University of Texas El Paso (Papers and Videos) http://www.math.utep.edu/Faculty/sewell/ Peer-Reviewed Paper Investigating Origin of Information Endorses Irreducible Complexity and Intelligent Design - Casey Luskin - July 2010 Excerpt: It has often been asserted that the logical entropy of a non-isolated system could reduce, and thereby new information could occur at the expense of increasing entropy elsewhere, and without the involvement of intelligence. In this paper, we have sought to refute this claim on the basis that this is not a sufficient condition to achieve a rise in local order. One always needs a machine in place to make use of an influx of new energy and a new machine inevitably involves the systematic raising of free energies for such machines to work. Intelligence is a pre-requisite. http://www.evolutionnews.org/2010/07/peer-reviewed_paper_investigat036771.html Evolution Vs. Thermodynamics - Open System Refutation - Thomas Kindell - video http://www.metacafe.com/watch/4143014 "there are no known violations of the second law of thermodynamics. Ordinarily the second law is stated for isolated systems, but the second law applies equally well to open systems." John Ross, Chemical and Engineering News, 7 July 1980 "...the quantity of entropy generated locally cannot be negative irrespective of whether the system is isolated or not." Arnold Sommerfel, Thermodynamics And Statistical Mechanics, p.155 "Bertalanffy (1968) called the relation between irreversible thermodynamics and information theory one of the most fundamental unsolved problems in biology." Charles J. Smith - Biosystems, Vol.1, p259.
bornagain77
February 1, 2012
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Work does not violate any second law principles. Conservation laws do not apply to systems that learn via feedback. As long as there is an energy gradient, work can be done without any violation of any second law principle. If genetic entropy were actually a problem, the fastest replicators -- viruses, bacteria -- would go extinct. Doesn't happen. Current laboratory experiments -- Lenski, Thornton -- support a functional space that can be connected.Petrushka
February 1, 2012
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I didn't say "what did happen at the ool". Thats taken, it seems to me, as axiomatic, and then you can look at bacteria, metazoans , etc.Starbuck
February 1, 2012
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Petrushka, and why is there 'no point' in asking what happened at the origin of life because 'We’ll never know', yet at the same time you claim we can know for certainty what subsequently happened right past the OOL??? i.e. Why the double standard? And why are not current laboratory experiments good enough for you to refute Darwinism and ANY OOL scenarios as completely ludicrous??? Do you find a loophole around the Second Law (Sewell)??? Did you find a loophole around COI (Dembski-Marks)??? Did you find a loophole around the First Rule (Behe)?, or Genetic Entropy (Sanford)? Exactly why are you so biased as to the point of complete scientific blindness?bornagain77
February 1, 2012
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I see no point in asking what did happen at OOL. We'll never know. We can, however, explore whether it is possible for replicators to arise through regular processes.Petrushka
February 1, 2012
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I think there is one key difference between your perspective on front-loading, and Mike Gene's. That is, in my opinion, that Mike Gene doesn't really concern himself with the question of how "How could sophisticated molecular systems be front-loaded?" For him it's not a matter of what can or can't happen, but what did happen. As such I don't think he allows ID type complexity arguments into his thinking on FLE, unless I'm mistaken.Starbuck
February 1, 2012
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Biological complexity. Front-loading predicts that the last universal common ancestor (LUCA) was quite complex, complete with genes necessary for the origin and development of metazoan life forms.
That sounds like an impressive spec, but what with horizontal transfer, it becomes problematic defining what you mean by LUCA. The first metazoans would have most of the genes found in modern ones, since they were invented by microbes.
The front-loading hypothesis proposes that the universal optimal genetic code was present at the dawn of life: in other words, we won’t find precursors of sub-optimal genetic codes, because the genetic code was optimal from the start.
So OOL research is relevant or not, assuming it eventually supports a bootstrap scenario?Petrushka
February 1, 2012
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