Home » 'Junk DNA', Intelligent Design, News » Not only is genome alteration for placental pregnancy a “huge cut-and-paste operation,” study finds, but …

Not only is genome alteration for placental pregnancy a “huge cut-and-paste operation,” study finds, but …

File:Pregnancy comparison.jpg

26 vs 40 wks

See PaV here, talking about:

From “Invasion of Genomic Parasites Triggered Modern Mammalian Pregnancy, Study Finds” (ScienceDaily, Sep. 26, 2011), we learn:

“In the last two decades there have been dramatic changes in our understanding of how evolution works,” said Gunter Wagner, the Alison Richard Professor of Ecology and Evolutionary Biology (EEB) and senior author of the paper. “We used to believe that changes only took place through small mutations in our DNA that accumulated over time. But in this case we found a huge cut-and-paste operation that altered wide areas of the genome to create large-scale morphological change.” nonlocalizability, …

Cut and paste from where, guys?

The Yale team studying the evolutionary history of pregnancy looked at cells found in the uterus associated with placental development. They compared the genetic make-up of these cells in opossums — marsupials that give birth two weeks after conception — to armadillos and humans, distantly related mammals with highly developed placentas that nurture developing fetuses for nine months.

They found more than 1500 genes that were expressed in the uterus solely in the placental mammals.

Which natural selection completely accounts for, operating in a glacially slow series of steps …

It gets better:

Intriguingly, note the researchers, the expression of these genes in the uterus is coordinated by transposons — essentially selfish pieces of genetic material that replicate within the host genome and used to be called junk DNA.

So the Darwinists fronting junk DNA were and are wrong. The Christian Darwinists who preach that junk DNA proves that Christians must embrace Jesus n’ Darwin are wrong.

Notice how the announcement is cloaked in “we’ve figured it out now” language and mysterious talk of “genomic parasites”.  You mean the ones crawling all over the dead Darwin? Yes, Darwin is dead, no matter what his lobby forces scared people to say or dense people to believe.

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16 Responses to Not only is genome alteration for placental pregnancy a “huge cut-and-paste operation,” study finds, but …

  1. It’s true that the role of single point mutations has been (historically) overemphasized, but things like horizontal gene transfer are recognized as important evolutionary mechanisms. In addition to the transposition example above, I have previously given the example of balanced Robertsonian translocations as another form of chromosomal rearrangement. However, these discoveries do not alter the material basis of evolution.

    Transposable elements and an epigenetic basis for punctuated equilibria.
    Evolution is frequently concentrated in bursts of rapid morphological change and speciation followed by long-term stasis. We propose that this pattern of punctuated equilibria results from an evolutionary tug-of-war between host genomes and transposable elements (TEs) mediated through the epigenome. According to this hypothesis, epigenetic regulatory mechanisms (RNA interference, DNA methylation and histone modifications) maintain stasis by suppressing TE mobilization. However, physiological stress, induced by climate change or invasion of new habitats, disrupts epigenetic regulation and unleashes TEs. With their capacity to drive non-adaptive host evolution, mobilized TEs can restructure the genome and displace populations from adaptive peaks, thus providing an escape from stasis and generating genetic innovations required for rapid diversification. This “epi-transposon hypothesis” can not only explain macroevolutionary tempo and mode, but may also resolve other long-standing controversies, such as Wright’s shifting balance theory, Mayr’s peripheral isolates model, and McClintock’s view of genome restructuring as an adaptive response to challenge.

    This is just one way that evolution can credibly explain: a natural, refined search constrained by transposon mechanics; a role for limited epigenetic inheritance that supports both the periods of “stasis” and “explosive creativity”; and a use for a sizable chunk of “junk DNA.”

    As best as I can determine, the 500-bit-FSCI criteria isn’t going to be be very help in this regard. So ID theory has another challenge — how to explain chromosomal rearrangements outside of material evolutionary processes?

  2. rhampton7:

    So ID theory has another challenge — how to explain chromosomal rearrangements outside of material evolutionary processes?

    Actually, it’s the other way around. ID has never said anything other than the genetic changes leading to macroevolution must, perforce, by intelligently “guided”. ID can explain these “chromosomal rearrangements”, whereas material evolutionary processes cannot. All you have done is to say this is what must be happening; but you don’t posit any kind of driving force or mechanism.

    For example, quoting from the abstract:

    With their capacity to drive non-adaptive host evolution, mobilized TEs can restructure the genome and displace populations from adaptive peaks, thus providing an escape from stasis and generating genetic innovations required for rapid diversification.

    The obvious, pertinent, and unanswered, question is this:

    If all of these changes are “non-adaptive”, then what is the driving force?

    ID would simply say that an intelligent agent is behind them.

    They found more than 1500 genes that were expressed in the uterus solely in the placental mammals.

    What is the probability of blind, non-Darwinian forces effecting even 100 promoter changes at once? Do you have any measure of the improbability of this happening through “random mutations” given the known mutation rates of mammmals?

  3. Here’s the Darwinian explanation for all of this:

    “Mammals were invaded by ‘genetic parasites’.”

    It sounds like some alien invasion, not science. This is grasping at straws. Facts are determined; and, then, based on a politically correct way of thinking, words are used to obfuscated the fact that they don’t know what’s going on. Ignorance masquerading as knowledge. I’m afraid the “emperor has no clothes”!

  4. Houston we have a problem! Neo-Darwinists have no clue where these 1500 genes came from for placental mammals!!! Nor do they have a clue for any ORFans!!!

    A survey of orphan enzyme activities
    Abstract: We demonstrate that for ~80% of sampled orphans, the absence of sequence data is bona fide. Our analyses further substantiate the notion that many of these (orfan) enzyme activities play biologically important roles.
    http://www.biomedcentral.com/1471-2105/8/244

    Proteins Did Not Evolve Even According to the Evolutionist’s Own Calculations but so What, Evolution is a Fact – Cornelius Hunter – July 2011
    Excerpt: For instance, in one case evolutionists concluded that the number of evolutionary experiments required to evolve their protein (actually it was to evolve only part of a protein and only part of its function) is 10^70 (a one with 70 zeros following it). Yet elsewhere evolutionists computed that the maximum number of evolutionary experiments possible is only 10^43. Even here, giving the evolutionists every advantage, evolution falls short by 27 orders of magnitude.
    http://darwins-god.blogspot.co.....d-not.html

    Moreover this ‘anomaly’ of unique ORFan genes/proteins is found in every new genome sequenced:

    Widespread ORFan Genes Challenge Common Descent – Paul Nelson – video with references
    http://www.vimeo.com/17135166

    Estimating the size of the bacterial pan-genome – Pascal Lapierre and J. Peter Gogarten – 2008
    Excerpt: We have found >139 000 rare (ORFan) gene families scattered throughout the bacterial genomes included in this study. The finding that the fitted exponential function approaches a plateau indicates an open pan-genome (i.e. the bacterial protein universe is of infinite size); a finding supported through extrapolation using a Kezdy-Swinbourne plot (Figure S3). This does not exclude the possibility that, with many more sampled genomes, the number of novel genes per additional genome might ultimately decline; however, our analysis and those presented in Ref. [11] do not provide any indication for such a decline and confirm earlier observations that many new protein families with few members remain to be discovered.
    http://www.paulyu.org/wp-conte.....genome.pdf

    Moreover, even though it is shown that there is a ‘pool of genes’ that are shared within different environments, this ‘sharing is found to be ‘limited’, As well, it is also shown that there is a large portion of ‘dedicated genes’

    Intercellular DNA transfer. J Shapiro (page 12)
    Excrpt: Molecular genetics began with the study of intercellular DNA transfer in bacteria.(113,114) We now know that all prokaryotes have elaborate transmembrane systems for transferring DNA to other cells (even to higher plants) and many also possess them for taking up DNA from the environment.(115–117) This exogenous genetic information can be incorporated into the genome in the form of “islands” encoding specialized adaptive functions.(118) Eukaryotic cells are also capable of taking up and integrating exogenous DNA, but there has been little study of the molecular mechanisms involved.
    http://shapiro.bsd.uchicago.ed.....0Dogma.pdf

    Estimating the size of the bacterial pan-genome Page 108
    The bacterial pan-genome. Each gene found in the bacterial genome represents one of three pools: genes found in all but a few bacterial genomes comprise the extended core of essential genes (250 gene families that encode proteins involved in translation, replication and energy homeostasis); the character genes (7900 gene families) represent genes essential for colonization and survival in particular environmental niches (e.g. symbiosis and
    photosynthesis); and finally, the accessory genes, a pool of apparently infinite size, contains genes that can be used to distinguish strains and serotypes; the function of most genes in this category is unknown. At the genomic level, a typical bacterial genome is composed of 8% of core genes, 64% of character genes and 28% of accessory genes. Although the character genes contain only 7900 gene families, they are the most abundant at the genomic level. Expanding the gene centered approach to 573 bacterial genomes or sampling of 508 genomes, excluding highly reduced genomes, yields similar results (Table S2), except that the total number of families in the accessory pool is increased as expected for an open pan-genome.
    http://www.paulyu.org/wp-conte.....genome.pdf

    Thus basically we have evolutionists postulating a completely unsubstantiated claim for radical ‘cut and paste’ of new genes from some magical mystery land where completely new genes apparently materialize out of thin air with no need from Intelligence:

  5. Three years ago, these same authors decided that the entire difference between placental and marsupial mammals had to do with ONE gene: HoxA-11. I remember reading this and being astonished that one single gene could do so much.

    Oops! It turns out that it takes 1523 transcription factors. Oh, this is a really big “Oops!”.

    Here’s a link.

    And here’s a quote from the link:

    By analyzing DNA from many species of mammals, including resurrecting genes from the extinct ancestors of mammals, the researchers found that a crucial regulatory link in the evolution of pregnancy involved the altered function of a transcription factor protein, HoxA-11.

    The specific change they found in HoxA-11 is present in all known placental mammals — from elephants, the most primitive lineage with a placenta, to humans — but does not exist in marsupials, like opossums or wallabies, where there is a brief and rudimentary pregnancy followed by development of the offspring outside the mother, or in egg-laying mammals like the platypus.

    The textbook story is that regulatory proteins, like HoxA-11, are ancient, universal and unchanging tools, and that new functions arise by using an existing tool from the gene regulatory ‘toolbox’ in a new or different place.

    The “textbook” story now contains 1523 transposons of unknown origin.

  6. ID has never said anything other than the genetic changes leading to macroevolution must, perforce, by intelligently “guided”.
    -&-
    It sounds like some alien invasion, not science

    You may have heard of retrovirus, well they are just one kind of transposon. I’m not aware of any ID research that claims transposons are either irreducibly complex or exhibit FSCI greater than 500 bits in length, so I have to conclude that ID theorists currently accept that a purely natural mechanism is the best explanation. As Stephen Meyer explains;

    Moreover, as Dembski has shown, neither low probability events nor high probability events allow intelligent design to be unambiguously detected. Instead, intelligent design can be unambiguously detected only in specified events of very small probability … Indeed, if design theorists are correct, design can not be inferred for every effect, even if intelligent design is a possible cause of all effects. Because intelligent agents, and presumably the Divine Agent, have causal powers that nature does not have, intelligent design may always be a possible explanation. Nevertheless, possible explanations are not necessarily the best explanations. Intelligent design is not always the best explanation for a variety of reasons. Human action or special (that is, detectable) divine action may not have played a causal role in certain natural events; intelligent design, whether human or divine, may not always be detectable even when it has played a causal role; natural objects and processes have real causal powers (even for theists who accept God’s sustaining governance of nature) that may be clearly evident in a given phenomenon. Thus, at least for those scientists who seek the best explanations, intelligent design can not be invoked as a theory of everything. It may function as a possible theory of everything, but it can function as the best explanation or best theory of only some things. Intelligent design need be neither vacuous nor unconstrained.

  7. I’m not aware of any ID research that claims transposons are either irreducibly complex or exhibit FSCI greater than 500 bits in length, so I have to conclude that ID theorists currently accept that a purely natural mechanism is the best explanation. As Stephen Meyer explains;

    You’re perhaps missing the forest for the trees here.

    First, the tree.

    Transposons have to insert themselves into the DNA, something that requires certain enyzmes. Those enzymes are specified. And each of those enzymes is very likely long enough to constitute CSI, i.e., more than 500 bits.

    So, the tree suitably fits the ID perspective.

    Now, for the forest.

    Certainly you will admit that 1523 transposons inserting themselves in just the right position along the length of the genome all via random processes defies all odds. In fact, it looks like what we would expect from a genetically engineered system.

  8. rhampton:

    Of course ID and the 500 bit limit have a lot to say about chromosomal rearrangement, transposons, and so on.

    Maybe you miss the basic point: any variation either is random or is designed. Chromosomal rearrangements and transposon intervention are no exception.

    Any random variation can be evluated by a probabilistic analysis. It is not important if the variation is a point mutation, a chromosomal rearrangement, an inversion, a frameshift mutation, or any other event. The important point is that the variation is random, that is it is completely blind and in non way related to a functional purpose. For all these variations, each single result is just an attempt in a random walk. The probabilities oh hitting a functional target are the same.

    The situation is completely different for designed variations. Obviously, as discussed often, design can be implemented in different ways. Guided variation is one possibility, random variation followed by intelligent selection is another. Anyway, the important point is that here the result is not random, but is guided towards a pre-defined purpose. That makes the search tractable. Design works.

    And I must say that I have already suggested here, some time ago, that transposons appear to be very good candidates as instruments for design implementation. I maintain that view.

  9. Authors: ” a crucial regulatory link in the evolution of pregnancy involved the altered function of a transcription factor protein, HoxA-11.”

    PaV: “the entire difference between placental and marsupial mammals had to do with ONE gene: HoxA-11.”

    A crucial=The entire?

  10. That transposons “select” from a constrained set of locations does not deny the randomness of the transposition itself. For example, flipping a coin (or detecting the radioactive decay of an atom) generates a random sequence despite an outcome limited to only two possibilities.

    In this comprehensive study which used data collected from P-element gene disruption projects in Drosophila melanogaster, it was shown that transposons exhibit a 14 base-pair palindromic hydrogen bonding pattern. Yet given this preference of targets;

    We have further shown that there is no local or genome-wide strand bias for P-element insertion, consistent with a model of random strand integration. We conclude that staggered-cut palindromic target site model is a sufficient to explain the insertion preferences of the D. melanogaster P-element and, together with the widespread occurrence of staggered-cut palindromic target sites in disparate taxa, suggest that this model may apply generally to other cut-and-paste DNA transposons as well.

    As you might imagine, it’s a great deal more complicated then that. Now Intelligent Design researchers might want to take a closer look at transposons and see if there is means to detect intelligence via some new theoretically model or application of an exisiting one. In the meantime, however, a natural, mechanical process remains the best explanation.

  11. DrREC:

    Obviously you don’t know how it was reported at the time.

    The authors studied the HoxA-11 gene and were convinced—at the time—that it alone determined placental versus marsupial.

    From an ID perspective, this didn’t seem right. But from a Darwinian perspective, it fit like a glove.

    They were only wrong by 152300%. So much for what Darwinism will get you.

  12. PaV-

    Maybe I need to again suggest the importance of reading the scientific literature. I provided a direct quote from the authors above.

    “From an ID perspective, this didn’t seem right.”

    Why? What principle of ID would rule out that hypothesis? Why not design a system with a master regulator?

    And the “1523 transposons of unknown origin” isn’t quite correct. The authors found 1523 genes regulated by the insertion of a transposon containing regulatory elements, namely responsive to progesterone. A regulatory module got picked up and transposed about the genome. Duplication and divergence.

  13. rhampton7:

    I wonder if you’re misreading this article.

    There appears to be two things going on here: (1) preferences shown for “staggered-cut palindromic target sites”, and (2) no preference for which strand of the chromosome it attaches to.

    I think you’re confusing the one with the other.

    They write:

    As structure and sequence are intimately related at the DNA sequence level, we make no claim about which of these factors is causal. We have also shown that the local, nonrandom pattern of P-element spacing is uniquely predicted by the palindromic TSM, and that match to the TSM is a better predictor of P-element insertion frequency than palindromicity itself. We have further shown that there is no local or genome-wide strand bias for P-element insertion, consistent with a model of random strand integration. We conclude that staggered-cut palindromic target site model is a sufficient to explain the insertion preferences of the D. melanogaster P-element and, together with the widespread occurrence of staggered-cut palindromic target sites in disparate taxa, suggest that this model may apply generally to other cut-and-paste DNA transposons as well.

    This appears to be non-random attachment sites they’re dealing with. This can’t be good news for Darwinism.

    Another day; another bad day for Darwinism.

  14. The non-randomness of the insertion (when there is non-randomness) relates to the physical mechanism of transposition.

    It has not shown to relate to the ‘need” of the organism.

    Therefore still random with respect to need. By comparison, most types of mutations are non-random, and relate to the mechanism that created them. UV induced mutations, for example.

    Actually, unchecked transposons cause reduced fitness in populations, and disease in humans.

    http://journals.cambridge.org/.....id=1777952

  15. The non-randomness of the insertion (when there is non-randomness) relates to the physical mechanism of transposition.

    It has not shown to relate to the ‘need” of the organism.

    Therefore still random with respect to need. By comparison, most types of mutations are non-random, and relate to the mechanism that created them. UV induced mutations, for example.

    Actually, unchecked transposons cause reduced fitness in populations, and disease in humans.

    http://journals.cambridge.org/…..id=1777952

  16. The “head” and “tail” of a coin are non-random, but the sequence generated from flipping a coin is random. Likewise the preference for a given site-type is non-random, but which one of the thousands of qualifying sites that ends up being selected is random.

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