Home » Intelligent Design » Front loading passes peer review in Cell Cycle

Front loading passes peer review in Cell Cycle

1: Cell Cycle. 2007 Jun;6(15):1873-7. Epub 2007 Jun 6. Links

Universal genome in the origin of metazoa: thoughts about evolution.

Sherman M.

Department of Biochemistry; Boston University Medical School, 715 Albany St., Boston, Massachusetts 02118, USA.

[email protected]

Recent advances in paleontology, genome analysis, genetics and embryology raise a number of questions about the origin of Animal Kingdom. These questions include:(1) seemingly simultaneous appearance of diverse Metazoan phyla in Cambrian period, (2) similarities of genomes among Metazoan phyla of diverse complexity, (3) seemingly excessive complexity of genomes of lower taxons and (4) similar genetic switches of functionally similar but non-homologous developmental programs. Here I propose an experimentally testable hypothesis of Universal Genome that addresses these questions. According to this model, (a) the Universal Genome that encodes all major developmental programs essential for various phyla of Metazoa emerged in a unicellular or a primitive multicellular organism shortly before the Cambrian period; (b) The Metazoan phyla, all having similar genomes, are nonetheless so distinct because they utilize specific combinations of developmental programs. This model has two major predictions, first that a significant fraction of genetic information in lower taxons must be functionally useless but becomes useful in higher taxons, and second that one should be able to turn on in lower taxons some of the complex latent developmental programs, e.g., a program of eye development or antibody synthesis in sea urchin. An example of natural turning on of a complex latent program in a lower taxon is discussed.

PMID: 17660714 [PubMed - in process]

HT to Gilbert T. for alerting me to this paper.

  • Delicious
  • Facebook
  • Reddit
  • StumbleUpon
  • Twitter
  • RSS Feed

57 Responses to Front loading passes peer review in Cell Cycle

  1. Sounds like front loading from the abstract, but what does the full paper say? What is the mechanism responsible for this “program” being in place? Is it blind watchmaker programming? A dash of luck, and a pinch of chance? Nothing is beyond belief in the world of Darwin, which is why I ask.

  2. So much for the saying that early, ie the first, population(s) of living organisms (single-celled) were “simple” compared with today’s single-celled organisms.

    There isn’t any justification for that now.

    However I still think that in order to use this data for front-loading or universal common descent someone needs to be able to account for the physiological and anatomical differences observed.

  3. Side note to whoever is in charge of the theme for this site: please make the font for the quoted text darker. It is way too light for easy reading. Instead of using 888, perhaps something like 333 would work.

    Thanks

  4. 4

    Very interesting abstract. This is the kind of paper I expect to see more and more of in the coming years, which avoid the word “design” but which have obvious design implications. The evidence for design is just too overwhelming to ignore indefinitely.

    But Dave, I would have been reluctant to post this until the paper actually appeared; aren’t you concerned that an anonymous Baylor student or faculty member will alert the editor that this paper may have ID implications. It could still disappear suddenly.

  5. 5

    Oh, my mistake. Looks like it has already appeared.

  6. And so it goes,,,They find the genetic data that is nothing like Darwinism predicted yet Darwinism must be true thus the genetic complexity we find in simple life must have purpose for a future evolutionary scenario since we know evolution to be true. Don’t bother with pesky how did the original information get there in the first place!

    They state:
    This has two major predictions, first that a significant fraction of genetic information in lower taxons must be functionally useless but becomes useful in higher taxons, and second that one should be able to turn on in lower taxons some of the complex latent developmental programs, e.g., a program of eye development or antibody synthesis in sea urchin.

    Thus the ID weak position of front loading is their most tenable position for materialistic evolution,,,Yet ID predicted this scenario years ago!!!
    I would like to think that the #1 major prediction of the ID strong position (my favorite) would be that the complexity of the Genetic code of these lower life forms is really barely understood by us right now and that the entire code will be found to have some type of function though we have not yet deduced its entire function as of now. IOW, The intelligent design that is found in the genetic code of simple life forms is so complex that it is currently beyond our ability to fully comprehend right now.

    To me this seems the strongest position and most reasonable position so far since it is truly the position that best reflects the evidence and the repeated failure of Darwinian predictions for the genome complexity we are finding.
    As well I am very weary of being burnt by my false presumptions I had from my Neo-Darwinism education.

    Thus I think when deciphering the function of a Genetic Code, scientists should wipe the blackboard totally clean of any Darwinists/materialists presumptions and then basic foundational engineering questions should seek to lay a new foundation for scientists to work with for deciphering the sheer complexity we are actually dealing with!

  7. In reading The God Theory, Bernard Haisch, a book I mostly don’t agree with, and mostly because of his undying pro-evolution stance, he makes an interesting argument centered around light. It basically goes like this.

    To make an image with pure white light, you must start subtracting portions of that light in order to create an image. If you are familiar with slides, or have Photoshop where you can view an image as made up of it’s different color components, you’ll see what he means. You’re removing purity from the source in order to create something.

    Well I read this post and it got me thinking. What if God does this with DNA. What if God started off with the purest form of DNA, containing infinite possibility and to create things, He masks or even chops away portions in order to create images. Us. Image of God. Interesting thought?

    Israel Anderson

  8. Cell Cycle paper: “This model has two major predictions, first that a significant fraction of genetic information in lower taxons must be functionally useless but becomes useful in higher taxons, and second that one should be able to turn on in lower taxons some of the complex latent developmental programs, e.g., a program of eye development or antibody synthesis in sea urchin.”

    I don’t see how this could have gotten past peer review. The clear implication is that all the complex developmental programs such as for eye development and antibody synthesis evolved in “a unicellular or a primitive multicellular organism shortly before the Cambrian period”. Such a primitive organism would have not had anything like complex eyes or immune systems, or so it would seem. So it is precarious to say they came about by RM & NS. Then where did they come from?

  9. Let’s notice that one of the proposals—turning on in lower taxon higher complexity latent programs–is every bit as proof-positive as lac-operon genes in bacteria. If they are able to do “turn these programs on”, then we can say that “front-loading” is a “fact”!!

    As Jackie Gleason used to say: “How sweet it issss!!!”

  10. I am no biologist but ever since I read about the mechanism of genetic code, I realized that shared genetic traits of species that is placed very far apart on the “Tree of Life”, must be traced back to an ancestor with vast amounts of genetic information ready to share with the rest of “the Tree” (i.e I deduced front loading).

    This was a logical conclusion that excluded the very small probability that, for instance, something like the eye can have several completely independent evolutionary emergences that is so strikingly similar for so many species on so many location on the “Tree of Life”. The eye is just a simple example of a plethora of similarities that has to relate back as far as logically necessary.

    Trying to account for the Cambrian Explosion force this reality through a logical bottleneck. It will be interesting to see more attempts to get through this bottleneck. We should also expect evo-biology to start to derelict their trusted geological coulomb if more of these results are “logically forced” into peer reviewed papers.

    This article seems to support my intuitive deduction. Thank you for sharing – it makes great academic discussions open to ID skeptics.

  11. I am afraid that Michael Sherman (Associate Professor Biochem) does not seem to be a materialist. I fear he will quickly be branded a neo-creationist. I admire his courage in seriously proposing such a novel idea. I am worried that the editor of Cell Cycle may soon get Sternberged for publishing this.

  12. The weak point in this argument (for both evolutionists and ID Frontloaders) is that beneficial mutations would still have to occur at the proper time in the proper place. Thus the assumption of beneficial mutations is at its core of these beliefs…Yet it hasn’t been clearly demonstrated, in the least, that the DNA itself has any beneficial flexibility to mutations in it. This one point of evidence, the actual flexibility of DNA to any random mutations, which happens to be a foundational piece of evidence, has not even been decisively proven to be true yet. Though it is commonly presumed to be true. This is very shabby science to say the % How can anyone dare judge the genetic data accurately if the foundational paradigm is not even set in stone yet!?!
    Point blank fact,,IF the DNA is in fact not flexible to mutations then intelligent design is most likely true by default. This one piece of evidence (Beneficial Flexibility of DNA) should easily be within science’s grasp at this present time. Indeed, Sanford in his book “Genetic Entropy” lists several studies that could find no beneficial flexibility to DNA (Spetner “NOT By Chance” list some studies as well). If rigorously proven true then analysis of genetic data would take on the appropriate engineering posture to deduce design instead of the “vainly” searching for natural explanations posture.
    This seems simple to me yet even in ID circles I find many people blindly gloss over the fact that they are vainly depending on some sort of beneficial mutations to occur that have not even been proven true in the first place.

  13. If I understand Sanford’s genetic entropy hypothesis (and I admit I haven’t read his book), he’s arguing that genomes are degrading, because mutations reduce fitness.

    But then how can front-loading work? If sequences that are under selection are degrading, surely sequences that are neutral (i.e. those that are waiting to be activated) must also be degrading, at least as fast as functional sequences. So the will probably have no function by the time they are called into action.

    Anyone care to make a refutation?

    Bob

  14. I don’t think Sanford claims front loading millions of years ago. And I don’t think the degrading of the genome is really a hypothesis of Sanfords, it is just an observation. However, the typical front loading scenerio is that after an organism reaches its terminal point is starts to degrade. Front loaders like Davison find support for this in the paleontology of Schindenwolf. They also see the patern in ontongeny. What begins as a single cell becomes a complex organism and then degrades.

  15. I agree that Sanford doesn’t discuss front-loading (or at least I’m not aware of him discussing it), but his claims about degradation are relevant to front-loading, so I’m interested in how the two can be squared.

    An obvious question arises – why doesn’t an organism degrade before its terminal point?

    Bob

  16. Bob

    An obvious question arises – why doesn’t an organism degrade before its terminal point?

    Observation has revealed great variation in the level of protection and repair of genetic code both from one organism to the next and from one stretch of code to the next in the same organism. From an engineering perspective it’s trivial to protect some memory regions better than others. It’s all a matter of how much protection you need and how much overhead you’re willing to use to protect it. Code that needs to be maintained without error for geologic timespans gets better error detection/correction applied to it.

  17. Bob O’H,
    Genetic degradation for single celled bacteria is still pretty much up in the air,,In fact I remember a PCR (Poly-merase Chain reaction) study of some 250 million year old bacteria that caused quite a stir for the study showed very little change in the genome of the bacteria when compared to its modern day descendants. Yet bacteria still display adherence to the overall principle of Genetic Entropy for they are commonly known to lose fitness for survival the further away from their original state they are selected for! As well in crops such corn we can see the principle of Genetic Entropy being adhered to, for it is easy to see that corn crops have much less variability (information) than the parent species of corn has..As well even the human species is clearly shown to obey the principle of genetic entropy for the younger races of humans (Chinese, Europeans, American Indians etc..) all have less information for skin color than the original race of humans that is thought to have migrated out of Africa 50,000 years ago.
    Degradation of the particular genomes of different species or phyla is still very much only in the rough outline phase, yet the principle of Genetic entropy is very strong in empirical validation for it lines up with many other lines of evidence such as the over 90% of mysterious extinctions in the fossil record that have no connection to any natural disasters. Plus it lines up with what is known about CSI generating by chance. And lines up with the strength of observed data for mutation rates to DNA.
    Genetic Entropy has some refining to go through but it has definitely asserted itself with more solid proof than Neo_Darwinism has at this point. If I were a betting man, all my money would definitely ride on Genetic Entropy being validated as the foundational law of biology in the not to distant future!

  18. bornagain77 – I assume then that you would disagree with DaveScot about front-loading.

    Can you give a reference to the PCR on the 250m year old bacterium – did they really extract DNA from something that old?

    The reason why corn (I assume you mean maize, although similar results would be seen for wheat and other agricultural cereals) lacks diversity is because the process of domestication introduced a huge bottleneck, and this has become worse with breeding. It has nothing to do with entropy. Your example of human skin colour is confusing – how exactly is the “less information” in “young races” measured? And how was it measured/estimated for a population 50 000 years ago?

    Bob

  19. When it comes to degeneration, a population on average is receiving so many deleterious mutations per individual, so each bacterium would have to be reproducing X amount to provide sufficient population resources to purge the deleterious mutations out of the population. Might be making a boneheaded comment but I’m assuming that bacterium reproduce often enough to avoid such problems as Nachman’s U-Paradox in humans? So perhaps genetic entropy isn’t much of an issue with high replicators such as bacteria.? Or am I missing something…

    “Observed baseline mutation ratesin bacteria are low: DRAKE et al. (1998) estimate the per base pair, per generation, mutation rate to be ubp = 5.4 x 10–10 in Escherichia coli “well adapted to laboratory conditions.”…They estimate the genomic rate of deleterious mutation to be ug = 2 x 10–4, as a lower bound.”

    link

  20. Yes Bob O’H here is the reference:

    http://www.nature.com/nature/j.....897a0.html

    You allude to a bottleneck, then why should Dawkins use dog breeding as an example of evolution when information is in fact being lost?
    Exactly why would artificial selection by men be vastly different that natural selection in the wild since the natural selection would ultimately be a random occurrence of selection for a desired trait, when taken into total context of how the selection operates? Thus the bottleneck you refer to is not a artificial phenomena but an inherent part of the genome when selection is placed on the genome and will and does occur in the wild!
    Do you think the younger races have more information for skin color than the younger races?
    I think it is fairly obvious that the East Africans have all the inherent traits of all the races in their genomes! Whereas it is also obvious that Europeans are much more deficient of the raw material to “make” other color races. To me it is clear that more information for skin color resides in the East Africans! It is commonly known that the black color is really a mixture of all the other colors when referring to materials, whereas white contains all the other colors when referring to light! As to how to extrapolate this basic fact for color information to the genome I do not know right now. As well you can clearly see genetic entropy in the wild with the sub-species of “horses” such as donkey and zebra. It is very easy to see which is closer to the parent species that was originally created by God and to see which has been “naturally selected” for to produce the “very limited variability” we can easily see in the sub-species!
    As far as front loading goes, I believe that “beneficial adaptations” will occur from preexisting information such as what we see in the polar bear from the grizzly bear but that the adaptation , though beneficial, will result in the loss of information from the original parent species. Such as the loss of information for hair color.
    As well the highly touted Lactase Persistence mutation that is offerred as conclusive proof of evolution in humans is actually the loss of a preexisting instruction to turn the Lactase Enzyme off. Thus, even in evolutionists “hardest proof” once again Genetic Entropy is obeyed and no new information was created in the genome!

  21. Yes Bob O’H here is the reference:

    http://www.nature.com/nature/j…..897a0.html

    Ah, thanks. Although it appears that the bacteria have changed:

    Thus the bottleneck you refer to is not a artificial phenomena but an inherent part of the genome when selection is placed on the genome and will and does occur in the wild!

    The bottleneck wasn’t a result of natural (or artificial) selection. It was a result of domestication starting from a small base population – the plants that happened to be in the right place at the right time (the story is clearer with bread wheat, which is a hybrid, so the parents in the hybridisation form a small base).

    Do you think the younger races have more information for skin color than the younger races?

    Well, as I don’t know what you mean by information in this context, I’ll repeat my questions:
    How exactly is the “less information” in “young races” measured? And how was it measured/estimated for a population 50 000 years ago?

    Bob

  22. Patrick –

    So perhaps genetic entropy isn’t much of an issue with high replicators such as bacteria.?

    That’s my understanding – IIRC Mike Lynch showed that the rate of mutational meltdown depends on population size.

    A related issue is the evolution of sex, which is favoured more in small populations (I recently blogged about Sally Otto’s talk on this at ESEB), and hence can be seen as a mechanism to escape these problems.

    Bob

    Bob

  23. As to how to extrapolate this basic fact for color information to the genome I do not know right now.

    Wiki has a nice page on this. It also links to a
    paper that shows that lighter skin is due to different genes in different areas of the world. If you want to get empirical support for your theory, you should go through the CEPH data and show that all of the genetic variants are present in the East African populations.

    Bob

  24. 24

    ex-xian:

    As far as I know, Michael Behe has never speculated about this.

    If the SETI (Search for Extraterrestial Intelligence) researchers ever receive the type of signal they are looking for, they will conclude there are intelligent beings out there, despite the fact that they probably will not be able to tell us anything else about these beings.

  25. Bob O’H you stated:

    Although it appears that the bacteria have changed:

    Yet researchers stated:

    These researchers extracted and cultured a bacterium from an inclusion body from what they claim is a 250 million-year (Myr)-old salt crystal. If substantiated, this observation could fundamentally alter views about bacterial physiology, ecology and evolution. Here we report on molecular evolutionary analyses of the 16S rDNA from this specimen. We find that 2-9-3 differs from a modern halophile, Salibacillus marismortui, by just 3 unambiguous bp in 16S rDNA, versus the approximately 59 bp that would be expected if these bacteria evolved at the same rate as other bacteria. We show, using a Poisson distribution, that unless it can be shown that S. marismortui evolves 5 to 10 times more slowly than other bacteria for which 16S rDNA substitution rates have been established, Vreeland et al.’s claim would be rejected at the 0.05 level. Also, a molecular clock test and a relative rates test fail to substantiate Vreeland et al.’s claim that strain 2-9-3 is a 250-Myr-old bacterium. The report of Vreeland et al. thus falls into a long series of suspect ancient DNA studies.

    I would also like to point out that Vreeland is adamant that His test are faultless and that his results are accurate. Whereas the molecular clock and relative rest rates used to refute him are themselves subject to suspicion and are based on assumptions rather than rock solid evidence. Also this test of Vreeland’s is not an anomaly for many other test have been done on other ancient bacteria recovered from amber crystals and also show “very little” change in the DNA…That is to say, that the change that is consistently found for ancient bacteria’s DNA is always way below Darwinian predictions.
    Again I point out this is observationally direct evidence whereas the supposed refutation is based on indirect evidence and assumption. I believe direct evidence still carries more weight in science than indirect assumption, thus I find Vreeland’s findings much more persuasive than the obviously weak attempts at refutation.

  26. Bob O’H you stated:

    The bottleneck wasn’t a result of natural (or artificial) selection. It was a result of domestication starting from a small base population – the plants that happened to be in the right place at the right time (the story is clearer with bread wheat, which is a hybrid, so the parents in the hybridization form a small base).

    Are you saying this following statement is false?
    “Whatever we may try to do within a given species, we soon reach limits which we cannot break through. A wall exists on every side of each species. That wall is the DNA coding, which permits wide variety within it (within the gene pool, or the genotype of a species)—but no exit through that wall. Darwin’s gradualism is bounded by internal constraints, beyond which selection is useless.” R. Milner, Encyclopedia of Evolution (1990)

    Are you saying that we would get different results from wheat plants in the wild? Are you saying this lack of variation found in sub-species will not consistently occur when pressure of selection is put on a parent species no matter if in the wild are if “artificially selected for by man?? If so why should I think that the chances for CSI generating in the wild for a larger population in the wild are vastly greater than a sample population of same? What are you really trying to say? Is a larger population going to solve your problem of generating CSI? Behe has demonstrated that malaria and HIV, though having a vastly larger population than your wheat will never generate CSI. I think you are barking up the wrong tree Bob!! You are trying to put the problem out of reach with an allusion to a larger population yet the problem of generating useful information is still very large for you!! Plus you run into problems with Gould’s punctuated equilibrium, since he requires small populations rapidly evolving to explain the gaps in the fossil record! Not to mention the problems you have for inherent small population sizes for animals!
    To me it seems like you are trying to have your cake and eat it too.
    So I ask what exactly what is going to be the exact differentiating factor for your wild natural selection for a species as opposed to the artificial selection imposed by man on a species? Is complex new information going to magically appear in the Genome of the species in the wild thus violating Dembski’s CSI.
    I truly would like to know how you can dare differentiate the two and claim that one is not similar to the other. Are you saying that a species under selection is not a species under selection? This is absurd! As stated before reproductive isolation is most likely, from the best evidence available, due to the fact that information for variability is being lost and thus the sub species has demonstratively less information for variation than the original parent species did. This principle includes your wheat example; i.e. your wheat example by no means escapes this principle of genetic entropy!!

  27. Thanks Bob, for the insight on tracking down Genetic Entropy in humans using genetic data: Thus as a result of your insight, this following quote garnered from the ID antagonists, no less, over at Wikipedia;

    Existing data on human genetic variation support and extend conclusions based on the fossil evidence. African populations exhibit greater genetic diversity than do populations in the rest of the world, implying that humans appeared first in Africa and later colonized Eurasia and the Americas (Tishkoff and Williams 2002; Yu et al. 2002; Tishkoff and Verrelli 2003).

    Thus Genetic entropy is readily admitted in the article. They are in effect saying that more information exists in the African population than is younger populations!

    full article is here:
    http://en.wikipedia.org/wiki/H....._variation

  28. bornagain –
    1. What I wrote doesn’t say anything about the truth of the Milner quote. And I wasn’t writing about selection – I was writing about a bottleneck. It’s this which is the primary cause of the low diversity in crop plants – selection doesn’t help of course.

    I also made no comment about CSI – it’s hard enough explaining simple population genetics around here, without having new concepts dragged in.

    I was well aware of the greater genetic diversity in Africa, but I’ve no idea about how it relates to genetic entropy, which is the (supposed) degradation of the genome due to fixation of deleterious mutations. I think you need to show how the accumulation of deleterious mutations relates to the information content of genomes.

    In a desperate attempt to get this thread back on-topic, I’ll repeat – do you disagree with DaveScot about frontloading?

    Bob

  29. Bob,
    Genetic Entropy IS THE LOSS OF INFORMATION!!!!!
    Thus a demonstrated lack of diversity, variability, reveals a loss of information thus a degradation of the genome!!!!!
    Can you see it now?

  30. I can’t stay long but just wanted to jump in with a thought, re the exchange by BornAgain77, Bob OH and Patrick:

    We observe that:
    1) “Lower” lifeforms (such as bacteria) out-reproduce higher lifeforms by leaps and bounds.

    2) Life is thought to have originated from lower lifeforms in both NDE and Frontloaded versions of origins.

    3) Genetic entropy applies inversely to reproductive rate: the higher the rate, the less affected by genetic entropy.

    4) Frontloaded lifeforms would need to stick around with non-degraded information for long time spans (according to FLE scenarios), so they can’t become too affected by genetic entropy, in order to complete their “mission”

    Tying these ideas together, and we solve a puzzle neatly.

    We have wondered out loud on here why higher lifeforms reproduce so slowly and sparingly compared to lower lifeforms. It is clear to see that such an observed trend cannot be the result of natural selection, because there is no reason decreasing reproductive success would keep being selected for.

    But maybe we have it backwards: the question isn’t why do higher organisms reproduce so sparingly but rather, why do lower lifeforms reproduce so quickly?

    If Frontloading is true, then we would need our original replicators to be robust against genetic entropy, since they are the root of many branches. The closer to the bottom of the tree, the longer their line will be around, and so the more robust they need to be. Hence they need to reproduce faster in greater numbers. As they diversify and branch out, they get closer to their “terminal” branches, and thus are closer in time to their destination. So as we move up the tree, the less roubst the replicators need to be. The terminal branches can be fully subject to genetic entropy, since they have already reached their destination.

    This accords well with observation, as much as I am aware.

    Davescot, others: thoughts?

  31. Atom,
    You have very keen observation-s of the current state of observed data!
    I would like to comment, since I support the “strong” ID position of later implementation of information, that the front loaded position, while somewhat tenable, is by no means set in stone for the ID theory.

    From the evidence we now have, We can say with assurance that we KNOW information was implanted in the genomes! With just as much assurance, from the current evidence, we can state that we are not exactly sure when the precise implementation of information in the genome was inserted!

    I believe myself, and I know I’m probably in the minority in this view on this site, that since the demonstrated harmful rate of mutations to DNA is known to approach +99.9999%, including the highly touted HOX gene mutations, I believe the information for the genome was implanted as late as parent species! and was not implanted much earlier than that.
    Many people point to genetic similarities between phyla and say “look proof of relationship!”,,yet this is the same type of shabby reasoning that evolutionists use to try to prove monkeys and humans are related. This Similarity , although suggestive, quickly fails under critical analysis!
    My own take on this is that we have barely touched the surface of understanding functionality in genomes and to infer relationship between phyla is very premature. Especially when the genomes could have required similarity due to required shape space configuration or any number of other functionally similar uses that have no bearing on relationship! Or I could be wrong and it could be relationship,,BUT The very point being that it is very early to be jumping to any solid conclusions!
    My own take on the preliminary evidence we have so far is that it seems front loading will be very limited in its scope,,,with beneficial adaptations to sub-species occurring, yet, and I believe the evidence for this position is strong, the “front loaded” beneficial adaptation will ultimately come at a loss of the original information that was inserted in the Genome,,Thus I believe staying within the principle of Genetic Entropy and, this is presuming on my part, staying within what is possible for the generation of meaningful information in a genome.
    Of course all I have, so far, to back this up this claim is the negative mutation rates to DNA,,,Yet until someone demonstrates some radical exception to the current mutation evidence my position holds up with the observed data better than a radical front loading scenario does,,, this includes high populations of bacteria,,,since, as of now, bacteria have never been “naturally” changed into any other type of bacteria (Venter’s work is interesting to this point). As well Behe’s work in EOE points to a very limited scope for the generation of meaningful information for high populations.
    I know many objections can be made against my position,,yet I still hold that my position holds up with observed data better that any other current scenario being offered.

  32. Genetic Entropy IS THE LOSS OF INFORMATION!!!!!

    OH REALLY????!!!1???

    So, does genetic entropy have nothing to do with the buildup of a negative mutation load? That’s what I glean from reading comments on the web about it.

    Bob

  33. If Michael Sherman is interested in doing research on this paper’s implications. Does anyone have any specific ideas for experiments they would like to see performed?

  34. Bob O’H

    So, does genetic entropy have nothing to do with the buildup of a negative mutation load? That’s what I glean from reading comments on the web about it.

    You have to understand the difference between information and noise.

  35. Bob O’H
    Ditto to Jehu’s comment!

  36. bornagain77 – can you give me a direct answer. Are you saying that genetic entropy has nothing to do with the buildup of a negative mutation load?

    Bob

  37. Genetic Entropy IS THE LOSS OF INFORMATION!!!!!

    OH REALLY????!!!1???

    So, does genetic entropy have nothing to do with the buildup of a negative mutation load?

    “Negative” implies a loss.

    And a “buildup of a negative mutation load” would definitely be “a degradation of the genome”.

    “Noise” wouldn’t necessarily be a “negative”.

  38. Bob O’H
    If you haven’t read it, I suggest you read Dr. J.C.Sanford’s book “Genetic Entropy”; 2005. Though, in my own personal opinion, he tries to stretch the evidence a bit to far in limiting the span of human existence to fit his YEC for humans of 6000 years. I believe the foundation he lays for the principle of Genetic Entropy is solid in its basic premise and irrefutable as a overriding principle of biology!
    No, I am not saying that Genetic Entropy has nothing to with the buildup of a negative mutational load. In fact, I am saying quite the opposite in that it is all connected! It is just that Genetic Entropy can be measured in a variety of ways. You seem to be looking at Genetic Entropy from strictly the molecular level. Yet the very usefulness of the information in the genome itself can only be measured from the macroscopic level when taking into consideration its positive or negative effects on a species!
    A negative mutational load in the genome, by definition, is the buildup of useless information in the genome that reduces the ability of the species to survive.
    The fact that a negative mutational load is building up in humans can be clearly demonstrated by this following fact.
    “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 (slightly detrimental recessive mutations) that have been accumulating in our genomes.
    (Sanford; Genetic Entropy; page 147)
    So as you can see Bob the negative mutational load has everything to do with Genetic Entropy yet our ability to measure it effectively is for the large part limited to its effects on the macroscopic level of the species.

  39. A negative mutational load in the genome, by definition, is the buildup of useless information in the genome that reduces the ability of the species to survive.

    How is this related to the loss of genetic diversity?

    Actually, can you point me to this definition? I couldn’t find one on the web, and from what I could find, Sanford didn’t seem to be discussing information theory.

    Also, what about neutral mutations? They are also “useless information”. Does Sanford include those in genetic entropy?

    Yet the very usefulness of the information in the genome itself can only be measured from the macroscopic level when taking into consideration its positive or negative effects on a species!

    Err, no. Precisely the opposite. My understanding of Sanford’s genetic entropy is that it was the accumulation of deleterious alleles, which had the effect of reducing mean population fitness – it’s the fitness reduction that’s key.

    Hopefully we’ll get back to frontloading soon.

    Bob

  40. Hopefully we’ll get back to frontloading soon.

    IMHO-Front loading, like universal common descent, is only good if and only if genotype translates into phenotype.

    However from what we do know, even though genes and genomes may influence development, they do not determine it.

    Having an influence over something is not the same as determining it.

    Workers on an assembly-line influence the product’s quality. However they do not determine what the product is.

  41. Joseph,
    Is not the evidence that is currently coming in suggesting similar genotypes across phyla while phenotype appears to be vastly different?
    Would not this fact severely hamper the radical front loading scenario?

  42. Bob,
    Dr. Sanford does talk about neutral mutations (or really the lack thereof). I highly recommend his book to you! It will clear up a lot of the misconceptions we have between each other.

  43. If biology was my specialty I would research which is the mechanism that selects the front-loaded potential.
    According to New Scientist article mentioned here there could be another mechanism besides natural selection called “epigenetic” modifications. It seems to do subtle chemical changes to DNA according to the nutrition and living habits of the subject.
    I believe that this could be the thing that changes the way we see change in organisms completely when researched further. Too bad I am not a biologist.

    Article: New Scientist
    Men inherit hidden cost of dad’s vices

    06 January 2006
    Rowan Hooper
    Magazine issue 2533

  44. The problem with DNA is that it’s hard to know which mutation is beneficial, which neutral and which is negative because we don’t know the “islands” of functionality. However to my knowledge there is virtually zero data that supports the claim that the functionality we can get through different encodings of DNA is even nearly as plastic as most Darwinists seem to believe. As we can learn from programming languages the syntax that has to be used is precise and random binary coding offers diminishing returns.

  45. bornagain77 – Sanford may “talk about” neutral mutations, but does he include them in his genetic entropy?

    Oh, and please answer this question (directly!):

    How is this related to the loss of genetic diversity?

    I’m asking about your claims.

    Bob

  46. Bob,
    Yes, He does!

    Are you asking how Genetic Entropy is related to the loss of Genetic Diversity?
    Bob, The answer is clear. Genetic Entropy is the measurable loss of information and or function in a genome! If diversity is lost to a sub-species that was present in the parent species it came from, this is clearly the loss of functional information in the genome of the sub-species from the parent species, thus the “sub-speciation” stays within the overriding principle of Genetic Entropy! This rule applies to all known cases of sub-speciation I have looked at!
    I really don’t think I can make this any clearer Bob. I really do recommend Dr. Sanford’s book “Genetic Entropy” to you. He truly has a gift for taking a complex subject and breaking it down into easy to learn lessons that are easy to understand. He is much like Dr. Behe in this manner. I believe he can do a much better job of teaching you the principle of Genetic Entropy than I can.

  47. Yes indeed I find it funny that the breeding example used by evo-devo proponents seems to offer exact opposite conclusions when data is researched.
    My current hypothesis:

    Front-loaded original species
    ->

    Time+RM(genetic entropy)+NS+some not so well known mechanism for example epigenetic modifications
    ->

    Multiple sub-species that don’t have the front-loaded potential anymore, but retain some of it.

  48. Is not the evidence that is currently coming in suggesting similar genotypes across phyla while phenotype appears to be vastly different?

    That doesn’t account for the differences. If anything it tells us that genotype does not determine phenotype.

    Would not this fact severely hamper the radical front loading scenario?

    It all depends on where “form” resides.

    Suggested reading:

    “Why is a Fly Not a Horse?” by geneticist Giuseppe Sermonti.

    Chapter VI:

    The scientist enjoys a privilege denied the theologian. To any question, even one central to his theories, he may reply “I’m sorry but I do not know.” This is the only honest answer to the question posed by the title of this chapter. We are fully aware of what makes a flower red rather than white, what it is that prevents a dwarf from growing taller, or what goes wrong in a paraplegic or a thalassemic. But the mystery of species eludes us, and we have made no progress beyond what we already have long known, namely, that a kitty is born because its mother was a she-cat that mated with a tom, and that a fly emerges as a fly larva from a fly egg.

  49. Joseph,
    I wonder if “form” may be tentatively found (roughly defined) by comparing the differences between Genome sequence similarities with specific gene sequence similarities across phyla.

  50. Genetic Entropy is the measurable loss of information …

    I’ve only ever seen you claim that – everything I’ve read by Sanford suggests that he means something else (a loss of fitness). If I ordered his book now, it would take over a week to arrive, by which time this thread would have died. So, I’ll ask again for you to point me to a definition of genetic entropy that accords with what you’re claiming.

    Bob

  51. I’ve only ever seen you claim that – everything I’ve read by Sanford suggests that he means something else (a loss of fitness).

    Loss of function and loss of information are basically the same thing. Function generally requires information. When the informatin is lost the function is lost as well. Sometimes a loss of information creates improved fitness and maybe even function in the same way burning a bridge can have the function of slowing down an invading army.

  52. Bob,
    Since evidence has primary authority in science, let’s look at the evidence. If I read you right, You want Genetic Entropy to “only” mean a loss of fitness. Whereas, I hold that Genetic Entropy is a broader overriding principle of biology and includes not only loss of fitness but also loss of functional information, although fitness can “temporarily” be gained for a species.
    Many times naturalists will offer “conclusive” proof for evolution by showing bacteria that have become resistant to a certain antibiotic such as penicillin. When penicillin was first discovered, all the gram positive cocci were susceptible to it. Now 40% of the bacteria Strep pneumo are resistant. Yet, the mutation to DNA that makes Strep pneumo resistant to penicillin results in the loss of a protein function for the bacteria (called, in the usual utilitarian manner, penicillin-binding-protein). A mutation occurred in the DNA leading to a bacterial protein that no longer interacts with the antibiotic and the bacteria survive. Although they survive well in this environment, it has come at a cost. The altered protein is less efficient in performing its normal function. In an environment without antibiotics, the non-mutant bacteria are more likely to survive because the mutant bacteria cannot compete as well. So as you can see, the bacteria did adapt, but it came at a loss of function in a protein of the bacteria, loss of genetic information in the DNA of the bacteria, and it also lessened the bacteria’s overall fitness for survival. Scientifically, it is better to say that the bacteria devolved in accordance with the principle of genetic entropy, instead of evolved against this primary principle of how “poly-constrained information” will act in organisms (Sanford; Genetic Entropy 2005). As well, all other observed adaptations of bacteria to “new” environments have been proven to be the result of such degrading of preexisting molecular abilities. Sometimes a complex adaptation in bacteria is exhibited by naturalists (Hall, gene knockout experiments) that defy tremendous mathematical odds. Yet far from confirming evolution as they wish it would, the demonstration of a complex adaptation of a preexisting protein actually indicates another higher level of complexity in the genetic code of the bacteria that somehow found (calculated) how to adapt a preexisting protein with the very same ability as the protein that was knocked out to the new situation (Behe, Evidence For Design pg. 138). To make matters worse for the naturalists, the complex adaptation of the protein still obeys the principle of genetic entropy for the bacteria, since the adapted bacteria has less overall functionality than the original bacteria did. Thus, even naturalists supposed strongest proof for evolution in bacteria is found to be wanting for proof of evolution since it still has not violated the principle of genetic entropy. Even the most famous cases of adaptations in humans, such as lactase persistence, the sickle cell/malaria adaptation (Behe, The Edge of Evolution 2007), and even long term immune system responses of humans, genetic entropy is still being obeyed when looked at on the level of overall functional genetic information. For naturalists to “conclusively prove” evolution they would have to clearly demonstrate a gain in genetic information that does not in fact decrease functionality of the species. Naturalists have not done so, nor will they ever. The overall interrelated complexity of the information for the integrated whole of a life-form simply will not allow the generation of meaningful information to happen in its DNA by chance alone.

    “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)

    “There is no known law of nature, no known process and no known sequence of events which can cause information to originate by itself in matter.” Werner Gitt, “In the Beginning was Information”, 1997, p. 106. (Dr. Gitt was the Director at the German Federal Institute of Physics and Technology) His challenge to scientifically falsify this statement has remained unanswered since first published.

    Naturalists also claim stunning proof for evolution because bacteria can quickly adapt to detoxify new man-made materials, such as nylon and polystyrene. Yet once again, when carefully looked at on the molecular level, the bacteria still have not demonstrated a gain in genetic information, i.e. though they adapt they still degrade preexisting molecular abilities of the bacteria in order to adapt (genetic entropy). Indeed, it is not nearly as novel as they think it is, for the bacteria are still, only, complacently detoxifying the earth of toxins as they have always been doing for billions of years. Even though naturalists claim this is something brand new, that should be considered stunning proof for evolution, I’m not nearly as impressed, with their stunning proof, as they think I should be (Answers in Genesis; Nylon Eating Bacteria; 2007)! This overriding truth of never being able to violate the entropy of poly-constrained information by natural means applies to the “non-living realm” of viruses, such as bird flu, as well (Ryan Lucas Kitner, Ph.D. 2006). I would also like to point out that scientists have never “naturally” changed any one type of bacteria into any another type of bacteria, despite years of exhaustive experimentation trying to change any bacteria type into any other bacteria type. In fact, it is commonly known that the further scientists deviate any particular bacteria type from its original state, the more unfit for survival the manipulated population will quickly become. As esteemed French scientist Pierre P. Grasse has stated:
    “What is the use of their unceasing mutations, if they do not change? In sum, the mutations of bacteria and viruses are merely hereditary fluctuations around a median position; a swing to the right, a swing to the left, but no final evolutionary effect.”
    Needless to say, this demonstrated limit to the variability of bacteria is extremely bad news for the naturalists.
    Bob I could go on and on, and site evidence after evidence..Yet the very point is that evolutionists have no evidence for evolution that withstands scrutiny; to “conclusively” prove evolution, evolutionists will have to produce solid evidence for for an increase in fitness as well as an increase in obvious functional information for the species. Evolutionists should have countless examples they could produce , since evolution is “a fact of life” yet I can find none anywhere I look! Do you have any examples that can withstand scrutiny Bob”?

  53. I wonder if “form” may be tentatively found (roughly defined) by comparing the differences between Genome sequence similarities with specific gene sequence similarities across phyla.

    No one has found it yet. But they have figured out what I have already posted- that DNA may lend itself to those forms but the DNA does not determine it.

  54. Thank you bornagain. I asked you to provide evidence that your definition of genetic entropy accords with Sanford’s. You wrote over a thousand words, and didn’t answer my request. I guess this means you’re not going to, so I think we’re done here.

    Bob

  55. Bob,
    If you noticed in the article, I definitely referenced Sanford in regards to how information acts in regards to the “fitness” adaptation of a bacteria. So yes! I did answer your question in vivid detail as to how Sanford views Genetic Entropy. As stated before his book is very easy to read and will clear up the misconceptions you seem to have about the limits you seem to think he has on the principle of Genetic Entropy.
    In fact he does several pages on mutations to what he terms “poly-constrained” information!
    He definitely does not hold to your view that Genetic Entropy is limited to (a loss of fitness) but also, emphatically, supports its origination in the information of the genome!
    Please read the book Bob.

  56. I think that Bob is right about genetic entropy in a sense that it seems to lower the total fitness of the species in question. However it lowers the total fitness in multiple fitness landscapes and might improve fitness in a few. For example the antibiotic resistance in bacteria acts just like that increasing fitness against acting antibiotic but the bacteria loses fitness in every other fitness landscape that don’t have that antibiotic.

  57. [...] Front loading passes peer review in Cell Cycle [...]

Leave a Reply