Intelligent Design

BBC’s Tree of Life – Review of Attenborough’s programme

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Andrew Halloway offers his review of David Attenborough’s recent BBC1 prime time documentary ‘Charles Darwin and the Tree of Life’ highlighting the out of date material and poor reasoning.

Andrew comments ‘I’m astonished that the BBC still included this [material about the Tree of Life], and what’s more made it the title of the programme, considering that only last month the country’s leading scientific journal, New Scientist, carried a major article called “Why Darwin was wrong about the Tree of Life” (21 January). The article clearly stated that there is “no evidence at all” for the Tree of Life, and this was even backed up by the editorial of the journal, despite the fact that the New Scientist is known for its strong pro-evolution stance.

Read the full article here Charles Darwin and the Tree of Life

26 Replies to “BBC’s Tree of Life – Review of Attenborough’s programme

  1. 1
    Domoman says:

    Don’t you know that’s how neo-Darwinists try and dupe the public? They ignore negative evidence and then state the theory of evolution is fact. Like when they say that bacterial resistance to anti-biotics is evidence of large scale macroevolution, while ignoring the fact that the resistance is due to a loss of genetic information. :-p

  2. 2
    Dave Wisker says:

    I was unaware New Scientist was a peer-reviewed journal. If it is, does it have a higher impact factor than Nature?

  3. 3
    Dave Wisker says:

    Looking at the New Scientist article in question, it looks more to me that the metaphor of the tree of life is stronger than ever– the “root system” is more complex, due to HGT occurring rampantly at the prokaryotic-archaeic base. But the levels of HGT drop off precipitously in eukaryotic organisms higher up, where vertical gene transmission is far more common, giving the tree its familiar form.

  4. 4
    halo says:

    For UK people:

    The Expelled DVD is now available in multi-region format for UK viewers – CMI (Creation Ministries International) have managed to obtain a limited number of region-free copies, they only have about 40 left.
    Call 0845 6800 264.

  5. 5
    WeaselSpotting says:

    Like when they say that bacterial resistance to anti-biotics is evidence of large scale macroevolution, while ignoring the fact that the resistance is due to a loss of genetic information

    I have a question for the biochemists on board: given this loss of information, would that mean that the back mutation (to the original sequence) would be less probable than the original mutation? It would seem like this would be easy to check out in a lab…perhaps the evolutionists are afraid of what they’d find.

  6. 6
    Dave Wisker says:

    I have a question for the biochemists on board: given this loss of information, would that mean that the back mutation (to the original sequence) would be less probable than the original mutation? It would seem like this would be easy to check out in a lab…perhaps the evolutionists are afraid of what they’d find.

    Mutations that result in losses of information are common and not controversial. Simple deletions are an example. But mutations whih increase information are also uncontroversial. Duplications followed by subsequent mutations to one copy are one example. Observed mutations that result in novel promiscuous functions in proteins are another. Still other examples are genes that arise de novo from the cobbling together of non-coding DNA sequences (T-urf13 in maize and BSC4 in yeast are two well-known ones). The notion that mutations always result in losses of information is false.

  7. 7
    IRQ Conflict says:

    “The notion that mutations always result in losses of information is false.”

    Who said they did?

  8. 8
    Dave Wisker says:

    “The notion that mutations always result in losses of information is false.”

    Who said they did?

    Parsing this passage from Halloways article leads one to that conclusion:

    Mutations do not result in new genetic information capable of constructing new complex biological structures. All the experiments conducted over many decades prove this. Mutations are nearly all negative, resulting in damage to genetic information, not improvements. The tiny minority that are neutral do not help the argument either. There are some mutations that give a temporary advantage to some creatures, but they involve a LOSS of genetic information, that ultimately prevents evolution. Attenborough’s programme, of course, chose to ignore this massive hole that undermines the entire theory.

    If they are detrimental they involve damage to information. Presumably that is a loss. If they are beneficial they involve a loss of information. Neutral mutations (ignoring the obvious error in stating that they are a tiny minority) aren’t specifically said to be losses of information, but then, why would beneficial ones incur losses of information and neutral mutations not? The only difference between detrimental, neutral and beneficial mutations is their effects on reproductive success in comparison with other alleles. And those differential effects are always dependent on the environmental context in which they find themselves. Thus a neutral mutation can be beneficial under different environmental conditions. So there is no particuarly logical reason to exclude neutral mutations from being losses of information, since they can be beneficial under some circumstances, and thus must be losses of information as well.

  9. 9
    jerry says:

    Dave Wisker,

    I am a little confused and you seem to be fairly knowledgeable on this. Most of know a little about the various ways a genome can mutate and understandably know that most are not advantageous or more than likely dangerous. So there is probably a relatively easy way of understanding just what is known and just what is conjecture.

    Positive mutations can be a loss of information but can also be a change in a nucleotide or two or even additions to the genome. I also understand that the changes can be environmentally context sensitive. How prevalent is each?

    Neutral mutations can be just that and not affect the organism in any way. This might be that the place on the genome that changes has no function, or that the change does not affect the function such as when a mutation just represents another codon for the same amino acid. These should have no effect on selection.

    Negative mutations theoretically will be selected against very quickly.

    I guess it is possible that a mutation could move from one category to the other depending upon the circumstances.

    So what I am asking is if you could add to this brief discussion of the categories with some thoughts and examples or expand the categories which were put together very quickly. Basically I am asking for a brief synopsis of what is known assuming we know some basics. If you do not have the time, I understand. Or maybe you could point to a source that is friendly to the average person interested in these topics.

  10. 10
    Patrick says:

    Dave and jerry,

    I’d also add that we should not forget deleterious mutations that also happen to be beneficial in limited environments. I also think it’d help the discussion to make the distinction between deleterious/junk/constructive variation and negative/neutral/positive selection.

    For example, the famous blind cave fish apparently lost their eyes due to a couple mutations. But it was also restored with just a couple. The information pertinent to the eyes could have gotten scrambled via deleterious mutations but these changes would still have been neutral in reference to selection (that’s assuming the usage of information does not overlap with other systems[is true junk], which might be unlikely considering the results of the ENCODE project[when the code is pleiotropic you have to have multiple concurrent changes that work together to produce a functional result.], so I’m speaking of information that’s specific to only the vision system). Or presumably these deletions could have eventually resulted in a different functional system that is then positively selected. Kind of like the flagellum-to-T3SS story.

  11. 11
    Domoman says:

    From what I’ve gathered on mutations they are essentially like this:

    Information-gaining mutations < deleterious mutations < near-neutral mutations.

    Essentially, information-gaining mutations are extremely rare. Deleterious mutations not near as rare, and near-neutral mutations occur almost all the time. As you could expect the reason nobody really notices the near-neutral mutations is because they’re just that, essentially, neutral. If an organism mutates a single nucleotide (if that’s even technically possible) that doesn’t mean the whole system goes down (generally), but it would be a basically neutral mutation.

  12. 12
    Dave Wisker says:

    Frankly, I don’t see a correlation between information gain/loss and adaptive value.

    As Patrick points out loss can be neutral or beneficial. I can think of gains in information that could be detrimental: a gene arising <de novo for a protein that binds to an essential regulatory protein, preventing its proper function, would be an example.

  13. 13
    Dave Wisker says:

    Jerry,

    I’m afraid a comprtehensive review of mutations and their adaptive value is probably beyond the scope of this venue (and my available time). However, I can recommend a reasonably accessible (hopefully not too mathematically dense for a layman) text on population genetics: John Gillespie’s Population Genetics: A Concise Guide.

  14. 14
    Patrick says:

    I can think of gains in information that could be detrimental:

    Or monkey tails on a human. Or anchors on a bird. Or cows with extra limbs attached to their heads. Or extra mammary glands that are non-functional. Or flies with eyes with all over their bodies. Or systems that allow suicidal individuals to “shut down” with a thought. Or…you get the idea.

    There’s more destructive changes that can be positively selected. For example, the trypsinogen gene in Antarctic notothenioid fish. This beneficial mutation is destructive in that while all other fish have two globin genes–alpha1 and beta globin–it turns out that ice fish carry a partially deleted copy of alpha1 and lack the beta globin gene altogether. These deletions are inextricably linked to its lower blood viscosity and have seemingly produced a key adaptation.

    The bulk of the best examples of Darwinian evolution are destructive modifications like passive leaky pores (a foreign protein degrading the integrity of HIV’s membrane) and a leaky digestive system (P. falciparum self destructs when it’s system cannot properly dispose of toxins it is ingesting, so a leak apparently helps) that have a net positive effect under limited/temporary conditions (Behe terms this trench warfare).

    In any case, I would say that in order for Darwinism to be true there needs to be a majority of constructive and beneficial mutations. Exceptions will happen but they can’t be the rule.

  15. 15
    Dave Wisker says:

    In any case, I would say that in order for Darwinism to be true there needs to be a majority of constructive and beneficial mutations. Exceptions will happen but they can’t be the rule.

    I disagree. Much constructive complexity can occur via neutral mutations. I suggest, as an example, Micheael Lynch’s excellent book Origins of Genomic Architecture. The main thesis of the book is that the majority of the complexity seen in the genome arose via non-adaptive forces, i.e, genetic drift. He makes an interesting and compelling argument, IMHO.

  16. 16
    Upright BiPed says:

    “Much constructive complexity can occur via neutral mutations.”

    “When light strikes the retina of the eye, a photon interacts with a molecule called 11-cis-retinal, which rearranges within picoseconds to form trans-retinal. The change in the shape of retinal forces a change in the shape of the protein, rhodopsin, to which the retinal is tightly bound. The protein’s metamorphosis alters its behavior, making it stick to another protein called transducin. Before interacting with activated rhodopsin, transducin had tightly bound a small molecule called GDP. But when transducin interacts with activated rhodopsin, the GDP falls off and a molecule called GTP binds to transducin. GTP-transducin-activated rhodopsin now binds to a protein called phosphodiesterase, located in the inner membrane of the cell. When attached to activated rhodopsin and its entourage, the phosphodiesterase acquires the ability to chemically cut a molecule called cGMP. Initially there are a lot of cGMP molecules in the cell, but the phosphodiesterase lowers its concentration, like a pulled plug lowers the water level in a bathtub. Another membrane protein that binds cGMP is called an ion channel. It acts as a gateway that regulates the number of sodium ions in the cell. Normally the ion channel allows sodium ions to flow into the cell, while a separate protein actively pumps them out again. The dual action of the ion channel and pump keeps the level of sodium ions in the cell within a narrow range. When the amount of cGMP is reduced because of cleavage by the phosphodiesterase, the ion channel closes, causing the cellular concentration of positively charged sodium ions to be reduced. This causes an imbalance of charge across the cell membrane which, finally, causes a current to be transmitted down the optic nerve to the brain. The result, when interpreted by the brain, is vision.” -Behe

  17. 17
    Dave Wisker says:

    Sometimes, it is remarked that neutral alleles are by definition not relevant to adaptation, and therefore biologically unimportant. I think this is too short-sighted a view. Even if the so-called neutral alleles are selectively equivalent under a previaling set of environmental conditions of a species, it is possible that some of them, when a new environmental condition is imposed, will become selected. Experiments suggesting this possibility have been reported by Dykhuisen & Hartl (1980), who called attention to the possibility that neutral alleles have a ‘latent potential for selection’. I concur with them and believe that ‘neutral mutations’ can be the raw material for adaptive evolution.

    Kimura, M (1986). DNA and the neutral theory. Phil. Trans. R. Soc. Lond. B 312:343-354

  18. 18
    Upright BiPed says:

    Dave, with all due respect, neutral mutations may very well be a “raw material” for adaptive selection in some circumstances, this should not be particularly controversial (I think an example or two has already been illiminated on this thread) but the functional coordination within living tissue hardly presents itself to be the result of a mechanism driven by neutral mutation.

    It is the source of that coordination that alludes explanation by such mechanisms. Your Kimura quote, even if taken at full value (which I am prepared to do) is interesting but trivial.

  19. 19
    Dave Wisker says:

    Upright, I’m afraid I don’t see how Behe’s laying out of a particular extant pathway tells us anything significant about the plausibility of the mechanism(s) by which it arose. That has always been a problem with Behe’s concept of IC, IMO.

  20. 20
    Dave Wisker says:

    To get back to Lynch’s thesis:

    From the abstract of a paper by Lynch and Conery which summarize part of the argument in Lynch’s book:

    Complete genomic sequences from diverse phylogenetic lineages reveal notable increases in genome complexity from prokaryotes to multicellular eukaryotes. The changes include gradual increases in gene number, resulting from the retention of duplicate genes, and more abrupt increases in the abundance of spliceosomal introns and mobile genetic elements. We argue that many of these modifications emerged passively in response to the long-term population-size reductions that accompanied increases in organism size. According to this model, much of the restructuring of eukaryotic genomes was initiated by nonadaptive processes, and this in turn provided novel substrates for the secondary evolution of phenotypic complexity by natural selection. The enormous long-term effective population sizes of prokaryotes may impose a substantial barrier to the evolution of complex genomes and morphologies

    Lynch M and JS Conery (2003). The origins of genome complexity. Science 302: 1401-1404

  21. 21
    Upright BiPed says:

    Dave: “I’m afraid I don’t see how Behe’s laying out of a particular extant pathway tells us anything significant about the plausibility of the mechanism(s) by which it arose.”

    I would think that laying out our observations next to their explanations is gernerally seen as a fruitful excercise.

    That was the reason for my post at #16.

    If you did not intend your comment that “Much constructive complexity can occur via neutral mutations” was to be interpreted as a viable explanation for the existence of complexity – then I made a mistake.

  22. 22
    Domoman says:

    Dave Wisker said,

    Frankly, I don’t see a correlation between information gain/loss and adaptive value.

    As Patrick points out loss can be neutral or beneficial. I can think of gains in information that could be detrimental: a gene arising <de novo for a protein that binds to an essential regulatory protein, preventing its proper function, would be an example.

    Well, I’m not saying that information gain is necessary for adaptive value, only that is necessary for neo-Darwinian evolution to occur in the long run. Of course there are certain times when a loss of information can lead to an adaptive benefit, such as anti-biotic resistance. But this isn’t what’s needed for bacteria to evolve in the long run. In fact, if the losses in information continued to occur, the bacteria would eventually not be able to function at all.

  23. 23
    Borne says:

    Mutations can be seen as noise. There are virtually no non-zero effect mutations according to Kimura and others.

    See Kimura’s selection distribution diagrams. All the mutations occur to the left (non-zero negative) of center (completely neutral). Interestingly, there is nothing at all on his graph to the right of neutral (beneficial)

    All mutations, under accumulation, end up being harmful in the end.
    John Sanford, in Genetic Entropy, says,

    If Kimura’s estimate is correct that fitness typically has a heritability of only about .004, then only about 0.4% of phenotypic variation for fitness is selectable. This represents a signal to noise ratio of 1:250. One way of expressing this is that 99.6% of phenotypic selection for fitness will be entirely wasted. This explains why simple selection for total phenotypic fitness can result in almost no genetic gain.

    In 2000, Crowell (University of Arizona Department of Ecology and Evolutionary Biology), published a paper estimating the human mutation rate at around 175 mutations per person per generation. Kondrashov published a paper in 2002 estimating the rate of point substitution mutations alone at 100 per person per generation.

    Kondrashov’s numbers only include point mutations. They do not include numbers for deletions, insertions, duplications, translocations, inversions, macro-mutations and mitochondrial mutations.

    Mutations in a population increase genetic load and will tend to move towards eventual mutational meltdown = extinction – not new and better or “higher” (as Darwin said it) species.

    It is estimated that we are undergoing about 100 mutations/person/generation. In the overall population (+- 6billion = 600 billion total mutations) this means that the genetic load will dramatically increase and that we are in fact devolving, not evolving at all. The human genome is degenerating and always has been.

    It was estimated, by geneticists, decades ago that a mutation rate of 1/person/generation would lead to genetic meltdown. We now know that the rate is conservatively estimated at near 100.

    Thus Darwinian evolution is literally impossible.

    Questions remain – among which :
    1. how did the information get there in the first place?
    2. if that information has been deteriorating since mutations first started how could anything ever have positively evolved at all?
    3. if we are now all mutants, and still undergoing mutations, just how long ago did the genome get started? Iow, can we trace the time line back? Say by reversing the process and tracing backwards? If so what kind of date we would be looking at?

    In any case “Genetic Entropy” explains it all way better than I have and I strongly recommend that book.

  24. 24
    jerry says:

    Dave Wisker,

    I tried reading the Lynch article and the terminology overwhelmed me. From the abstract you have provided from the article, here is what I infer in simple laymen’s language:

    Lynch believes that duplicated genes lie around and over time are mutated at a slow rate but eventually the extent of the change leads it to become functional in a way that was different from the original form. Since there is no selection value in this genetic sequence there is some other process that leads this gene to spread to many organisms before it becomes functional. Otherwise there is no reason for it to pass on and it should get eliminated. So I assume this is a random process with a zillion duplications and only a few eventually making it very far. Maybe you could explain briefly this stepwise process where one duplicated gene in one organism eventually ends ups as a new functional protein in the gene pool and then gets selected.

    And how many examples of this do they know about? Also if this process led to morphological changes in eukaryotes, then it must also be happening today and there are instances of these changes going on in genomes of various species. Any examples?

    Sounds like interesting stuff.

  25. 25
    bornagain77 says:

    Here is a video on genetic entropy:

    Evolution vs. Genetic Entropy

    http://www.youtube.com/watch?v=B8B0RcNWi-I

    Loss of information in a genome not only occurs with natural selection but also with slightly deleterious mutations, which accumulate in the genome over time. The fossil record agrees with this line of evidence. Genetic entropy can first be seen being obeyed by the loss of morphological variability, for all sub-species of a parent species. This is true in the fossil record as well as in living species (Trilobites, Webster: Dog Breeding etc..) Yet the next phase of Genetic Entropy is when the vast majority of mutations, which are slightly deleterious in nature, build up in the genomes of the entire population and eventually lead to Genetic Meltdown for the entire population. (This can be seen in the fossil record by the over 90 percent of species that have gone extinct in the fossil record with no explanation from any natural disaster (Indeed it explains it very well since the extinction rate is fairly constant overall for all species, with a few notable exceptions of longevity)) This is because the “slightly deleterious” mutations are far below the power of natural selection to remove from any one individual’s genome before the negative mutations spread throughout the entire population. (i.e. The slightly deleterious mutations are never dealt with)

    “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.” (Sanford; Genetic Entropy page 24)

    “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.” Dr. Lee Spetner (Ph.D. Physics – MIT – Not By Chance)

    Evolutions try to circumvent this crushing fact by implying that the majority of the DNA is Junk DNA and then postulating some imagined pathway, Yet this dodge has effectively been crushed by the findings of ENCODE.

    “The science of life is undergoing changes so jolting that even its top researchers are feeling something akin to shell-shock. Just four years after scientists finished mapping the human genome – the full sequence of 3 billion DNA “letters” folded within every cell – they find themselves confronted by a biological jungle deeper, denser, and more difficult to penetrate than anyone imagined.”

    Since evolution was forced, by the established proof of Mendelian genetics, to no longer view the whole organism as to what natural selection works upon, but to view the whole organism as a multiple independent collection of genes that can be selected or discarded as natural selection sees fit, this ‘complex interwoven network’ finding is extremely bad news, and absolutely crushing, for the population genetics scenario of evolution (modern neo-Darwinian synthesis) developed by Haldane, Fisher and Wright (page 52 and 53: Genetic Entropy:
    Sanford 2005)!

  26. 26
    Dave Wisker says:

    Hi Jerry.

    So I assume this is a random process with a zillion duplications and only a few eventually making it very far. Maybe you could explain briefly this stepwise process where one duplicated gene in one organism eventually ends ups as a new functional protein in the gene pool and then gets selected.

    Well, first of all, Lynch’s work is concerned primarily with how the complexity of the genomic architeture (how genes are structured) arose. Eukaryotic genomes are structured quite differently from prokaryotic ones, with genes being broken up into the coding sequences (exons) and the non-coding sequences in between them (introns). This makes protein synthesis more complex, because the introns in the messenger RNA transcripts of the genes must be spliced out before they can be sent to the ribosomes for translation into proteins. However, with that complexity comes much more flexibility in generating variation than that found in the prokaryotic architecture. Breaking genes up into exons and introns allows swapping of coding sequences to occur in mechanisms like exon-shuffling and alternative splicing, in addition to the high level of variation basic sexual reproduction and recombination can provide.
    I chose Lynch’s work because it was an interesting (and somewhat counterintuitive) mechanism by which complexity could arise primarily through neutral–non-adaptive– processes. I didn’t intend to use it as an explanation for subsequent morphological complexity, necessarily. I think part of the answer to that lies in the fact that architecture of the eukaryotic genome provides much more flexibility in generating variation than the prokaryotic architecture does. However, in his book Lynch does touch upon the possibility that his approach to non-adaptive forces may help answer some knotty problems that have previously only been examined through the adaptive lens.

    Getting back to your original question, I’m not sure I can adequately address it here. Having said that, I can recommend a very readable and accessible book by Sean Carrol called The Making of the Fittest, in which he describes how gene duplications play a role in the formation of entire gene and protein families. Not only that, he is far more eloquent than I am.

    Sounds like interesting stuff.

    Indeed it is.

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