Thursday, August 11, 2011

Junk & Jonathan: Part 9—Chapter 6

This is part 9 of my review of The Myth of Junk DNA. For a list of other postings on this topic see the links below. For other postings on junk DNA check out the links in Genomes & Junk DNA in the "theme box" below or in the sidebar under "Themes."
Jumping Genes and Repetitive DNA
The title of Chapter 6 is "Jumping Genes and Repetitive DNA." Wells describes transposons as jumping genes and includes them in the category of "Repetitive Non-Protein-Coding DNA." This category makes up 50% of the genome, according to Wells. The breakdown is as follows. LINES 21%; SINES 13%; retroviral-like elements 8%; simple sequence repeats 5%; and DNA-only transposons 3%. These percentages are similar to those published in a wide variety of textbooks and scientific papers. [What's in Your Genome?] [Junk in your Genome: LINEs] [Junk in Your Genome: SINES]


Many LINES and SINES are Functional

Most of the transposons in the human genome are fragments or otherwise mutated versions of the original mobile elements. This is a good reason for assigning them to the junk DNA category. They are a form of pseudogene. What this means is that half of our genome is composed of defective transposons that can't "jump." This is non-functional DNA, otherwise known as "junk."

This conclusion is unacceptable to Jonathan Wells. In order to prove that junk DNA is a myth he must show that most of this DNA has a function. He begins with a section called "Many LINES and SINEs are functional.

Theme

Genomes
& Junk DNA
The first evidence for functionality comes from the data showing that most of the genome is transcribed—the main theme of Chapter 3. If most of these defective transposons are transcribed then it seems likely that they have a function. But the evidence for widespread transcription is not widely accepted and one of the main criticisms is that it's extremely difficult to tell which repeated sequences are actually transcribed and which ones just happen to be very similar to a family member that is transcribed. We know that active LINES and SINES have to be transcribed at some time and we know that many defective transposons will still be transcribed even if they are non-functional. The question is not whether any transposons are transcribed, it's whether all (or most) of them are. The answer is almost certainly that very few are transcribed on a regular basis. The pervasive transcription reported in some papers is most likely accidental transcription at a very low level or artifact.1
Nishihara, H., Smit, A.F., and Okada, N. (2006) Functional noncoding sequences derived from SINEs in the mammalian genome. Genome Res. 16:864-874.
The first "function" paper Wells mentions is Nishihara et al. (2006). These workers characterized a new class of SINES in the human genome. They consist of a hybrid of 5S RNA and a tRNA (~300 bp). These SINES are found in most vertebrates (fish, amphibians, birds, mammals). There are about 1000 of these SINEs in the human genome and in 105 of them there seems to be more sequence conservation in the central portion of the sequence than expected from junk DNA. For example, the overall sequence similarity between human and zebrafish is about 59% in a stretch of 338 nucleotides. (The authors refer to these as regions that are "under strong selective constraint." That's a bit exaggerated.)

This section contains three other examples of sequence similarities in a small class of transposons. These are the only examples where he makes the case for widespread functionality of defective transposons.

Wells is happy to accept the arguments that sequence similarity is evidence of homology and also of function.2 Several possible functions were ruled out in these studies but it's possible that they have some undiscovered function that results in moderate sequence conservation. If this turns out to be true it would mean that 0.01% of the genome should be moved from the "junk" category to the "functional" category.

Some Specific Functions of LINES and SINES

Wells then proceeds to a discussion of papers that demonstrate a function for individual transposon fragments. Before we look at those studies, it's worth keeping the big picture in mind. A typical eukaryotic genome has a million defective transposons and a dozen or so functional transposons that are still capable of jumping to new locations. If you examine the genomes of a dozen or so eukaryotes you can expect to find some examples where these bits of DNA have been co-opted to perform some new function. If you collect together all these examples from many different species then it looks like an impressive array of functional transposon sequences but impressions can be deceptive. It's still true that 99.9% of defective transposons are junk.

This section of the book consists of four pages of specific examples of presumed functional transposon-like sequences from mouse, rat, human, hamster, silkworm, fruit fly, and Arabidopsis (plant). There are 54 references to the scientific literature. Wells makes no attempt to asses the reliability of these studies, nor does he indicate whether the claims have been independently confirmed by other labs.

It's a typical ploy of creationists to focus on specific examples of unusual adaptations and ignore the context. In this case, all those specific individual examples don't amount to a hill of beans when compared to the vast majority of junk in eukaryotic genomes.

However, in fairness it's not just Jonathan Wells and the creationists who fail to see the forest for the trees. There are many scientists who also think that the evidence quoted by Wells is conclusive proof that junk DNA is a myth. Wells has no trouble finding such scientists whose views are expressed in the scientific literature.
Walters, R.D., Kugel, J.A., and Goodrich, J.A. (2009) Critical Review (sic): InvAluable Junk: The Cellular Impact and Function of Alu and B2 RNAs. Life 61:831-837.

Finding that Alu and B2 SINEs are transcribed, both as distinct RNA polymerase III transcripts and as part of RNA polymerase II transcripts, and that these SINE encoded RNAs indeed have biological functions has refuted the historical notion that SINEs are merely "junk DNA."
Endogenous Retroviruses

About 8% of your genome consists of endogenous retroviruses. Most of them are defective, usually because large parts of them have been deleted. Some are still capable of producing viable retrovirus, like HIV or hepatitis B. There are about 30,000 loci in your genome where endogenous retroviruses are located.

Endogenous retroviruses contain strong transcriptional promoters since they have to produce a lot of transcripts when they are induced. Some of these small promoter regions (called "LTRs") have become incorporated into the promoter regions of regular genes. What happened is that millions of years ago a retrovirus accidentally integrated into the genome near the 5′ end of a gene and when parts of the endogenous retrovirus were lost by deletion the remaining retroviral promoter region became active leading to enhanced transcription of the adjacent gene. Over time this piece of the retrovirus evolved to become an integral part of the regulation of the gene.

Wells describes several examples of such events in different mammals. He also describes a famous example where expression of a modified envelope protein from a defective endogenous retrovirus has taken on a role in the development of the mammalian placenta. Together, these examples of co-opted retroviral sequences account for about a dozen of the 30,000 copies in your genome. Naturally, this is assumed to be proof that none of the defective endogenous retroviruses are junk. That's the logic of creationists.

Francis Collins and Repetitive Elements

The last section of this chapter is pure rhetoric. Wells is upset because Francis Collins, a Christian, wrote the following in The Language of God (pages 135-136):
Even more compelling evidence for a common ancestor comes from the study of what are known as ancient repetitive elements (AREs). These arise from "jumping genes," which are capable of copying and inserting themselves in various other locations in the genome, usually without any functional consequences. Mammalian genomes are littered with such AREs, with roughly 45 percent of the human genome made up of such flotsam and jetsam. When one aligns sections of the human and mouse genomes, anchored by the appearance of gene counterparts that occur in the same order, one can usually also identify AREs in approximately the same location in these two genomes.

Some of these may have been lost in one species or the other, but many of them remain in a position that is most consistent with their having arrived in the genome of a common mammalian ancestor, and having been carried along ever since. Of course, some might argue that these are actually functional elements placed there by the Creator for a good reason, and our discounting them as "junk DNA" just betrays our current level of ignorance. And indeed, some small fraction of them may play important regulatory roles. But certain examples severely strain the credulity of that explanation. The process of transposition often damages the jumping gene. There are AREs throughout the human and mouse genomes that were truncated when they landed, removing any possibility of their functioning. In many cases, one can identify a decapitated and utterly defunct ARE in parallel positions in the human and mouse genome.
Wells is upset because this is a double-barreled attack on intelligent design. Not only does Collins describe these sequences as junk but he also uses them as evidence of common ancestry. This is one of the reason why creationists like Wells maintain that junk DNA is used to support evolution.

Wells says,
Collins's argument rests on the assumption that those repetitive elements ... are nonfunctional. Yet their similar position in the human and mouse genomes could mean that they are performing some function in both. Given the rate at which functions are being discovered, Collins's assumption seems foolhardy, and his argument could easily collapse in the face of new scientific discoveries.
As long as most of these repetitive elements remain non-functional they pose a serious problem for Intelligent Design Creationists. The IDiots have been wishing for evidence of function for 20 years but "wishing" isn't a very scientific argument. Given the rate at which functions are being discovered, it's going to be a long, long time before all those hundreds of thousands of repetitive elements are assigned a function (i.e. never!). The vast majority of them are junk and discovery of a few co-opted sequences isn't going to change that fact.


1. As a general rule, Wells "forgets" to mention when one of his "facts" is disputed in the scientific literature. Like most creationists, he is delighted to quote any scientific studies that confirm his bias but he is somewhat more reluctant to quote papers that don't. In this case—pervasive transcription—the criticisms in the scientific literature are so well-known that he is forced to discuss them in Chapter 9.

2. This is a bit strange coming from someone who doesn't believe in evolution but logic has never been a strong point is Wells' writing. Note that Wells does not accept the corollary argument that lack of conservation implies lack of function.

36 comments :

  1. Dr Moran you posted:
    "Most of the transposons in the human genome are fragments or otherwise mutated versions of the original mobile elements. This is a good reason for assigning them to the junk DNA category."

    By "mutated" do you mean "changed" or do you mean corrupted/damaged/defective?
    As I understand what you have said repeatedly in other posts, the word "mutated" simply means "changed".

    If it simply means "changed", then that itself is no reason "for assigning them to the junk DNA category."

    Right?

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  2. Moran you posted:
    "Wells describes several examples of such events in different mammals. He also describes a famous example where expression of a modified envelope protein from a defective endogenous retrovirus has taken on a role in the development of the mammalian placenta."

    What evidence do we have that it was a "defective" endogenous retrovirus?
    I have studied this field fairly extensively and have never seen any actual evidence that the "vector" was defective. ("Vector" is a more neutral, objective term than "virus").
    Can you supply any evidence for that claim? A reference link to something peer-reviewed would be very helpful.

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  3. anonymous asks,

    What evidence do we have that it was a "defective" endogenous retrovirus?
    I have studied this field fairly extensively and have never seen any actual evidence that the "vector" was defective. ("Vector" is a more neutral, objective term than "virus").
    Can you supply any evidence for that claim? A reference link to something peer-reviewed would be very helpful.


    Your "fairly extensive" study wasn't very effective. Here's one paper that covers a lot of bases.

    Cáceres, M. and Thomas. J.W. (2006) The Gene of Retroviral Origin Syncytin 1 is Specific to Hominoids and is Inactive in Old World Monkeys J. Hered. 97:100-106. [doi: 10.1093/jhered/esj011]

    Syncytin 1 is one of the best known examples of recent acquisition of a new gene from an endogenous retrovirus (HERV) in the human genome and has been implicated in placental physiology. Within primates, Syncytin 1 is conserved in all hominoids but has not been characterized in Old World monkeys (OWMs). In this study, we investigated the status of Syncytin 1 in 14 hominoid and OWM species. We show that although the HERV-W provirus responsible for the origin of this gene was present in the genome of the most recent common ancestor of hominoids and OWMs, Syncytin 1 is inactive in OWMs. In addition, we were able to determine that the evolution of Syncytin 1 in hominoids involved an accumulation of amino acid changes and showed signatures of both positive and purifying selection. Our results indicate that Syncytin 1 is indeed a hominoid-specific gene and illustrate the complex and dynamic process associated with the origin of new genes.

    ...

    The best known and most studied of the human env-derived genes is Syncytin 1 or ERVWE1, which was originated from a human endogenous retrovirus (HERV) of the HERV-W family inserted in human Chr.7q21 (Blond et al. 1999; Mi et al. 2000). Multiple inactivating mutations were found in the gag and pol coding sequences of the provirus. Conversely, the env gene maintained an ORF coding for a 538 amino acid polypeptide that has all characteristic features of Env proteins and mediates intercellular fusion in vitro (Blond et al. 2000; Frendo et al. 2003; Mi et al. 2000). Recently, a molecular evolution study of the HERV-W provirus in several ape species and in 24 humans showed that in all of them Syncytin 1 was conserved and retained its receptor-mediated fusogenic activity (Mallet et al. 2004). However, an analysis of the synonymous and nonsynonymous substitutions indicated a relatively high degree of amino acid changes in hominoids (Bonnaud et al. 2004), which could be consistent with a low degree of selective constraint. Although it has been documented that the HERV-W invasion of the primate genome occurred before the divergence of hominoids and Old World monkeys (OWMs) (Kim et al. 1999; Voisset et al. 1999), the Syncytin 1 locus in OWMs has not been described previously (Mallet et al. 2004). In this study, we have taken advantage of current sequencing efforts focused in targeted genomic regions of diverse species (Thomas et al. 2003) to analyze in detail the Syncytin 1 region in primates. In addition, by using the OWM Syncytin 1 sequence as the outgroup, we have been able to better characterize the amino acid changes related to the acquisition of this new gene in hominoids.


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  4. Those references do not label them as "defective".
    That was my point.
    Do you have any evidence for your claim that they were "defective"?

    ReplyDelete
  5. anonymous the IDiot says,

    Those references do not label them as "defective".
    That was my point.
    Do you have any evidence for your claim that they were "defective"?


    I suppose there might be a parallel universe out there where "multiple inactivating mutations ... in the gag and pol coding sequences of the provirus" don't make a virus defective.

    It's even possible that anonymous lives on a different planet where the word "defective" has a different meaning.

    That would explain a lot.

    ReplyDelete
  6. It is the same question again.
    Does "mutating" simply mean "changing" or not?

    Mutating is not defective.
    You keep playing this ambiguity word game that I mentioned earlier.
    Sometimes you innocently claim that mutate just means change and then you use it to mean "defective".

    Just look at what you are saying if we replace the word "mutate" with "change":

    "multiple inactivating CHANGES ... in the gag and pol coding sequences of the provirus".

    How do you want to play this? Does mutate simply mean "change" or not?
    This is a dishonest game that evolutionists play. I have seen it many times.
    You are not the only one.

    ReplyDelete
  7. anonymous the IDiot asks,

    How do you want to play this?

    I'm not going to play with an IDiot like you. If you don't understand what the word "inactivating" means then there's little hope that you'll ever understand anything else.

    Goodbye.

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  8. I knew that response was coming.
    Now the focus turns to the word "inactivating".
    Why is it so hard to admit that you use the word "mutation" with different meanings?

    An inactivating change is not a defect.
    Inactivation is not the issue.
    The issue is the word "mutation".
    Why not just stop using it since it just means "change"?

    I understand why you want to stop the discussion when the jig is up.

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  9. All,

    I have been interested in transposable elements for 20 yrs or so for their intrinsic weirdness and as evidence for common descent. For a recent summary of TEs in the human genome see:

    http://www.ncbi.nlm.nih.gov/pmc/articles/ PMC3123540/table/T2/ remove space from url

    There are about 3 million detectable TEs. Nearly all are conserved with chimps, excepting those species- specific and dimorphic recent insertions which are the focus of a lot of recent research. (Fascinating stuff-somewhere around 1 in 20 of us probably has a new L1 or Alu insertion in our genome. With whole genome sequencing we will know the rate before long.)

    One thing that I haven't seen anyone comment on is that if you deny common descent, but accept that the repetitive elements are TEs, you must accept that 3 million insertions comprising half the genome got there after special creation. So you are in fact accepting a huge amount of genomic evolution, and if you insist that they are all or mostly functional, then it is a huge amount of functional evolution.

    So you really aren't denying evolution at all. You are asserting that there was massively parallel evolution going on in separate species, exactly reproducing the site of insertion, subtype, and temporal order of insertion (since TEs very often insert in older TEs and the order can be shown to be the same in different species) of hundreds of thousands to millions of TEs, depending on how close the species are that are being compared.

    I have just last week asked Cornelius Hunter over at Darwin's God to explain how he thinks about this. I didn't get much of an answer - just the usual assertion that it is all somehow the result of my religion. In fact I am a Christian, so I'm not clear how we Christians arrive at such different conclusions starting from the same place. He tells me that it is because I am a pure rationalist and he is a reasonable empiricist. It looks like the opposite to me.

    Thanks for reviewing Well's book. It saves me the trouble of buying it.

    ReplyDelete
  10. Hello PNG.
    Would the situation be resolves if there was common ancestry but the higher intelligence made certain significant genetic changes at certain points?
    In other words, directed evolution (or more precisely directed development).

    ReplyDelete
  11. Anus the utmost IDiot,

    When you put an adjective with a noun, the adjective is qualifying and thus often referring to a subset of the noun. In the case of "inactivating mutation" the word "inactivating" refers to a subset of "mutations," whose effect is that of "inactivation." Other mutations can have effects other than "inactivation."

    That "mutation" "simply" means "changes" does not mean that there are no inactivating ones.

    I know you have a hard time understanding basic semantics and that reading comprehension is discouraged among "apologists." Otherwise they would be quickly out of a job. But you should understand that at least you should not be too obvious about your pretended hyper-stupidity. Unless, of course, it is not "pretended" ("pretended" being a subset of possible "stupidities").

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  12. Seems that because Larry wrote "are fragments or otherwise mutated versions of the original mobile elements," instead of "are fragments or otherwise versions carrying inactivating mutations of the original mobile elements," Anus., the utmost IDiot, thinks Larry is playing an "evolutionist dishonest game." Honest mistakes out of too much familiarity and expectation that people will understand what is meant are not a possibility when it comes to "evolutionists."

    Anus., Aren't you ashamed that your arguments reduce to imbecilic wordplay? If you aren't you should. Now begone you imbecile.

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  13. Sorry, In my last answer to Anus. The IDiot I should have written:

    Anus., Aren't you ashamed for being responsible for that bullshit? Have you no sense of shame? Aren't you ashamed that you built an "argument" on wordplay and ignorance?

    Thanks and sorry for the mess.

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  14. Hello PNG.
    I was hoping you would respond to what I posted earlier:

    Would the situation be resolved if there was common ancestry but the higher intelligence made certain significant genetic changes at certain points?
    In other words, directed evolution (or more precisely directed development).

    ReplyDelete
  15. Perhaps PNG will respond. I hope so.
    My point is that evolution theory explains adaptation but cannot explain the origin of new species.
    The mechanisms of evolution theory are completely insufficient for the origin of new species.
    A number of scientists have come to that conclusion.
    And to highlight the point new species appear abruptly.

    So there must be an additional factor in action, to account for what we clearly see in the fossil record.
    And that additional factor could be a higher intelligence (eg. Nature) which "made certain significant genetic changes at certain points".

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  16. Examples of the abrupt changes include the Cambrian Explosion and the explosion of animals in the Eocene.
    Evolution theory cannot explain the explosion of new species at these points.
    An additional factor is active.
    That additional factor is the living being we call Nature.

    This thinking accepts common ancestry but is supplemented by the intelligent influence of Nature at key points.

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  17. The wordplay over "mutation" is amusing. A common complaint is that mutations are always bad, so they can't have a role in a creative process of adaptation. So when we have a mutation that causes a loss of function (one of the "bad" kind), we can't use that word because the fact that a change has occurred is not necessarily an indication that it is deleterious. But then, it has never been argued that genetic mutation carries any connotations of detriment without a qualifier. You can get tied up in knots by your own misunderstanding of usage.

    If it's mutated, it's simply changed. If it's consequently inoperable then that may be good bad or indifferent depending on whether you are rooting for the transposon or the wider genome.

    An important point to note in all this is that transposons include the genes for transposing within themselves. Yet transposition frequently damages these, at least as far as transposing ability is concerned. If you have a genome-level adaptive need to have transposons, the last place you should keep such assumed 'valuable' genes is in a transposon. It's crap design. So an ID research programme might be to find a non-transposon-located control system for transposition.

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  18. "So an ID research programme might be to find a non-transposon-located control system for transposition."

    How about DNA transposons?
    http://en.wikipedia.org/wiki/Transposon
    "Class II (DNA transposons): By contrast, the cut-and-paste transposition mechanisms of class II transposons do not involve an RNA intermediate. These transpositions are catalyzed by various types of transposase enzymes. Some transposases can bind non-specifically to any target site, while others bind to specific sequence targets. The transposase makes a staggered cut at the target site producing sticky ends, cuts out the transposon and ligates it into the target site. A DNA polymerase fills in the resulting gaps from the sticky ends and DNA ligase closes the sugar-phosphate backbone. This results in target site duplication and the insertion sites of DNA transposons may be identified by short direct repeats (a staggered cut in the target DNA filled by DNA polymerase) followed by inverted repeats (which are important for the transposon excision by transposase). The duplications at the target site can result in gene duplication, which plays an important role in evolution."


    NATURE has a number of strategies for modifying itself.

    ReplyDelete
  19. A few lines down from where Anonymous quoted in the wiki article:

    "Both classes of transposons may lose their ability to synthesise reverse transcriptase or transposase through mutation, yet continue to jump through the genome because other transposons are still producing the necessary enzymes."

    So even the wiki article you cited states that genes for the enzyme transposase are contained within DNA transposons (although not all transposons contain a functional transposase gene).

    However, it is possible that a gene for transposase could exist outside of the transposon if a transposase mRNA is reverse transcribed and inserted into the genome. I suppose a transcribed transposase retrogene could even survive for some length of time in a lineage, if that lineage already contained endogenous siRNA against part of the transposase sequence.

    Anyways, I suppose that the endogenous siRNA pathway which acts to prevent transposable elements from proliferating counts as a non-transposon-located control system. I don't see how that could possibly count as evidence for intelligent design though.

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  20. NATURE has a number of strategies for modifying itself.

    Why, by golly, yes i does! I think we're all agreed that nature is remarkable. We wouldn't be interested in it otherwise.

    The point is, if transposons serve a useful function, one would expect to see genomic mechanisms promoting them, and doing things a damn sight better thn the shoddy opportunism displayed.

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  21. Allan Miller - so you believe in the intelligence of Nature as I do then?
    Nature as a living, intelligent being.

    ReplyDelete
  22. Allan Miller - so you believe in the intelligence of Nature as I do then?
    Nature as a living, intelligent being.


    No, I'm afraid I don't. Let's just take those three words:

    Living ... To me, to be living is simply to be a viable instance of a replicating system. Replication is the essence, the sine qua non, whatever school biology texts may emphasise. They tend to put replication at the end of the list, and look instead to homeostasis, or organisation, metabolism etc. But I think of these as secondary. The essence of life is replication - of nucleic acids, in the modern implementation. All derived states serve this objective, while the very fact of replication in a finite world creates the basis of evolution - imperfect replication and concentration of variants by sample error and selection. Nature itself does not replicate, and so I can't see it as living. I'm aware that my emphasis would also have viruses as living, within the world that they inhabit. I don't have a problem with that.

    Being ... there are a number of hierarchic levels capable of being considered an evolutionary 'being'. Ant colonies and wasp nests are one such, then we have multicellular individuals, themselves composed of cells that are also capable of evolutionary change, even when not free-floating as single-celled organisms. Even lower, I think a case can be made for certain sub-genome elements, which behave for all the world like 'conventional' biological entities within their subgenome world. But the whole collection - Nature itself? No, I wouldn't say so.

    Intelligent ... This is kind of interesting, in a purely philosophical manner. I do think that the operation of Natural Selection has parallels with intelligence. It examines alternative strategies and discards those less worthy. That's pretty close to 'intelligent' in my book. But I would extend it no further than that. Conflating intelligence with purpose or consciousness (because that's what it always associates with in our particular implementation of it) doesn't get us anywhere, and I don't see where such purpose or awareness could reside.

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  23. When I refer to "Nature" I have been referring to the "biosphere":

    "Our biosphere is the global sum of all ecosystems. It can also be called the zone of life on Earth, a closed (apart from solar and cosmic radiation) and self-regulating system.[1] From the broadest biophysiological point of view, the biosphere is the global ecological system integrating all living beings and their relationships, including their interaction with the elements of the lithosphere, hydrosphere and atmosphere. The biosphere is postulated to have evolved, beginning through a process of biogenesis or biopoesis, at least some 3.5 billion years ago.[2]"

    If someone wants to claim that Nature is not intelligent then you are saying that in your thinking a non-intelligent entity (Nature) is composed of intelligent entities.

    All living entities are part of Nature.

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  24. Anonymous:

    "The mechanisms of evolution theory are completely insufficient for the origin of new species.
    A number of scientists have come to that conclusion."

    You really should put "scientists" in quotes. These people have degrees but generally they aren't professional scientists - they are just critics.

    Mutations happen. Speciation happens. The directedness or non-directness of any particular mutation, whether by "Nature" or God or anyone else is a metaphysical question that science has no access to.

    Science can look at the statistical distribution of events of particular classes and see whether they fit some model with a random aspect, but individual mutations are not analyzable with statistics.

    Any conclusion we draw about directedness is an intuition, which may be right or wrong, but it isn't part of what we mean by "science" at this point in history.

    That's my take anyway.

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  25. If someone wants to claim that Nature is not intelligent then you are saying that in your thinking a non-intelligent entity (Nature) is composed of intelligent entities.

    And that's a problem because ... ? There aren't that many intelligent entities to be honest. Most organisms don't even have a nervous system, which I would insist is an absolute prerequisiste for the kind of intelligence you have in mind - purposive and aware. Until the early Cambrian, Nature definitely contained no intelligence, and it has only shown vague sparks since. Your notions seem vaguely Gaian, and I don't buy that either.

    All living entities are part of Nature.

    That doesn't make Nature anything special outside of its component parts. All smoked pork products are part of Charcuterie.

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  26. Is Charcuterie self-regulating?

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  27. Is Charcuterie self-regulating?

    No. And neither is Nature. Nature contains self-regulating elements, but is not itself self-regulating (which, in any case, is not a sufficient condition for Life, or intelligence).

    Life is, in very broad terms, a runaway chain reaction that commenced when the property of replication arose. A replicator able to make even a slight excess of copies possessing that same property has the potential to organise the whole planet. By organising disordered molecules with the property of spreading that organisational capacity, what you call 'Nature' grew from a couple of molecules into something absolutely huge, clothing the planet and almost completely scrubbing the atmosphere of the substantial concentrations of carbon that were there in the prebiotic earth. It's just blind chemistry, self-perpetuating but hardly, on the broad scale, self-regulating.

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  28. With all due respect Allan Miller, I will go with the wikipedia entry (citing The Columbia Encyclopedia) rather than a fellow on a blog like you who has his own personal opinion.

    http://en.wikipedia.org/wiki/Biosphere
    "Our biosphere is the global sum of all ecosystems. It can also be called the zone of life on Earth, a closed (apart from solar and cosmic radiation) and self-regulating system.[1] From the broadest biophysiological point of view, the biosphere is the global ecological system integrating all living beings and their relationships, including their interaction with the elements of the lithosphere, hydrosphere and atmosphere. The biosphere is postulated to have evolved, beginning through a process of biogenesis or biopoesis, at least some 3.5 billion years ago.[2]"

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  29. PNG posted:
    "Mutations happen. Speciation happens. The directedness or non-directness of any particular mutation, whether by "Nature" or God or anyone else is a metaphysical question that science has no access to."

    PNG, do you generally accept theories of the form:
    "Mutations happen. Speciation happens.".

    For example, would an explanation like: apples fall to the ground. Falling happens. Would that be acceptable?

    What is the difference between
    "Mutations happen, Speciation happens"
    and
    we don't know?

    To say that "mutations happen and speciation happens" is no explanation at all.

    Right?

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  30. With all due respect Allan Miller, I will go with the wikipedia entry (citing The Columbia Encyclopedia) rather than a fellow on a blog like you who has his own personal opinion.

    Arf arf arf! You do realise that Wikipedia is written by Internet jockeys like myself and yourself, don't you? Some experts get involved, but any one statement could have been written by absolutely anybody - even if quoted with approval from the Columbia Encyclopedia!

    That there is no outside organisation is not disputed. As in: a self-regulating advertising industry. But you are saying something more, that the sum of all ecosystems (each the sum of all organisms within them) is itself possessed of organisational properties that belong to the wider system, not simply emergent upon the activities and interactions of its component parts. I disagree.

    A balanced ecosystem is a complex web of interactions between the organisms that compose it. That does not mean that any one ecosystem is intelligent, aware or purposive. The biosphere is just a big ecosystem, or the set of all ecosystems. Why is it special - why declare it possessed of organisational and regulatory capacities that you would not ascribe to a local ecosystem - my back yard, say, or the Sahara?

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  31. Allan Miller you have made some progress. You are past the point of comparing Nature to smoked pork products.
    You are moving in the right direction.

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  32. You are moving in the right direction.

    You are right - backing away slowly and groping behind me for the door-handle. :0)

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  33. Well if you are backing away from what you were saying then that is good.

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  34. Well if you are backing away from what you were saying then that is good.

    OK, let's review ...

    There is no evidence that having transposons serves a purpose for the organism. Uh-huh, happy with that.

    Nature lacks the qualities necessary to entitle it to be called
    a) living
    b) a being
    c) intelligent
    No problem here either.

    Global feedback loops involving the biosphere do not constitute homeostatic, self-regulatory mechanisms in the organismal sense. Check! (an error you share with James Lovelock).

    Collections of entities do not necessarily share qualities possessed by their component subdivisions. And vice versa. Check!

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  35. I like being in the company of someone like James Lovelock, except that my position is more modest.

    I am not as impressed with your opinions as you are. No matter how dogmatically you state them.

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  36. Allan Miller I had said:
    "Allan Miller you have made some progress. You are past the point of comparing Nature to smoked pork products.
    You are moving in the right direction."

    In that sense you are moving in the right direction.

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