Darwin's Doubt, by Stephen C. Meyer

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Darwin's Doubt: The Explosive Origin of Animal Life and the Case for Intelligent Design
by Stephen C. Meyer (2013)

This is Stephen Meyer's sequel to Signature in the Cell (2009). Signature focused on the problem of the origin of genetic information and the case for intelligent design, using some arguments similar to those of Shiller in 5th Option. I found that book to be really well written. The explanations were clear, arguments well structured, lots of good references. This one is no different. It focuses on the mystery of the Cambrian explosion, when numerous new animal forms appeared quite suddenly in the fossil record, seemingly with no transitional ancestors that would explain their unique features according to gradual Darwinian processes. Part 1 examines the first problem posed by the Cambrian explosion: the missing forms and fossils. If Darwinism is true, there should be innumerable transition fossils, but they're wholly missing. Part 2 zeroes in on genetics and the problems it has accounting for the new Cambrian creatures. And Part 3 takes a look at some post-Darwinian theories, including intelligent design. Here's some summary notes I took while reading. Hopefully it covers the main points, but if you want the details, you'll just have to read the book (or ask).

Chapter 1 lays out the problem, which Darwin acknowledged. The fossil record shows an 'explosion' of new body plans in the Cambrian period representing most animal phyla, phyla which weren't present in the pre-Cambrian fossil record. Assuming Darwinism is true, a reliable fossil record should show a progressive, gradual development of animal forms, but the record is discontinuous. Darwin, and his followers, hypothesized that perhaps the fossil record was simply incomplete (i.e., the forms existed, but didn't fossilize, or couldn't, perhaps because they were too small or too soft). Chapter 2 describes the discovery of fossils in the "Burgess Bestiary" and the problems it suggested, for example, the fact that it seemed as if big changes came first, not later, after many small-scale changes, the opposite of Darwin's hypothesis. New phyla seemingly arrived fully formed, without transitional forms between them and their presumed common ancestor. Chapter 3 tackles the explanations proposed in response to this contradiction and shows that they hold no water. Small organisms (single cells) and soft body parts can and do get fossilized, and there IS a fossil record of pre-Cambrian creatures. Chapter 4 further demonstrates that the fossils are not simply missing. The known pre-Cambrian fossils do not represent ancestors for the new phyla that crop up during the Cambrian (at least in the vast majority). In the few comparisons to be made, pre-Cambrian forms are either too dissimilar from later Cambrian forms (compounding the problem of missing fossils showing gradual change) or too differentiated (meaning they can't be common ancestors to various known phyla). The fossil record may not be complete, but it is well enough represented to imply that the picture it presents is largely complete (i.e., discontinuous appearance of new forms). We're just looking at it in the wrong way (i.e., assuming universal descent via only natural selection and random mutation).

Chapter 5 looks at the comparative study of genes supposedly proving a pre-Cambrian common ancestor. But Meyer shows that molecular studies produce widely divergent results, and are based on the assumption of universal common descent. (In other words, to use such studies and their estimated molecular dating to prove common descent is circular reasoning.) The hypothetical dates of a common ancestor vary so widely that they don't prove much at all. Chapter 6 looks at the hypothetical trees of life created based on molecular and anatomical comparison between organisms. Meyer shows that comparisons of different molecules produce totally different trees, comparisons between anatomy and molecules produce different trees, and comparisons of different anatomies also produce different trees. The trees contradict each other and are mutually exclusive. In other words, there's currently no reliable picture of the proposed tree of life.

Chapter 7 looks at Gould and Eldredge's theory of 'punctuated equilibrium' (punk eek), proposed in order to explain the discontinuity in the fossil record and the fact that organisms tend to remain the same for long periods of time. But by proposing the idea that speciation proceeds too rapidly to appear in the fossil record, the theory ran into its own problems. Populations needed to be large enough to produce viable mutations, and then small enough to promote that trait. And the only way to get those mutations in the first place was by the same gradual neo-Darwinian process of random mutations (bottom-up, not top-down, as the fossil record suggests). In other words, 'punk eek' ran into the same problems: more transitional fossils should be in the fossil record from the time when variations cropped up between competing species. The Cambrian explosion was still a mystery.

Chapter 8 introduces the second problem posed by the Cambrian explosion. What exactly produced all the new genetic information required for the new cell types and organs seen in the Cambrian phyla? Can this be explained using neo-Darwinian models? Chapter 9 highlights the problem: DNA contains the information for forming proteins, and random changes to specified information (like words in a book) almost inevitably lead to degraded meaning. It becomes gibberish. Wouldn't DNA suffer the same fate, with mutations inevitably producing non-functional proteins? Proteins are typically made of hundreds of amino acids. How many of the astronomical number of possible amino-acid sequences are functional, and how likely is it that random mutation would stumble upon one of those functional sequences? Chapter 10 answers that question, with an in-depth explanation of Doug Axe's work on proteins. While sequences of any length contain many possible functional proteins, compared with the total number of sequences, they are extremely rare. For proteins 150 amino acids in length, the ratio of proteins that fold correctly to those that don't is 1 to 10^74. But the ratio for properly folded proteins that are also functional is 1 to 10^77. Even by generously assuming that one organism can randomly search through these possibilities and come up with a new gene for a new protein in its lifetime, given all the organisms that ever lived in life's 3.8-billion-year history, the probability of reaching a new functional protein is still about 1 in 10^37. In other words, no dice. Such odds are as slim as slim can be. And keep in mind that the Cambrian explosion was mere millions of years long and required the creation of new cell types requiring whole sets of novel genes. Random mutation followed by natural selection CANNOT account for the necessary amount of new genetic information. There simply wasn't enough time for neo-Darwinist processes to do their thing. Chapter 11 deals with the response to Axe's ideas: that known gene-producing processes can explain the production of new genes and proteins. Meyer shows that they cannot. These processes, like exon-shuffling, either presuppose existing genetic information, thus begging the question, or posit 'de novo' creation of genes (i.e., creation out of nothing, new genes with no known precursors). And either way, they don't explain how these processes can solve the problem of searching 'combinatorial space' for the specific functional sequences among way more non-functional ones. Chapter 12 describes experiments showing that genes requiring more than 2 coordinated mutations to produce a new gene are implausible given the entire time and populations available for evolution. In short, neo-Darwinism can't account for the arrival of new genes, new proteins, new traits. The probabilities are too astronomical given the assumed processes at work. Something else is going on. (This has led many researchers to propose new theories for the origin of novel genetic information, which Meyer analyses in Chapters 15 and 16.)

Chapter 13 looks at the origin of body plans and the highly complex processes that go into the growth of embryos to their final form. New forms require new regulatory networks, which switch genes on and off in the right places at the right time in order to differentiate cells, organs, and make sure they're all in the right place in the body. But mutations to these regulatory genes inevitably result in faulty organisms. A new regulatory network requires numerous coordinated mutations, since every part of the system works together, and the system as a whole is hierarchically structured. You can't just change one part of the system to make a new network. Chapter 14 poses perhaps the biggest problem with the development of new forms: epigenetic information, i.e., inherited information that isn't contained in the genes. While genes are necessary for proper development, other things are at work. For example, sea urchin embryos can develop up to 500 cells after their nuclei (which store their DNA) have been removed. How is this possible? It turns out that the pre-existing form of the cell (including its cytoskeleton, centrosome, cell membrane targets, ion channels, and sugar structures that form on the membrane, all of which are essential to the development of an organism's form) is inherited directly from cell to cell. Genes don't code for forms, so new forms require new epigenetic information, wherever and whatever it is. (Random mutation and natural selection can't account for the creation or adaptation of this epigenetic information.)

Chapter 15 looks at the post-neo-Darwinist theory of 'self-organization' that has been proposed to account for some deficits of neo-Darwinism. However, Meyer shows that these theories, too, presuppose genetic information (like gene regulatory networks) and do not explain how epigenetic information self-organizes. It cannot. The shape and location of morphogenic cell features are inherited directly and not determined by their chemical properties. They, too, are a form of pre-existing information that must be presupposed in order for the theory to work. Chapter 16 looks at some other modern theories (like James Shapiro's 'natural genetic engineering', neo-Lamarckism, evo-devo), and shows that they run into similar problems (presupposing large amounts of pre-existing information). Chapters 17, 18, and 19 focus on intelligent design. Meyer argues that it is a valid scientific theory that uses abductive reasoning, like much historical science, and is the best and only explanation for all the problematic features of the Cambrian (rapid top-down appearance, hierarchical genes and gene networks, new animal forms and later variations on those forms that stick to the basic body plan, modular genes, novel information, etc.). He argues that there is no rational reason for denying its status as 'science.'

My only beef with the book is a relatively small one. Meyer seems to think there is only one definition of 'naturalism' (other than methodological naturalism): materialism. Funny that the last footnote is a quote from Alfred Whitehead, who developed a naturalistic philosophy that makes room for mind AND a cosmic mind (God, perhaps). Yet Meyer doesn't raise this possibility that materialism is just one form of naturalism, which would go a long way to reconciling scientific methodology and even some of its core philosophical assumptions with the subject matter of religion (values, questions of the ultimate, soul, free will, etc.). David Ray Griffin has written many good books arguing for an expanded naturalism, showing that one doesn't have to believe the only options are materialistic naturalism and supernaturalism (i.e., God creating the world out of nothing and intervening in it whenever he wants), which has its own serious philosophical problems. So while Darwin's Doubt if a great argument for intelligent design, I think it should be rounded out with a read of some of Griffin's books, like Religion and Scientific Naturalism or Reenchantment without Supernaturalism. But that's a minor point, as so little of the book has to do with theology. The focus is pretty tight on the science and Meyer does a good job despite what I see as one minor weakness in what is really an inessential part of his argument (relegated to the final chapter or two).
 

Laura

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Oh dear, another book to read! And I'm drowning in FISC management!
 

Gaby

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Approaching Infinity said:
Chapters 17, 18, and 19 focus on intelligent design. Meyer argues that it is a valid scientific theory that uses abductive reasoning, like much historical science, and is the best and only explanation for all the problematic features of the Cambrian (rapid top-down appearance, hierarchical genes and gene networks, new animal forms and later variations on those forms that stick to the basic body plan, modular genes, novel information, etc.). He argues that there is no rational reason for denying its status as 'science.'
Does the book mentions "Heat Shock Proteins" or anything among those lines? I was thinking about it today as someone was inquiring about the possibility of combing a "Heat Shock Protein" supplement along with DMSO as a relieving therapy for high stress.

Here is the relevant excerpt from "Speculation on Laura's new book- Horns of Moses"

http://cassiopaea.org/forum/index.php/topic,27881.msg375025.html#msg375025

Cells have very effective emergency programs to cope adverse environmental conditions. Remarkably, cellular stress response is rather uniform irrespective to the stress factor nature. Some cellular functions that are not essential for survival, for example cell division, are temporarily suspended. Besides special kind of genes, the so called heat shock proteins (HSP), will be activated. Their major function is the proper refolding of the damaged proteins. Heat shock proteins, notably the HSP70, were first discovered while investigating cellular responses to a heat shock, hence the name. Tokalov et al. (2003) studied effects of three different stressors on the induction of several heat shock proteins and on the cell division dynamics. The stress was produced by 200 keV X-ray irradiation, by exposure to a weak ELF electromagnetic field (50 Hz, 60 ± 0.2 µT ), or by a thermal shock (41°C for 30 min)....

The fact that weak electromagnetic fields can induce the stress proteins indicates that cells consider electromagnetic fields as potentially hazardous (Goodman & Blank 2002). This is surprising enough, because the magnitude of an effective magnetic stimulus is very small. Electromagnetic fields can induce the synthesis of HSP70 at an energy densities fourteen orders of magnitude lower than heat shock (Goodman & Blank 2002). Such extra sensitivity to the magnetic field must have good evolutionary grounds. Interesting thermo-protective effect of the ELF electromagnetic field exposure mentioned above, and the absence of any effects of weak electromagnetic fields on the cell proliferation, may indicate that cells are not really expecting any damage from the weak electromagnetic impulse, but instead they are using this impulse as some kind of early warning system to prepare for the really hazardous other stress factors which often follow the electromagnetic impulse. There is another aspect of this problem also: some recent findings in evolutionary biology suggest that heat shock proteins play important role in evolution. HSP90 guides the folding process of signal transduction proteins which play a key role

HSP70 guides the folding process of signal transduction proteins which play a key role in developmental pathways. When HSP70 functions normally, a large amount of genetic variation, usually present in genotype, is masked and does not reveal itself in phenotype. However, under the stress Hsp70 is recruited to help chaperone a large number of other cellular proteins. Its normal role is impaired and it can no longer buffer variation. Therefore some mutations will become unmasked and individuals with abnormal phenotype will appear in the population. If a mutation proves to be beneficial in the new environmental conditions, the related traits will be preserved even after the HSP70 resumes its normal function. Therefore HSP70 acts as a capacitor of evolution. If environmental conditions are stable, the buffering role of HSP70 ensures the stability of phenotype despite increased accumulation of hidden mutations in genotype. When the environmental conditions suddenly change, as for example after the asteroid impact, which is believed to cause the dinosaur extinction 65 million years ago, this great potential of genetic variation is released in phenotype and the natural selection quickly finds the new forms of life with greater fitness. The Drosophila experiments of Rutherford and Lindquist (1998) demonstrated this beautiful mechanism, which may constitute the molecular basis of evolution....

Further studies have shown that the HSP70 and HSP60 protein families also buffer phenotypic variation (Rutherford 2003). As was mentioned above, experiments demonstrated that ELF electromagnetic fields can induce various heat shock proteins and in particular HSP70. Therefore we can speculate that ecological and genetic consequences of the Tunguska event are possibly not related to mutations which happened during the event, but are manifestations of the latent mutations, already present in the Tunguska biota, which were unmasked due to the stress response. ELF/VLF radiation from the Tunguska bolide might act as a stressor thereby explaining why the effect is concentrated towards the trajectory projection. …
 

Approaching Infinity

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Psyche said:
Does the book mentions "Heat Shock Proteins" or anything among those lines? I was thinking about it today as someone was inquiring about the possibility of combing a "Heat Shock Protein" supplement along with DMSO as a relieving therapy for high stress.
He doesn't specifically mention heat shock proteins, but he does discuss the work of James Shapiro and Eva Jablonka, both of whom discuss epigenetics and the process of 'directed mutations' (i.e., adaptive mutations in response to environmental threat). In context, Meyer makes two points about such phenomena. First, they require a form of preprogramming (the genome needs to be programmed to respond adaptively as opposed to just reacting blindly, which is what neo-Darwinism predicts). But the bigger point is this: even if an environmental stressor accelerated the mutation rate to a ridiculous level, it would still be impossible to generate a wholly NEW gene. The 'combinatorial space' between 2 functional genes/proteins is so large that it needs intelligence to direct the search. It simply can't occur randomly. And there's no known genetic program that can direct or channel mutations to get one totally novel gene from a prior one. (That would be like programming a computer to somehow make rearrange the text of a novel in order to make a totally different novel that still makes sense.)

So, for these quotes from HOM:

When the environmental conditions suddenly change, as for example after the asteroid impact, which is believed to cause the dinosaur extinction 65 million years ago, this great potential of genetic variation is released in phenotype and the natural selection quickly finds the new forms of life with greater fitness.
"Quickly finding new forms of life" may be what occurs, but there's probably something EXTRA going on. As Laura then writes:

Therefore we can speculate that ecological and genetic consequences of the Tunguska event are possibly not related to mutations which happened during the event, but are manifestations of the latent mutations, already present in the Tunguska biota, which were unmasked due to the stress response.
That would make more sense. The stressor turns certain genes on or off. This could be similar to what happens in queen/worker bees. They have the same genome, but different epigenomes, which turn certain genes on or off, resulting in the differences we see between them. So, theoretically, certain environmental changes could result in something similar in humans, like turning a worker into a queen bee.

But if the process DOES create totally new genes, then I think that has to be directed by intelligence. Whether that is hyperdimensional or by our own influence would be an interesting question to answer (my own hypothesis is that new genes are created by telepathy and psychokinesis :cool2:).
 

Approaching Infinity

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A couple more points:

When the environmental conditions suddenly change, as for example after the asteroid impact, which is believed to cause the dinosaur extinction 65 million years ago, this great potential of genetic variation is released in phenotype and the natural selection quickly finds the new forms of life with greater fitness. The Drosophila experiments of Rutherford and Lindquist (1998) demonstrated this beautiful mechanism, which may constitute the molecular basis of evolution....
I'm not familiar with Rutherford and Lindquist (Meyer doesn't cite them), but he does cite other Drosophila experiments conducted over the last 100 years or so. What they uniformly show is that mutations to developmental gene regulatory networks are fatal. They produce a ton of interesting phenotypic variations, but they're all literally mutants: they can't survive in the wild (e.g., legs where antenna should be, double sets of wings but without the necessary stabilizers or muscles to make flight possible, etc.).

Also, just a note that Meyer is the guy Thomas Nagel got so much flak for supporting (Nagel positively reviewed his first book, Signature in the Cell and cited it in Mind and Cosmos).
 

shijing

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Approaching Infinity said:
In context, Meyer makes two points about such phenomena. First, they require a form of preprogramming (the genome needs to be programmed to respond adaptively as opposed to just reacting blindly, which is what neo-Darwinism predicts). But the bigger point is this: even if an environmental stressor accelerated the mutation rate to a ridiculous level, it would still be impossible to generate a wholly NEW gene. The 'combinatorial space' between 2 functional genes/proteins is so large that it needs intelligence to direct the search. It simply can't occur randomly. And there's no known genetic program that can direct or channel mutations to get one totally novel gene from a prior one. (That would be like programming a computer to somehow make rearrange the text of a novel in order to make a totally different novel that still makes sense.)

[...]

Therefore we can speculate that ecological and genetic consequences of the Tunguska event are possibly not related to mutations which happened during the event, but are manifestations of the latent mutations, already present in the Tunguska biota, which were unmasked due to the stress response.
That would make more sense. The stressor turns certain genes on or off. This could be similar to what happens in queen/worker bees. They have the same genome, but different epigenomes, which turn certain genes on or off, resulting in the differences we see between them. So, theoretically, certain environmental changes could result in something similar in humans, like turning a worker into a queen bee.

But if the process DOES create totally new genes, then I think that has to be directed by intelligence. Whether that is hyperdimensional or by our own influence would be an interesting question to answer (my own hypothesis is that new genes are created by telepathy and psychokinesis :cool2:).
Thanks AI for this review of Meyer's new book! There are a couple of other books I've read recently that might provide some extra information on this topic: The first is Symbiotic Planet by Lynn Margulis (ex-wife of Carl Sagan), which is a fairly short but good book where she argues that most (if not all) evolution arises not via traditional Darwinian genetic mutation but through symbiotic relationships which develop between already existing organisms.

Then there's Alfred De Grazia, who was a contemporary of Velikovsky and promotes a punctuated equilibrium model of biological and environmental evolution based on catastrophism and plasma cosmology which he calls 'quantavolution'. I just finished reading his book The Iron Age of Mars, which is a broad case study on one of the more recent catastrophic periods in history where, interestingly enough (in view of our recent research on iron overload), he argues that large amounts of iron were transferred to Earth from other bodies (he also promotes a theory where Mercury was originally the largely iron core of another planet -- either Mars or the former planet which was destroyed and left the current asteroid belt between Mars and Jupiter). He also argues that man's original evolution occurred as the result of a much earlier quantavolution which left him with multiple selves as the result of an imbalance in hemispheric communication (he calls this new being Homo Schizo, and he's written a couple of books on the topic).

(As an aside, there's another book he's written called God's Fire which I haven't read yet, but flipping through it it looks like he's reached at least some of the same conclusions as Laura regarding the nature of Moses and the catastrophic context in which the 'Exodus' occurred.)
 

Approaching Infinity

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Shijing said:
Thanks AI for this review of Meyer's new book! There are a couple of other books I've read recently that might provide some extra information on this topic: The first is Symbiotic Planet by Lynn Margulis (ex-wife of Carl Sagan), which is a fairly short but good book where she argues that most (if not all) evolution arises not via traditional Darwinian genetic mutation but through symbiotic relationships which develop between already existing organisms.
Meyer is supposed to have a criticism of this theory on his website, but I don't think it's up there yet. But right away, I can see it running into some problems, namely the origin of NEW genes, proteins, and body plans. Any combination of already existing forms presupposes what it intends to explain (i.e., the original body plan, which was at one point 'new'). It also can't solve the 'combinatorial search' problem. I think symbiotic sharing may have occurred, but again, it can't be the whole explanation. Without some panpsychism it's just another materialistic theory doomed by its reliance on chance and necessity. (I haven't read Margulis's work though, so correct me if I'm wrong or making too many assumptions!)
 

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Found this from Meyer's original paper on the Cambrian:

_http://www.discovery.org/articleFiles/PDFs/Cambrian.pdf

In any case, evolutionary biologists have not offered any detailed neo-Darwinian account of the origin of the eukaryotic cellular system. True, Lynn Margulis’s endosymbiotic hypothesis seeks to explain how eukaryotes acquired their mitochodria, the organelle responsible for much of the eukaryotic cell’s energy production. Yet her hypothesis (which is fraught with difficulties on its own terms)[134] does not attempt to explain the origin of the eukaryotic cell as a whole. According to Margulis, prokaryotic bacteria somehow incorporated a primitive cellular system (without digesting it), and this system eventually became an independent subsystem within the emerging eukaryotes. Whatever its merits or difficulties, the endosymiotic hypothesis gives no account for the origin of the other organelles specific to eukaryotes, or the cytoskeloton, or the eukaryotic information processing system (with its many complex and specialized proteins). Nor does the endosymbiotic hypothesis attempt to explain the origin of the system of proteins and nucleic acids operating within mitochondria itself. Instead, it merely posits the absorption of one tightly integrated system by another, without explaining how any mutually interdependent system of proteins could arise by neo-Darwinian means in the first place.

footnote 134: According to the serial endosymbiotic theory (SET), a proto-eukaryote engulfed, via the complex process of phagocytosis, an alpha-proteobacterium (which then evolved into mitochondria) and cyanobacterium (which then evolved into plastids [chloroplasts]). Obviously an essential step in this hypothesis would be the ability to engulf another organism – yet SET provides no candidates for the proto-eukaryote equipped with this function. “The proto-eukaryote,” J.R. Brown and W.F. Doolittle note, “was proposed to have a rudimentary cytoskeleton, since such innovation would be necessary for phagocytosis...Although bacteria living intracellularly in a different bacterial species have been reported, phagocytosis by a bacterium has never been observed. Nor is there any evidence for the existence of the sophisticated RNA-based organisms with cytoskeletons” (“Archaea and the Prokaryote-to-Eukaryote Transition,” Microbiology and Molecular Biology Reviews 61 (1997): 456-502; p. 463
 

shijing

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Approaching Infinity said:
I think symbiotic sharing may have occurred, but again, it can't be the whole explanation. Without some panpsychism it's just another materialistic theory doomed by its reliance on chance and necessity. (I haven't read Margulis's work though, so correct me if I'm wrong or making too many assumptions!)
No, I think you're quite correct in asserting that it can't be the whole explanation (new genes, proteins, and body plans). In her book, Margulis speculates about the ultimate origin of cells (focusing on liposomes and RNA), but doesn't go beyond that -- Meyer's quote above also highlights what are probably the biggest questions about her SET hypothesis. That being said, there are some interesting things she describes, for example the fact that chloroplasts in plant cells are closer genetically to cyanobacteria than they are to the other parts of the cell that they're a part of (a similar situation is true for mitochondria and proteobacteria -- those are the two cases that Meyer mentions above re: the problem of phagocytosis).

One of my (very open-ended) questions is what the possibilities are during a catastrophe in which sudden, dramatic shifts in the environment occur, specifically those which involve high-energy electrical events. It might be the case, for instance, that symbiotic events could happen that would be otherwise precluded during long periods of relative homeostasis. That's the one thing that Meyer may be missing in his critique, in that he's looking at things from the perspective of what we observe in the present -- but just as with cosmic events, it may not be the case that things always work the way that we observe during the part of history we happen to be experiencing. But now I want to read his book to see what he says about all of this!
 

Laura

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Yeah, the prokaryote to eukaryote problem is generally unsolvable as far as I can see. What is postulated is so unlikely that it is more parsimonious to accept intelligent input such as information theory.
 

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Then, how about the viral properties of DNA? Does the book mention anything that could be linked? Keeping in mind that authors rarely say "viral", but use "junk" DNA terms such as retrotransposable elements, introns, etc.

Here is a synthesis on the subject:

On viral 'junk' DNA, a DNA-enhancing Ketogenic diet, and cometary kicks
http://www.sott.net/article/257631-On-viral-junk-DNA-a-DNA-enhancing-Ketogenic-diet-and-cometary-kicks

And considering the working hypothesis here:

After reading this book about viruses, we have the idea that viruses may be the means by which genetic manipulation {as in intentional coming from other densities} has taken place on this planet for millions, if not billions, of years.

A: Yes

Q: (L) Does that mean that a virus is a transdimensional manifestation?

A: Yes. Thoughts made manifest! Compare to some crop circles!

Q: (Psyche) Some viruses in the atlas DO look like crop circles. [wind noise muffles Ark's question] (Ark)...of course virus is just pure DNA, or what? (Psyche) It can be both DNA or RNA depending on the type of virus, and usually coated to protect itself. There are so many types of viruses; it can be just a piece of genetic code. (Ark) Okay, so my question is whether there is a particular part of the virus that has the property that is not just described by normal quantum physics or quantum chemistry and so on, or its the whole organization of virus that has this property?

A: Yes. Information field aggregates matter.

Q: (talk of thought vs. information) (Belibaste) Does information command or direct the aggregation of different proteins or amino acids to form a virus? Materialization?

A: Yes.

Q: (Psyche) It's very interesting because they have found in our "junk" DNA, properties of viruses that are close in location to those of stem cells, and also cells that end up producing cancer. It is quite interesting. (Perceval) That means our DNA is thought made manifest?

A: More or less!

Q: (Perceval) Except when we do the thinking, we mess it up. So we should stop thinking and interfering with the manifestation of our DNA! (laughter)
It seems to me the last paper quoted in the article above is very interesting in its implications. Full text available on the link below, but here are some relevant excerpts:

{It touches the experiments of the Drosophila species}
{There is a glossary box within the article... Transposable elements (TE) - which were once considered "junk" DNA - are viral in their origin}

Transposable elements and viruses as factors in adaptation and evolution: an expansion and strengthening of the TE-Thrust hypothesis

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3501640/

Abstract

In addition to the strong divergent evolution and significant and episodic evolutionary transitions and speciation we previously attributed to TE-Thrust, we have expanded the hypothesis to more fully account for the contribution of viruses to TE-Thrust and evolution. The concept of symbiosis and holobiontic genomes is acknowledged, with particular emphasis placed on the creativity potential of the union of retroviral genomes with vertebrate genomes. Further expansions of the TE-Thrust hypothesis are proposed regarding a fuller account of horizontal transfer of TEs, the life cycle of TEs, and also, in the case of a mammalian innovation, the contributions of retroviruses to the functions of the placenta. The possibility of drift by TE families within isolated demes or disjunct populations, is acknowledged, and in addition, we suggest the possibility of horizontal transposon transfer into such subpopulations. “Adaptive potential” and “evolutionary potential” are proposed as the extremes of a continuum of “intra-genomic potential” due to TE-Thrust. Specific data is given, indicating “adaptive potential” being realized with regard to insecticide resistance, and other insect adaptations. In this regard, there is agreement between TE-Thrust and the concept of adaptation by a change in allele frequencies. Evidence on the realization of “evolutionary potential” is also presented, which is compatible with the known differential survivals, and radiations of lineages. Collectively, these data further suggest the possibility, or likelihood, of punctuated episodes of speciation events and evolutionary transitions, coinciding with, and heavily underpinned by, intermittent bursts of TE activity.

Introduction

The importance of transposable elements (TEs) to stress responses and adaptation was first proposed by Barbara McClintock who was also the discoverer of TEs (McClintock 1956, 1984). Since then much groundbreaking work has substantiated the view that TEs play a significant role in evolution (Georgiev 1984; Syvanen 1984; Finnegan 1989; Brosius 1991; McDonald 1993; Kidwell and Lisch 1997; Fedoroff 1999; Shapiro 1999; Bennetzen 2000; Bowen and Jordan 2002; Jurka 2004; Kazazian 2004; Biémont and Vieira 2006; Volff 2006; Wessler 2006; Feschotte and Pritham 2007; Muotri et al. 2007; Beauregard et al. 2008; Böhne et al. 2008; Hua-Van et al. 2011; Werren 2011). Building on this body of work, we have proposed TEs as powerful facilitators of evolution (Oliver and Greene 2009a) and have subsequently gone further than others by formalizing this general concept into an explicit, comprehensive, predictive, and testable hypothesis, which we call the “TE-Thrust hypothesis” (Oliver and Greene 2011). The basis of the TE-Thrust hypothesis is that TEs are powerful facilitators of evolution that can act to generate genetic novelties in both an active mode and a passive mode. Active mode: by transposition, including the exaptation of TE sequences as promoters, exons, or genes. Passive mode: when present in large homogeneous populations, TEs can cause ectopic DNA recombination resulting in genomic duplications, deletions or rearrangements (including karyotypic changes). Fecund lineages, those with many species (e.g., rodents and bats, which together make up 60% of mammals), are generally rich in viable (i.e., capable of activity) and active TEs, whereas nonfecund lineages (e.g., monotremes) have mainly nonviable (i.e., incapable of activity) and inactive TEs. Evolutionary transitions, for example, the evolution of the higher primates and evolutionary innovations, such as the mammalian placenta, also appear to be facilitated by TEs (Oliver and Greene 2011). An outline of the TE-Thrust Hypothesis is:

Many eukaryote lineages are able to tolerate some sacrifices in the present, that is, a genomic “load” or population, of mostly controlled, but possibly fitness-reducing TEs. Such lineages may, thereby, fortuitously, gain a continuum of “intra-genomic potential” whose extremities are conveniently described as “adaptive potential” and “evolutionary potential.” This intragenomic potential may be realized in the present, and/or in the descendant lineage(s) of the future. Note that this does not imply any “aim” or “purpose” to evolution, or any ability of evolution to “see” into the future.

As environmental or ecological factors change, or the lineages adopt new habitats, these intragenomic potentials can be realized. For example, adaptive potential can be realized to give small adaptive changes within a lineage, over short periods of time, such as the evolution of insecticide resistance, when insecticides become prevalent in the environment. Evolutionary potential can be realized, over much longer periods of time, perhaps in adaptive radiations, as in some rodents or bats.

At least some unicellular eukaryotic organisms do not appear to tolerate a genomic load of TEs (Galagan and Selker 2004; Pritham 2009), which suggests that TE-Thrust does not operate in all extant biological lineages. However, it is noteworthy that most eukaryotic species known to lack TEs are intracellular parasites with small genomes, including members of the Babesia, Cryptosporidium, and Plasmodium genera (Pritham 2009). This could be due to selection for small cell size and/or because the genomic plasticity engendered by TEs may not provide a net advantage to nonfree-living organisms that exist within a stable environment.

TE-Thrust and Punctuated Equilibrium

Eldredge and Gould (1972) posed the concept of punctuated equilibrium from studies of the fossil record, as opposed to the then prevailing concept of phyletic gradualism. There is now independent support for punctuated equilibrium from studies of extant taxa (Cubo 2003; Pagel et al. 2006; Mattila and Bokma 2008; Laurin et al. 2012), from co-evolution (Toju and Sota 2009), and in extant and ancient genomes of Gossypium species due to intermittent TE activity (Palmer et al. 2012). TE-Thrust provides an intragenomic explanation of punctuated equilibrium (Oliver and Greene 2009a,b, 2011), as has also been suggested by Zeh et al. (2009), via epigenetic changes, and/or endogenization of retroviruses, in response to stress, and Parris (2009), via endogenization of retroviruses and environmental change.

The actual processes of speciation events seem to be poorly understood, but new species are said to emerge from many differing and rare single events (Venditti et al. 2010). However, two almost essential components seem to be necessary: reproductive isolation and intragenomic variation. Of these, intragenomic variation can be readily supplied by the hypothesized TE-Thrust (Oliver and Greene 2011), and reproductive isolation can be provided by a variety of means, including karyotypic changes, polyploidy, hybridization, and physical environmental or ecological factors (Venditti et al. 2010).

Much TE activity (active TE-Thrust) is thought to occur in intermittent bursts that interrupt more quiescent periods of low activity (Bénit et al. 1999; Marques et al. 2005; Cantrell et al. 2005; Pritham and Feschotte 2007; de Boer et al. 2007; Ray et al. 2008; Zeh et al. 2009; Erickson et al. 2011). These punctuation events can occur especially after intermittent infiltrations or amplifications of TEs. New acquisitions of TEs can be due to:

Intermittent horizontal transposon transfer (HTT) (Schaack et al. 2010). This appears to be relatively rare, and probably tends to occur more often with some DNA-TEs, LTR retro-TEs, and the Bov-B LINE.
The de novo synthesis of chimeric elements, for example, the hominid specific SVA (Wang et al. 2005). This is probably rare.
The de novo syntheses of various SINEs, the younger ones (<100 Myr) of which are lineage specific (Piskurek et al. 2003; Kramerov and Vassetzky 2011). This is probably rare.
Intermittent endogenizations of various RNA viruses (Bénit et al. 1999; Belyi et al. 2010; Horie et al. 2010). This may be relatively common, especially in mammals.
Hybridization, especially in angiosperms (Michalak 2010). This appears to be common.
Intermittent de novo modifications to successive families of TEs (e.g. L1 LINEs). This is relatively common.

An example of an intermittent burst is the L1 LINE in ancestral primates, where among a large number of overlapping families, L1PA6, L1PA7, and L1PA8 were apparently amplified intensively around 47 Mya. This seemingly contributed to a very large Alu SINE, and retrocopy, amplification at this time (Ohshima et al. 2003). TEs can result in the acceleration of the evolution of genes in a myriad of ways (Böhne et al. 2008; Goodier and Kazazian 2008; Hua-Van et al. 2011), providing a means for rapid species divergences in the affected lineages.

Modes of TE-Thrust

All the hypothesized modes of TE-Thrust shown below are consistent with the data tabulated in Oliver and Greene (2011), but are expressed herein in different ways. All of them refer only to the potential for adaptation or evolution due to the hypothesized TE-Thrust. As other facilitators of evolution will possibly also be active in addition to TE-Thrust, and as environmental and ecological factors can frequently change, all these hypothesized capabilities of TE-Thrust need to be predicated by “if all else is equal”. These modes of TE-Thrust are extremes of continuums, so intermediate modes must occur.

Mode 1. Evolutionary potential may be realized, in concert with, or following, significant intermittent bursts of TE activity, in viable and heterogeneous TE populations, whether large or small. This can underlie what we designate as “Type I” punctuated equilibrium (stasis with punctuation events), due to intermittent active TE-Thrust.

Mode 2. Evolutionary potential may be realized, in concert with, or following, significant bursts of TE activity, in large viable and homogenous TE populations. This can result in what we designate as “Type II” punctuated equilibrium (gradualism with punctuation events) due to both ongoing TE-Thrust (largely passive), and to intermittent active TE-Thrust. If the TE population is small, then only intermittent active TE-Thrust is likely to occur as per mode 1.

Mode 3. Nonviable heterogeneous TE populations, whether large or small, may result in evolutionary stasis, due to a lack of both active and passive TE-Thrust.

Mode 4. If a nonviable TE population is both large and homogeneous, and not too degraded by mutations, then gradualism type evolution may occur, due largely to passive TE-Thrust. If the TE population is small, then little TE-Thrust is likely to occur as per mode 3.

An Expansion of the TE-Thrust Hypothesis

Herein, the TE-Thrust hypothesis is further expanded from its original formulation. We acknowledge that in addition to TE-Thrust, other nongenomic facilitators of evolution may play a part in radiations and evolution, such as dynamic external factors, including geological, environmental, and ecological changes. Such factors may result in fragmentation of populations into small local demes, or larger disjunct sub-populations, which can result in reproductive isolation with possible divergence into novel taxa (Wright 1931; Eldredge 1995; Jurka et al. 2011). In addition to alleles drifting to fixation or extinction in demes, TE families likely also do so (Jurka et al. 2011) and we are in agreement with this. Additionally, in TE-Thrust we hypothesize that novel TEs as described above, may very occasionally be introduced into, or arise within, some demes or disjunct populations, but not into others, ultimately causing evolutionary transitions or the evolution of new taxa. We view the carrier subpopulation (CASP) hypothesis (Jurka et al. 2011) to be complementary to TE-Thrust, as it is about the fixation of TEs in populations and the details of mechanisms, or origins, of speciation, which were previously not included in the TE-Thrust hypothesis. The CASP hypothesis gains some support from the cotton genus (Gossypium) specific Gorge retro-TEs (Palmer et al. 2012), as Gorge seems to have spread to fixation in a small progenitor population of Gossypium. Indeed, both hypotheses are in agreement in strongly relating TEs to speciation and evolution. However, we suggest that karyotypic changes due to TE presence and activity, are among the factors that produce the reproductive isolation necessary for speciation, although we agree that geographic isolation into demes, niche availability, and many other phenomena (e.g., pheromone changes in insects) are also important factors.

We note that adaptive evolution via natural selection is, but one of the forces of evolutionary change. Other important forces, all of which are nonadaptive, comprise mutation, recombination, and random genetic drift (Lynch 2007). As TE-Thrust emphasizes a key intragenomic role for TEs in mutation and recombination, it fits comfortably with a growing body of evidence indicating that a significant portion of evolutionary changes are not adaptive in nature, but result from the accumulation of mildly deleterious mutations that can become fixed by genetic drift in populations of relatively small size (Fernández and Lynch 2011). Indeed, although the occasional highly deleterious TE insertion will be rapidly culled by purifying selection, TE insertions can themselves be viewed overall as an accumulation of neutral to mildly deleterious mutations that are subject to genetic drift. Activation of TEs, for example, during stress, or horizontal transfer of TEs etc., provides powerful complements to genetic drift. Thus, TEs accumulate by nonadaptive processes and can underpin nonadaptive change, and they also readily provide the raw material for future beneficial traits capable of undergoing positive selection.

We recognize that there are many known genomic facilitators of evolution, besides TE-Thrust. A few apposite examples are: symbiosis (Ryan 2007, 2009); hybridization (Ryan 2006; Larsen et al. 2010); noncoding RNA (Heimberg et al. 2008; Mattick 2011); horizontal gene transfer (Richards et al. 2006); whole genome duplications (Hoffmann et al. 2012), and viral driven evolution (Villarreal 2005, 2009; Ryan 2007; Villarreal and Witzany 2010; Feschotte and Gilbert 2012). Some facilitators of evolution may have greater importance in some clades than in others. For example, whole genome duplication (polyploidy) is apparently quite important in the evolution of angiosperms (Soltis et al. 2004). Ryan (2006) includes several of the examples above under the general descriptor “genomic creativity”.

Horizontal Transfer of TEs in TE-Thrust

Mobile DNA has been classified into Class I retro-TEs (e.g., LTR elements, LINEs, and SINEs), and Class II DNA-TEs, composed of subclasses 1 (e.g., Tc1-Mariner and hAT) and 2 (Helitron and Maverick), as have been described and reviewed elsewhere (Wicker et al. 2007; Böhne et al. 2008; Goodier and Kazazian 2008; Kapitonov and Jurka 2008; Hua-Van et al. 2011). The horizontal transfer of TEs (horizontal transposon transfer or HTT) has previously been proposed as a major force driving genomic variation and biological innovation (Schaack et al. 2010). DNA-TEs have long been known to be capable of HTT, for example, the P-element DNA-TE in Drosophila (Anxolabéhère et al. 1988; Daniels et al. 1990); the Mariner DNA-TE in various insects (Maruyama and Hartl 1991; Robertson and Lampe 1995; Lampe et al. 2003), and DNA-TEs in the bat Myotis lucifugus (Pritham and Feschotte 2007; Ray et al. 2007). However, HTT of retro-TEs, has been less well documented, except for some examples, including the patchily distributed Bov-B LINE, (Kordiš and Gubenšek 1998; Gogolevsky et al. 2008) and the Gypsy-like retro-TEs (Herédia et al. 2004).

Although probably infrequent, HTT is an important aspect of the TE-Thrust hypothesis that has so far only been given cursory attention (Oliver and Greene 2009a, 2011). Over 200 cases of HTT have been documented (Schaack et al. 2010), 12 of which were between different phyla. About a half of these known HTTs involved retro-TEs, most of which were LTR retro-TEs. The remaining HTTs involved a variety of DNA-TEs. Horizontal transfer is an important part of the life cycle of TEs, as they generally accumulate mutations and eventually become nonviable in the genomes they occupy. This can downgrade the efficacy of TE-Thrust. However, they are sometimes enabled, via chance events, to periodically make fresh starts with fully functional elements, in the genomes of other lineages. At least some TEs appear to be able to endure in the absence of HTT. For example, the LINE 1 (L1) retro-TE in mammals has persisted for 100 Myr with no known evidence of HTT (Furano et al. 2004; Khan et al. 2006), although it has now become nonviable in a few mammalian lineages (Casavant et al. 2000; Boissinot et al. 2004; Cantrell et al. 2008; Platt and Ray 2012).

Viruses and bacteria appear to be likely vectors of HTT (Piskurek and Okada 2007; Schaack et al. 2010; Dupuy et al. 2011), but endoparasites and intracellular parasites are among other possible vectors that have been proposed (Silva et al. 2004; Schaack et al. 2010). Empirical data (Anxolabéhère et al. 1988; Cantrell et al. 2005; de Boer et al. 2007; Pritham and Feschotte 2007; Ray et al. 2008) and simulations (Le Rouzic and Capy 2005) both suggest that TE amplification occurs immediately after HTT of a viable TE copy.

Holobionts and Holobiontic Genomes, and The Importance of the Highly Mobile Retroviruses

Exogenous retroviruses can become endogenized, and can be united with the host genome into a holobiontic genome in a new holobiont (Box 1). Holobiont is a symbiological term that means the partnership, or union, of symbionts (Rosenberg et al. 2007; Ryan 2007; Gilbert et al. 2010). For example, the ERVWE1 locus in the human genome comprises a conserved envelope (env) gene together with the conserved 5′ LTR of a retrovirus that contains regulatory elements. This locus, additionally, includes sections of human genetic sequences and these also play a role in regulation of the env gene, which codes for Syncytin-1 (Mi et al. 2000). Syncytin-1 has a crucial function in trophoblast cell fusion in ape placental morphogenesis (Mi et al. 2000), which strongly suggests that selection has occurred at the level of the holobiontic genome in the human plus retrovirus holobiont (Ryan 2006).

Box 1. Glossary of Terms

Parasite and Symbiont: To most contemporary biologists, a parasite is an often harmful organism in a partnership that benefits itself at the expense of the other partner, and a symbiont is an organism in a mutually beneficial partnership with another organism. However, Symbiologists define Symbiosis as: The living together of differently named (i.e., different species) organisms, including parasitism, commensalism, and mutualism (Ryan 2006, 2009) and this definition is used here.

TE-Thrust: A hypothesized pushing force generated by TEs within genomes, that can facilitate adaptation, and punctuated or major evolution, within the corresponding lineages (Oliver and Greene 2011).

Virus: Viruses are a part of biology because they possess genes, have group identity, replicate, evolve, and are adapted to particular hosts, biotic habitats, and ecological niches. Most viruses are persistent and unapparent, that is, not pathogenic (Villarreal 2005).

Viral Biogenesis: Exogenous retroviruses, and some other exogenous RNA viruses, can act in mutualism when endogenized in other genomes, and their genomes are united with the host genome into a “holobiontic genome”.

Holobiont: The partnership, or union, of symbionts (Ryan 2007; Gilbert et al. 2010).

Mobilome: A general term for the total content of the mobile DNA in any genome. Mobilome Consortium (Villarreal) implies that the presence or activity of each individual or category of TE, within the Mobilome, likely affects the mobilome as a whole, e.g., SINE viability is coupled to LINE compatibility and viability.

Adaptive potential: The potential of a lineage to adapt over decades or centuries. Such adaptation can be associated with one to several genes.

Evolutionary potential: The potential of a lineage to evolve and radiate, possibly by punctuation events, over thousands or millions of years. Such evolution may be associated with major organizational and architectural genomic changes. Note: Adaptive potential and Evolutionary potential are not distinct entities, but are useful descriptors for the extremities of an Intra-genomic potential continuum.
Retroviruses appear to be the most mobile of all “mobile DNA” as they can exist exogenously as infectious, or persisting viruses, as well as by becoming endogenized in host germ lines (Hughes and Coffin 2001, 2004; Ryan 2006). Exogenous retroviruses are distinct entities to those species whose genomes into which they endogenize to become an ERV, and they have an extracellular or virion stage, with a protein capsid. ERVs then are a part of a holobiont organism. Other TEs in a genome are not considered to be a part of a holobiont, as they seemingly can only transfer from genome to genome, and can have no independent existence like that of an exogenous retrovirus species.

Endogenized retroviruses (ERVs) can multiply within a genome either by repeated endogenizations, or by retrotransposition within the genome (Belshaw et al. 2004; Wang et al. 2010). Over time, due to recombinations between their LTRs, and deletions, ERVs often exist mostly as solo LTRs or sLTRs, (Sverdlov 1998). Many Class I elements are related to retroviruses, namely the Copia, Gypsy, and BEL/Pao subclasses of LTR retro-TEs, which have LTRs (long- terminal repeats), but lack an env gene.

Retroviruses are present among all placental mammals (Bénit et al. 1999), are largely restricted to vertebrates, and are particularly abundant in mammals (Villarreal 2005). Retroviruses have been endogenized in mammalian germ lines many times during the evolution of mammals. These ERVs have been a very important factor in their evolution (Villarreal 2005), and are particularly associated with that mammalian innovation, the placenta (Oliver and Greene 2011). Endogenized retroviruses, and the role they play in evolution, have been extensively detailed elsewhere (Villarreal 1997, 2004, 2005, 2009; Ryan 2003, 2006, 2007; Feschotte and Gilbert 2012).

Endogenous nonretroviral RNA virus elements, notably Bornaviruses, have also been found in mammalian genomes, including several primates and several rodents, and these viral sequences appear to have function (Belyi et al. 2010; Horie et al. 2010). Indeed, all major types of eukaryotic viruses can give rise to endogenous viral elements or EVEs (Feschotte and Gilbert 2012). Thus, viral-eukaryote holobiont organisms appear to be not uncommon, and these could have lead to significant evolutionary innovation. This enhances the explanatory power of the TE-Thrust hypothesis.

Retroviruses and the Evolution of the Mammalian Placenta

The placenta represents a major evolutionary innovation that occurred over 160 Mya at the time of the divergence of the placental mammals. The circulatory and the metabolic benefits provided by this transient organ to the growing embryo and fetus have been well investigated, but less so well understood is the origin of the placenta. The invasive syncytial plate, the precursor to the placenta, and the rapidly growing trophoblast, are developmentally unique to mammals (Harris 1991). Harris proposes that prior to the divergence of placental mammals, developing embryos became infected at an early intrauterine stage with retroviruses, which gave rise to cellular proliferation and creation of the trophoblast. This may then have resulted in the formation of the highly invasive “tumor-like” vacuolated and microvillated syncytial plate and a primitive placenta (Harris 1991). Although to date, there is no proof that the fusogenic ERVs of premammals resulted in the evolution of the mammalian placenta (Harris 1991; Dupressoir et al. 2009) it seems likely to be correct. Supporting evidence comes from the egg-laying platypus, which has a genome that is devoid of ERVs, although there are some thousands of ancient Gypsy-class LTR retro-TEs (Warren et al. 2008). In contrast, all examined placental mammal genomes do contain many ERVs (Mayer and Meese 2005; Villarreal 2005), with ERV/sLTRs constituting approximately 8% and 10% of the human and mouse genomes, respectively (Waterston et al. 2002). Atypically, the placenta exhibits global DNA hypomethylation, which allows many ERVs and retro-TEs to retain transcriptional activity in this tissue (Rawn and Cross 2008). Such a permissive environment for expression of TEs facilitates their exaptation as coding or regulatory sequences, and indeed, the LTRs of ERVs contain promoter activity that can confer tissue-specific expression in the placenta, as for example, the CYP19A1, IL2RB, NOS3, and PTN genes, which are solely expressed by an LTR promoter (Cohen et al. 2009). Although there are few known unique placenta-specific genes, numerous genes expressed in the human placenta are derived from retro-TEs and ERVs (Rawn and Cross 2008). Most notable are the fusogenic, ERV env-derived, syncytin-1, and syncytin-2 (Mi et al. 2000; Blaise et al. 2003), with syncytin-2 also having an immunosuppressive function (Kämmerer et al. 2011). The efficient adaptive immune systems of mammals must fail to initiate an immune reaction to the antigens of their embryos and placentas, and mammals alone are very highly infected with the generally immunosuppressive endogenous retroviruses (Villarreal 1997). Intriguingly, retroviruses are abundant around sperm heads and also coat the female placenta (Steele 2009). The advantages of the placenta could possibly explain why extant placental mammals number well over 5,000 species, whereas there are less than 300 extant species of marsupials (Pough et al. 2009).

Evolvability and the TE-Thrust Hypothesis

Mutation, including gene duplication and other DNA changes, is the driving force of evolution at both the genic and the phenotypic levels (Nei 2005, 2007). Significantly, Shapiro (2010) proposes that it is mobile DNA movement, rather than replication error that is the primary engine of protein evolution. Along the same lines, Hua-Van et al. (2011) stress TEs as a major factor in evolution, whereas Muotri et al. (2007) proposes that “handy junk” can evolve into “necessary junk”. Wagner (Heard et al. 2010), in support of our original concepts (Oliver and Greene 2009a) states that, in general, “the kinds of genetic changes that are possible depend on what kinds of TEs are present and active at any particular time”, in the evolution of each lineage. Thus, the potential for evolutionary innovations differs over time, contradicting the concept of gradualism in lineages. Caporale (2009) posits that “selection must act on the mechanisms that generate variation, much as it does on beaks and bones”. Earl and Deem (2004), with no mention of TEs, propose the evolution of mechanisms to facilitate evolution, and describe evolvability as a selectable trait. Further to this, Woods et al. (2011) found experimental evidence, in a study of bacteria that long-term evolvability may be important for determining the ultimate success of a lineage, and that less fit lineages with greater evolvability may eventually out-compete lineages with greater fitness. All these lines of reasoning, and associated experimental data, are in good accord with the TE-Thrust hypothesis.

Reduced “Fitness” versus enhanced “Adaptive Potential” and “Lineage Selection”

Accumulation of TEs in the genome of Drosophila melanogaster has been found to be associated with a decrease in fitness (Pasyukova et al. 2004). The reduced “fitness” in Drosophila may be an extreme case, because in D. melanogaster TEs cause over 50% of de novo mutations (Pasyukova et al. 2004). In contrast to D. melanogaster, de novo disease-causing insertions in humans are relatively rare (Deininger and Batzer 1999; Kazazian 1999; Chen et al. 2005; Hedges and Batzer 2005), whereas TE activity in the laboratory mouse falls between these two extremes (Kazazian 1998; Waterston et al. 2002; Maksakova et al. 2006). There is, however, no conflict with the TE-Thrust hypothesis with this finding in Drosophila, as despite a fitness loss in some individuals in the present, there can be a fortuitous gain in adaptive potential to the lineage as a whole. TEd-alleles (TE- deactivated or destroyed alleles), for example, usually lower the fitness of the lineage. However, TEm-alleles (TE-modified alleles, which can be modified in either regulation or function, or duplicated), for example, increase the genetic diversity, and hence the adaptive potential, of the lineage. These TEm-alleles allow the lineage to adapt to environmental/ecological challenges in the present. Also, importantly, this adaptive potential may be latent in the present, and only be realized in the future, as environmental/ecological challenges change. This latent adaptive potential then, increases the chances of the long-term survival of the lineage. In other words, TE-Thrust can result in latent adaptive potential (also called standing variation), which can be realized, if needed, in the future, and can result in the differential survival of lineages. This is the rationale for positing lineage selection in the TE-Thrust hypothesis (Oliver and Greene 2009a,b, 2011).

Realizable “Adaptive Potential” Due to TE-Thrust

TE-Thrust is proposed to have facilitated adaptive change, as we highlighted in the simian lineage (Oliver and Greene 2011). The ongoing ability of TEs to provide realizable adaptive potential is illustrated by TE-generated polymorphic traits identified in isolated populations of laboratory-bred mice (Table 1), as well as by structural variation in the human genome still being created by L1 activity (Ewing and Kazazian 2010).

[...]A specific example of an adaptive benefit from TE activity is the development of insecticide resistance in the Hikone-R strain of Drosophila melanogaster. [...] These four steps have occurred within 70 years in the Hikone-R strain of Drosophila melanogaster, and the more derived the allele, the greater the resistance (Schmidt et al. 2010). Such allelic successions, whereby different adaptive alleles are substituted sequentially have been demonstrated in several other studies of insecticide resistance (Schmidt et al. 2010).[...]

The Failure of Mutation Breeding

In a review, Lönnig (2005), described how, despite early enthusiasm and sustained effort, mutation breeding (in either plants or animals) has never been successful. The mutations caused by mutagens usually produced weaker or nonfunctional alleles of wild type genes. In TE-Thrust, however, the TEs usually consist of functional coding or exaptable sequences, and often also of potent regulatory sequences, so that by insertion and in many other ways, for example, exon shuffling in the active mode and ectopic recombination in the passive mode, they can make many beneficial changes, although they may sometimes do damage (Oliver and Greene 2009a,b, 2011). TEs can alter the regulation or the structure of alleles, or duplicate them (Darboux et al. 2007; González et al. 2009, 2010; Schmidt et al. 2010) creating TEm-alleles. Therefore, although attempted breeding, adaptation or evolution, using mutagens to generate alternative alleles almost always does not work (Lönnig 2005), adaptation or evolution using TE-Thrust generating TEm-alleles relatively often does work. This is not to say that other types of mutation, such as point changes, are not important in evolution. In fact, in addition to their general importance in evolution, such mutations often complement TE-Thrust, for example, by modifying TE-duplicated sequences.

Reduced “Fitness” versus Enhanced “Evolutionary Potential”

The question of whether or not the possible lowering of fitness in a lineage by TEs can result in enhanced evolutionary potential may be simplified into two competing hypotheses:

The Null Hypothesis: TE-Thrust is not causal to adaptation, speciation, punctuation events, or evolution.

The Alternative Hypothesis: TE-Thrust is causal to adaptation, speciation, punctuation events, and evolution.

Testing the Hypotheses

Recent/ancient speciation and the alternative (TE-Thrust) hypothesis

In the absence of events, such as intermittent de novo modifications to successive families of TEs, de novo SINE synthesis, HTT, or de novo synthesis of chimaeric TE elements, TE bursts in lineages eventually tend to fade to inactivity, with TEs becoming nonviable and degraded by the accumulation of deleterious mutations. An example is the apparent loss of L1 element activity in a number of species. These include the spider monkey, thirteen-lined ground squirrel, megabats, and sigmodontinae rodents (Casavant et al. 2000; Boissinot et al. 2004; Cantrell et al. 2008; Platt and Ray 2012), although at least in the case of the sigmodontinae, which have undergone rapid fecund speciation with numerous karyotypic changes, the loss of viable LINEs appears to have been more than compensated for by massive endogenisations of ERVs (Cantrell et al. 2005; Erickson et al. 2011). As TE-Thrust predicts that lineages lose their adaptability as overall TE activity and integrity fades, the loss of TE viability over time provides an intragenomic explanation to help account for the high rate of background extinction that has been a prevalent feature of life on earth (Raup 1994). In contrast, lineages harboring young TE families are associated with recent speciation. This is well exemplified in the mammals where species with the highest numbers of young TE families, such as the mouse, rat, bat, rhesus macaque, and human, represent the largest extant mammalian orders of rodents, bats, and primates (Jurka et al. 2011). Very species-poor extant mammalian lineages, such as the alpaca, elephant, tenrec, armadillo, and platypus, do not harbor any young families of TEs (Jurka et al. 2011). Nevertheless, TE-Thrust predicts more ancient speciation events being attributed to older families of TEs, when they were young, and this is supported by phylogenetic analyses (Jurka et al. 2011). These data are consistent with the Alternative (TE-Thrust) Hypothesis.

The vesper bats and the alternative (TE-Thrust) hypothesis

The radiation of the vesper bats (family Verspertilionidae) appears to support the Alternative Hypothesis and the active mode of TE-Thrust. The vesper bats, which have an almost worldwide distribution (Nowak 1994), are a fecund lineage (407 species of the approximately 930 species of microbats or 8–9% of all extant mammal species), and include Myotis, the most speciose mammalian genus with about 103 members. Significantly, vesper bats are somewhat unique in having many viable and active DNA-TEs that have been nonviable in most other mammals for 37 Myr (Pace and Feschotte 2007).

The early radiation of the vesper bats is proposed to have been due to HTT of Helitron DNA-TEs, called Helibat, into the vesper bat lineage about 30–36 Mya (Pritham and Feschotte 2007).
Amplification of DNA-TEs is thought to follow HTT in a naive lineage, which can result in innovations in the genome (Pace et al. 2008).
Helibat has amplified explosively up to at least 3.4% of the Myotis lucifugus genome (Ray et al. 2008).
HTT of Helitrons, especially, can lead to diversification, and to dramatic shifts in the trajectory of genome evolution (Thomas et al. 2010).
HTT of of DNA-TEs can also lead to horizontal gene transfer (Thomas et al. 2010).
Although Helitrons have not been detected in other mammals besides the vesper bats, they are abundant in plants, invertebrates, and zebrafish, and have been implicated in large-scale gene duplication and exon shuffling.
There were other multiple waves of HTT of DNA-TEs in the bat lineage coinciding with a period of their rapid diversification 16–25 Mya (Teeling et al. 2005; Pritham and Feschotte 2007; Ray et al. 2008).
A further burst of New World Myotis diversification 12–13 Mya was noted (Stadelmann et al. 2007), corresponding well with the period that the most active transposition of a variety of DNA-TEs is estimated to have occurred (Ray et al. 2008).
Such repeated waves of TE activity suggest a mechanism for generating the genetic diversity needed to result in the evolution of such great species richness as is observed in the vesper bats (Ray et al. 2008).
Active retro-TEs, namely L1 LINEs (Cantrell et al. 2008) and VES SINEs (Borodulina and Kramerov 1999), have also been found in vesper bats.

This mix of viable DNA-TEs and retro-TEs, unknown in other mammals, could have resulted in large architectural and organizational changes in their genomes and aided in the Myotis diversification, enabling adaptation to very diverse ecological niches within this lineage (Pritham and Feschotte 2007; Thomas et al. 2011). This suggests that much active TE-Thrust has operated during the very large radiation of the vesper bats during the last 36 Myr. A lack of data presently obscures any conclusions regarding any possible involvement of passive TE-Thrust. The predicted evolutionary outcome of such intermittently active populations of TEs is either gradualism or stasis with punctuation events, (Type I or II punctuated equilibrium). Current data suggest that this is correct for the Verspertilionidae.
The Muridae Rodents and the Alternative (TE-Thrust) Hypothesis

The extensive radiation of the Old World Muridae (the Murinae) appears to support the Alternative Hypothesis, and both the active and the passive modes of TE-Thrust. The rodents are the most fecund mammalian order comprising about 40% of mammals with an almost worldwide distribution. The Muridae family, which include the true mice and rats, have been particularly successful and account for about two-thirds of all rodent species. Representatives of the subfamily Murinae (Mus and Rattus) possess large populations of relatively homogenous retro-TEs, many of which are viable and active (Table 2).
Table 2
Table 2
Presence and Viability of Transposable Elements (TEs) in Distinct Mammalian Species

The Old World mouse (Mus) and rat (Rattus), with some 50–60 species each in their respective genera, have genomes comprised of about 40% largely homogenous genomic TEs. These include numerous viable and mostly highly active L1 LINEs and few nonviable ancient L2 LINEs, giving a LINE total of 22%. SINEs comprise a further 7% and most (92%) are lineage specific, viable, and effective, although slightly diverse, with only few being the nonviable ancient MIR SINEs. Less than 1% of their genomes are composed of nonviable DNA-TEs (Waterston et al. 2002; Gibbs et al. 2004). The mouse has about 10% ERV/sLTRs, many of which are very active and are closely related to mouse exogenous retroviruses (Maksakova et al. 2006).
The fitness cost of their greatly enhanced evolutionary potential is higher than in humans, as previously noted (Maksakova et al. 2006).

Although the generally small size of many rodents probably aided in their diversification, there has seemingly been much active TE-Thrust, as indicated by the growing number of documented examples of rodent-specific traits generated by TEs (Table 3). They are also quite well suited to passive TE-Thrust, as they have large homogenous populations of TEs to facilitate TE-mediated duplications, inversions, deletions or karyotypic changes. The predicted evolutionary outcome of large homogenous and intermittently active populations of TEs is gradualism with punctuation events (Type II punctuated equilibrium), as in the hypothesized mode 2 of TE-Thrust.
Table 3
Table 3
Specific Examples of Transposable Elements (TEs) Implicated in Rodent-Specific Traits
The naked mole rat and the alternative (TE-Thrust) hypothesis

In sharp contrast to Mus and Rattus, which are both very rich in species and have abundant viable and active TEs (Waterston et al. 2002; Gibbs et al. 2004), the rodent genus Heterocephalus, also in the family Muridae, has only one species (Wilson and Reader 2005). In support of the Alternative Hypothesis, sequencing of H. glaber (Kim et al. 2011), the very atypical, physiologically unique, eusocial, and long-lived naked mole rat, has shown that it possesses a nonviable and relatively small mobilome consortium (Table 2).

The TEs of the naked mole rat, although they are homogenous and constitute 25% of the genome, are highly divergent, indicating they have been both nonviable and inactive for a very long time (Kim et al. 2011).
As most mammals have 35–50% TEs, this suggests that a substantial portion of its TEs may have been lost altogether.

The data indicate that H. glaber has had little or no TE-Thrust, except in the remote past, and if all else is equal, it is in stasis or gradualism. (Note: As viable and active TEs are known to occasionally cause harmful mutations, these data additionally suggest that there possibly could be less genetic disease and cancer in the individuals of species, such as H. glaber).[...]

Summary of the evidence for the alternative (TE-Thrust) hypothesis

It can, of course, be argued that this evidence in mammals (microbats, rodents, and the platypus), reptiles (the green anole lizard and the tuatara), and the evolution of the mammalian placenta, is all only circumstantial evidence, and therefore does not demonstrate a causal link between TE-Thrust and enhanced evolutionary potential. This argument is weakened by the abundance of young families of TEs in the largest extant mammalian orders of rodents, bats, and primates, and their absence in the elephant, alpaca, tenrec, armadilo, and platypus. The argument of “only circumstantial evidence” is further weakened by the wide range of known conserved and/or beneficial genomic modifications that are due to TEs in various lineages (Brosius 1999; Miller et al. 1999; Kidwell and Lisch 2001; Nekrutenko and Li 2001; van de Lagemaat et al. 2003; Jordan et al. 2003; Kazazian 2004; Shapiro and Sternberg 2005; Volff 2006; Böhne et al. 2008; Oliver and Greene 2009a, 2011). Therefore, it seems that a causal link between recent TE activity, sometimes resulting in reproductive isolation, and recent speciation events is indeed likely.

Some hard evidence can be provided with regard to adaptive potential and adaptive evolution in insecticide resistance by insects in the last 70 years, and adaptation to temperate climates in the last few centuries. However, a punctuation event is estimated to take between 15,000 and 40,000 years (Gould 2002). It appears then that, as yet, bursts of TE activity and punctuation events cannot be dated accurately enough to establish any definite relationship. However, some apparent correlations have been reported, suggesting that increased TE activity may indeed be basal to, or coincident with, punctuation events and evolutionary transitions, speciation, or large radiations. Some examples of these, in addition to those detailed above, are:

Ohshima et al. (2003) found bursts of Alu SINE and retrocopies coincident with the radiation of the higher primates 40–50 Mya.
DNA-TE activity coincided with speciation events in salmonoid fishes (de Boer et al. 2007).
Bursts of transposition of BS element transposition have also shaped the genomes of at least two species of Drosophila, D. mojavensis and D. recta (Granzotto et al. 2011).
There are numerous examples of bursts of TE activity that often follow polyploidization events (Comai 2000), or hybidization (Michalak 2010), in angiosperms, leading to speciation.

Some suggest that a role for TEs in speciation is speculative (Hua-Van et al. 2011), whereas others have given data, which they readily acknowledge specifically suggests TE involvement in taxon radiations (de Boer et al. 2007; Pritham and Feschotte 2007; Ray et al. 2008; Thomas et al. 2011). In our interpretation of the available data, we suggest that, if all else is equal, minimal or passive TE-Thrust is likely to result in stasis or gradualism, whereas active TE-Thrust is likely to be causal to innovative evolution (e.g., the placenta), punctuation events and radiations, as in our hypothesized four modes of TE-Thrust (Oliver and Greene 2011). However, we readily acknowledge that some punctuation events may be caused by other facilitators of evolution.

Conclusions

The field of evolutionary biology has seemingly paid more attention to the outcomes of genetic mutation in terms of the generation of variants and their selection within populations than the mechanisms by which mutations emerge in the first place. Although small-scale DNA base changes and deletions are important in evolution, TEs (and viruses) are uniquely placed, via TE-Thrust, to expeditiously cause complex and/or large-scale changes and thereby help explain macroevolutionary change and the emergence of highly innovative adaptations. Much still remains to be investigated, such as the relevance of TE-Thrust to other classes and phyla. Only a small number of lineages in the metazoans: the mammals and to a lesser extent, a very few lineages of the insects, plants, and reptiles, have been considered with regard to the TE-Thrust hypothesis to date. As increasing numbers of genomes are being sequenced, it would be interesting to investigate the link between TEs, exogenous viruses, and enhanced adaptive potential, enhanced evolutionary potential, evolutionary transitions, and the occurrence of punctuation events, in the lineages of other taxa. It seems likely that in the great diversity of extant lineages, TE-Thrust and other facilitators of evolution will have had a greater or lesser impact on adaptation and evolution. There seems to be little doubt, however, that TEs and viruses have played a major and prominent role in the evolution of almost all life on earth, and that TEs and viruses need to be recognized and included, as the TE-Thrust hypothesis, in a much needed extension and modification in evolutionary theory.
 

Approaching Infinity

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Psyche said:
Then, how about the viral properties of DNA? Does the book mention anything that could be linked? Keeping in mind that authors rarely say "viral", but use "junk" DNA terms such as retrotransposable elements, introns, etc.
He does talk about junk DNA and various proposed mechanisms for the creation of novel genes, like exon shuffling, gene duplication (leading to 'neutral evolution' where the functional gene continues to do its job and the other mutates without selection), retropositioning, lateral gene transfer, and subsequent point mutations. He doesn't work them into a theory, though. He mainly points out that they suffer the same problems as all other mechanisms for really accounting for novel genes, traits, and body plans. All these mechanisms 1) rely on previously existing information (thus the mechanisms themselves can't account for the original information; they all presuppose what they attempt to explain), and 2) can't solve the combinatorial search problem. In other words, they probably still need to be directed to some degree, at least in cases involving wholly NEW forms of information, like totally new genes or body plans (which rely on non-genetic information in addition to the relevant genes and proteins). To oversimplify, the genes need to 'know' where exactly to make all the cuts and pastes, and how to fit them together in context so that they work within the existing system. I don't think Meyer would deny that such mechanisms can (or even do) occur, but interpreting them in a materialistic, random or automatic framework doesn't work. So, for example, from the paper you cited:

Conclusions

The field of evolutionary biology has seemingly paid more attention to the outcomes of genetic mutation in terms of the generation of variants and their selection within populations than the mechanisms by which mutations emerge in the first place.
Yes, but no mechanistic process can solve the problem of finding new genes in 'sequence space.'

Although small-scale DNA base changes and deletions are important in evolution,
I think this type of mutation has been overemphasized. Genes require multiple, specific mutations in order to find new genes. It's not a matter of changing one letter at a time until you randomly find a new functional gene.

TEs (and viruses) are uniquely placed, via TE-Thrust, to expeditiously cause complex and/or large-scale changes and thereby help explain macroevolutionary change and the emergence of highly innovative adaptations.
This probably overstates the case. Macroevolutionary change doesn't just require genetic changes, but epigenetic changes as well (e.g., in cell architecture, cell membrane features, and multi-gene regulatory networks). Whatever the merits of TEs, they can't 'cause' large-scale changes (i.e., macroevolution and highly innovative adaptations) on their own.

Much still remains to be investigated, such as the relevance of TE-Thrust to other classes and phyla. Only a small number of lineages in the metazoans: the mammals and to a lesser extent, a very few lineages of the insects, plants, and reptiles, have been considered with regard to the TE-Thrust hypothesis to date. As increasing numbers of genomes are being sequenced, it would be interesting to investigate the link between TEs, exogenous viruses, and enhanced adaptive potential, enhanced evolutionary potential, evolutionary transitions, and the occurrence of punctuation events, in the lineages of other taxa. It seems likely that in the great diversity of extant lineages, TE-Thrust and other facilitators of evolution will have had a greater or lesser impact on adaptation and evolution. There seems to be little doubt, however, that TEs and viruses have played a major and prominent role in the evolution of almost all life on earth, and that TEs and viruses need to be recognized and included, as the TE-Thrust hypothesis, in a much needed extension and modification in evolutionary theory.
Just as with Margulis's theory, I think TE-thrust is probably important. But I think the whole mechanistic/materialistic framework is a doomed approach. An organizing 'information field' probably has a part to play in all these proposed mechanisms.
 

Gaby

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Approaching Infinity said:
Just as with Margulis's theory, I think TE-thrust is probably important. But I think the whole mechanistic/materialistic framework is a doomed approach. An organizing 'information field' probably has a part to play in all these proposed mechanisms.
Fascinating. So it is really like going in circles over and over again in more sophisticated ways. "Information field" is like the perfect fit and only explanation to make all the puzzle pieces fit together in a coherent way.
 

shijing

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Psyche said:
Approaching Infinity said:
Just as with Margulis's theory, I think TE-thrust is probably important. But I think the whole mechanistic/materialistic framework is a doomed approach. An organizing 'information field' probably has a part to play in all these proposed mechanisms.
Fascinating. So it is really like going in circles over and over again in more sophisticated ways. "Information field" is like the perfect fit and only explanation to make all the puzzle pieces fit together in a coherent way.
I think that's more or less it -- the research mentioned above on symbiogenesis and TE-thrust are entirely valid research hypotheses and very interesting, but they are parts of the evolution toolbox, not self-contained mechanisms. What's missing is the intelligent organizing principle (information theory and the information field) which it would be most parsimonious to suggest operates at a hyperdimensional level.
 

Approaching Infinity

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Shijing said:
Psyche said:
Approaching Infinity said:
Just as with Margulis's theory, I think TE-thrust is probably important. But I think the whole mechanistic/materialistic framework is a doomed approach. An organizing 'information field' probably has a part to play in all these proposed mechanisms.
Fascinating. So it is really like going in circles over and over again in more sophisticated ways. "Information field" is like the perfect fit and only explanation to make all the puzzle pieces fit together in a coherent way.
I think that's more or less it -- the research mentioned above on symbiogenesis and TE-thrust are entirely valid research hypotheses and very interesting, but they are parts of the evolution toolbox, not self-contained mechanisms. What's missing is the intelligent organizing principle (information theory and the information field) which it would be most parsimonious to suggest operates at a hyperdimensional level.
Exactly. And the image of going around in circles is perfect. When you read Meyer's books, that's the exact image that formed for me. With each new theory, it's like these scientists know at some level that they're dealing with a huge mystery, but every new theory they come up with only pushes the real problem back and suffers the same problems as all the other ones: the origin of specified information. Because they CAN'T admit mind into their equations, they're stuck trying to fit a square peg in a round hole, and it's quite maddening to see them continually miss the crux of the matter.
 
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