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Epigenetics: Why it is a problem for Darwinism

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Darwin's Doubt Considering Steve Meyer’s Darwin’s Doubt is just now (12:30 pm EST) at

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#3 in Books > Christian Books & Bibles > Theology > Creationism, here is a brief excerpt from the chapter on epigenetics:

These different sources of epigenetic information in embryonic cells pose an enormous challenge to the sufficiency of the neo-Darwinian mechanism. According to neo-Darwinism, new information, form, and structure arise from natural selection acting on random mutations arising at a very low level within the biological hierarchy—within the genetic text. Yet both body-plan formation during embryological development and major morphological innovation during the history of life depend upon a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. If DNA isn’t wholly responsible for the way an embryo develops—for body-plan morphogenesis—then DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process. Genetic mutations are simply the wrong tool for the job at hand.(p. 281)

See also: BioLogos spending millions (selling Darwin to Christians – while everyone else is dumpint the stock?)


If anyone cares, Biologos (Christians for Darwin) will now actually review Darwin’s Doubt  

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27 Replies to “Epigenetics: Why it is a problem for Darwinism

  1. 1
    markf says:

    Of course they are an even bigger problem for ID as they suggest a different method of inheritance and no reason why that method should be guided. So now ID has to show that epigenetics cannot account for life as well neo-Darwinism before it can jump to the conclusion “designed”.

  2. 2
    Andre says:


    Clearly you don’t seem to understand the engineering principles that epigentics bring to the table….

    Look up feedback loops…..

  3. 3
    bornagain77 says:


    Of course they are an even bigger problem for ID as they suggest a different method of inheritance and no reason why that method should be guided.

    So the entire ‘bottom up’ Neo-Darwinian framework is found wanting as an explanation of the rapid adaptions occurring in populations and you, in the twisted reasoning that can only come from a committed Neo-Darwinist, claim this is an even bigger problem for ID?

    You have got to be kidding! This is even further proof of intelligent design because it entails ‘foresight’ in the design of an organism that anticipated environmental cues so as to have a ready response in place once the environmental cue took place.

    The ‘blind-watchmaker’ of Darwinists, by definition, has no such foresight to appeal to explain why such complex ‘anticipatory’ mechanisms are in place!

  4. 4
    rhampton7 says:

    DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process

    True, but it misses the point. Mutations, called epimutations, also occur to epigenes. From Epigenetics and the Evolution of Darwin’s Finches.

    The prevailing theory for the molecular basis of evolution involves genetic mutations that ultimately generate the heritable phenotypic variation on which natural selection acts. However, epigenetic transgenerational inheritance of phenotypic variation may also play an important role in evolutionary change. A growing number of studies have demonstrated the presence of epigenetic inheritance in a variety of different organisms that can persist for hundreds of generations. The possibility that epigenetic changes can accumulate over longer periods of evolutionary time has seldom been tested empirically. The current study was designed to compare epigenetic changes among several closely related species of Darwin’s finches, a well-known example of adaptive radiation. Erythrocyte DNA was obtained from five species of sympatric Darwin’s finches that vary in phylogenetic relatedness. Genome-wide alterations in genetic mutations using copy number variation (CNV) were compared to epigenetic alterations associated with differential DNA methylation regions (epimutations). Epimutations were more common than genetic CNV mutations among the five species; furthermore, the number of epimutations increased monotonically with phylogenetic distance. Interestingly, the number of genetic CNV mutations did not consistently increase with phylogenetic distance. The number, chromosomal locations, regional clustering, and lack of overlap of epimutations and genetic mutations suggests that epigenetic changes are distinct and that they correlate with the evolutionary history of Darwin’s finches. The potential functional significance of the epimutations was explored by comparing their locations on the genome to the location of evolutionarily important genes and cellular pathways in birds. Specific epimutations were associated with genes related to the bone morphogenic protein (BMP), toll receptor, and melanogenesis signaling pathways. Species-specific epimutations were significantly over-represented in these pathways. Since environmental factors are known to result in heritable changes in the epigenome, it is possible that epigenetic changes contribute to the molecular basis of the evolution of Darwin’s finches.

    Epimutations are also suspected in cancers that strike generations of families. So I don’t see how this is a problem for evolutionary theory. It’s still a “natural” material causation that does not require intelligent intervention.

  5. 5
    bornagain77 says:

    as to “True, but it misses the point.”

    Actually to considered ‘directed mutations’ to the DNA methylation regions, (epimutations), mutations that are ‘non-random’ and are accomplished via extremely sophisticated feedback mechanisms and molecular machines, is the miss the point. ,,, In fact, it is to miss the entire ‘bottom up’ barn that Darwinism was shooting at in the first place!

    Plant’s Epigenome as Varied as Their Environments – Cornelius Hunter – March 24, 2013
    Excerpt: epigenetics would involve literally hundreds (and that is conservative) of changes required before any benefit would be realized.
    The tagging machines not only need to be built, or adapted from other machines, but they need to know where in all the genome to place the tags. Likewise for the machines that remove and move the tags. In other words, it is not good enough merely to evolve the machines. They somehow much know where to place the tags given a spectrum of environmental signals.
    And then the machines that interpret the tags would have to do so correctly. They would have to know what the tag means. So again, not only must these machines have evolved or adapted, but they must know what they are doing.
    That is astronomically unlikely to occur according to our knowledge of science.
    But that is not all. For even given such a miracle, such epigenetic tags would not be inheritable. And yet they are. So there are even more machines that must have arisen by chance to preserve the tags when the cell divides.
    This brings us to yet another set of problems with epigenetics: the machinery described above is not inheritable unless is evolves in the germline. But in the germline it doesn’t do anybody any good. Only when it is a passed on to the progeny can it help.
    But even then the epigenetics capability likely won’t help because this capability gives the organism the ability to respond to a wide range of environmental conditions—conditions that probably won’t even occur in the organism’s lifetime.
    In other words, we must believe that an astronomically unlikely capability arose by chance and though most of it wasn’t helpful, it was preserved anyway. Then, in future generations, when a particular environmental shift occurred, the epigenetics came to the rescue.
    These problems are highlighted by the new research discussed above, showing how the epigenetic tagging can be so different in the same species of plant, in different locations around the world.,,,

  6. 6
    AVS says:

    “If DNA isn’t wholly responsible for the way an embryo develops—for body-plan morphogenesis—then DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process.”

    That’s completely false. Just because we’ve come to find that DNA sequence isn’t the whole story behind inheritance patterns, that doesn’t mean it’s completely powerless. Mutations can occur anywhere in the genome and exert their effects not just on amino acid sequence but also regulatory mechanisms including the epigenetic machinery itself.

  7. 7
    Dionisio says:

    Indeed, what we see in research about cell differentiation and epigenomics is a growing mass of detailed knowledge (and believe me, it is really huge and daily growing) which seems to explain almost nothing.

    What is really difficult to catch is how all that complexity is controlled. Please note, at this level there is almost no discussion about how the complexity arose: we have really non idea of how it is implemented, and therefore any discussion about its origin is almost impossible.

    Now, there must be information which controls the flux. It is a fact that cellular differentiation happens, that it happens with very good order and in different ways in different species, different tissues, and so on. That cannot happen without a source of information. And yet, the only information that we understand clearly is then protein sequence information. Even the regulation of protein transcription at the level of promoters and enhancers by the transcription factor network is of astounding complexity.

    Please, look at this paper:

    Uncovering Enhancer Functions Using the ?-Globin Locus.


    In particular Fig. 2.

    And this is only to regulate the synthesis of alpha globin in red cells, a very straightforward differentiation task.

    So, I see that, say, 15 TFs are implied in regulating the synthesis of one protein, I want to know why, and what controls the 15 TFs, and what information guides that control. My general idea is that, unless we find some completely new model, information that guides a complex process, like differentiation, in a reliable, repetitive way must be written, in some way, somewhere.

    That’s what I want to know: where that information is written, how it is written, how does it work, and, last but not least, how did it originate?

    — gpuccio

  8. 8
    Andre says:


    Except PCD controls cell stability mutation occur when PCD be mows Dysregulated. When tat happens the organism dies.

  9. 9
    AVS says:

    I see 7-8 TFs in that figure, all controlled by sequence specific binding inherent to their amino acid sequence that is encoded by the genome. The expression of these proteins are also regulated by an array of transcription factors. It’s the different combinations of sequences, their availability and the available factors that largely controls gene expression.

  10. 10
    Andre says:


  11. 11
    AVS says:

    That’s the only thing you’re going to fix in that post Andre?

  12. 12
    Andre says:

    Auto correct on a cellphone is evil!

  13. 13
    Dionisio says:

    “The holy grail of cell biology is a ‘complete’ description of the structure and function of an organelle, cell, tissue, or even of an organism, at molecular resolution.”


  14. 14
    Dionisio says:

    During the development of the central nervous system, neural progenitors generate an enormous number of distinct types of neuron and glial cells by asymmetric division.

    Intrinsic genetic programs define the combinations of transcription factors that determine the fate of each cell, but the precise mechanisms by which all these factors are integrated at the level of individual cells are poorly understood.

    doi: http://dx.doi.org/10.1242/dev.113381

  15. 15
    AVS says:

    Uh ok, so we are pretty far from this “holy grail,” that’s nothing new… Thanks Dio.

  16. 16
    Dionisio says:

    Closing in???

    Receptor signaling: Closing in on a mechanism for activation

    DOI: http://dx.doi.org/10.7554/eLife.04909

    Nevertheless, precisely how these small proteins activate their receptors is still something of a mystery.

    This is essentially the opposite mechanism to that proposed by Kavran et al.

    Further work is needed to resolve these conflicting models of activation.

    Other key questions remain unanswered.

    The nature of this steric constraint is unknown.

    Thus, the juxtamembrane regions of the IGF1 receptor and insulin receptor hold mechanistic secrets yet to be revealed.

  17. 17
    Dionisio says:

    A Competitive Cell Fate Switch?

    Whereas tissue development and homeostasis depend on stem cell self-renewal and differentiation, the mechanisms that balance these processes remain incompletely understood.

    DOI: http://dx.doi.org/10.1016/j.devcel.2014.10.016

  18. 18
    AVS says:

    Slow down Dio, there’s no need for you to turn this into another completely pointless third way-esq posting extravaganza.

  19. 19
    Dionisio says:

    Regulation of patterning, cell fate specification, and neurocircuitry in the developing cerebral cortex.

    Creating this structure poses an extraordinary developmental challenge.


  20. 20
    goodusername says:


    Even with the mechanisms in organisms to limit mutations, they still occur. We all have mutations, many of them.

  21. 21
    Dionisio says:

    Transcriptional Switches During Development

    The general concepts of transcriptional regulation are now well established, a major challenge resides in understanding the logic and physical elements implementing these regulatory interactions within a given cell in a developing organism.

    A central problem to be addressed is how transcriptional programs are set up and then modified throughout the successive steps of embryonic development.


  22. 22
    AVS says:

    Earth to Dio…

    Too late I guess.

  23. 23
    Andre says:

    Yes and the mutations kill us.. .

  24. 24
    bornagain77 says:

    At 6 AVS states,,,

    “If DNA isn’t wholly responsible for the way an embryo develops—for body-plan morphogenesis—then DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process.” – Stephen Meyer
    That’s completely false. Just because we’ve come to find that DNA sequence isn’t the whole story behind inheritance patterns, that doesn’t mean it’s completely powerless. Mutations can occur anywhere in the genome and exert their effects not just on amino acid sequence but also regulatory mechanisms including the epigenetic machinery itself.

    Actually AVS’s claim that it is ‘completely false’ is what is completely false.
    Firstly, mutations to the regulatory regions of DNA are found to be ‘always catastrophically bad’,,

    A Listener’s Guide to the Meyer-Marshall Debate: Focus on the Origin of Information Question -Casey Luskin – December 4, 2013
    Excerpt: “There is always an observable consequence if a dGRN (developmental gene regulatory network) subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.” –
    Eric Davidson

    Darwin or Design? – Paul Nelson at Saddleback Church – Nov. 2012 – ontogenetic depth (excellent update) – video
    Text from one of the Saddleback slides:
    1. Animal body plans are built in each generation by a stepwise process, from the fertilized egg to the many cells of the adult. The earliest stages in this process determine what follows.
    2. Thus, to change — that is, to evolve — any body plan, mutations expressed early in development must occur, be viable, and be stably transmitted to offspring.
    3. But such early-acting mutations of global effect are those least likely to be tolerated by the embryo.
    Losses of structures are the only exception to this otherwise universal generalization about animal development and evolution. Many species will tolerate phenotypic losses if their local (environmental) circumstances are favorable. Hence island or cave fauna often lose (for instance) wings or eyes.

    Secondly, regulatory mechanisms in the DNA “depend on pre-existing spatial anisotropies that are defined by early embryonic axes, and those axes are established long before the embryo’s dGRNs are put in place.,,,”

    Membrane Patterns Carry Ontogenetic Information That Is Specified Independently of DNA – Jonathan Wells – 2014
    Excerpt: Embryo development (ontogeny) depends on developmental gene regulatory networks (dGRNs), but dGRNs depend on pre-existing spatial anisotropies that are defined by early embryonic axes, and those axes are established long before the embryo’s dGRNs are put in place.,,,
    DNA sequences do not specify the final functional forms of most membrane components. Still less does DNA specify the spatial arrangements of those components. Yet their spatial arrangements carry essential ontogenetic information. The fact that membrane patterns carry ontogenetic information that is not specified by DNA poses a problem for any theory of evolution (such as Neo-Darwinism) that attributes the origin of evolutionary novelties to changes in a genetic program—-whether at the level of DNA sequences or dGRNs.

    Thirdly, Neo-Darwinian evolution, which is predicated on reductive materialism, cannot explain the ‘form’ of DNA and proteins themselves much less can it explain the ‘form’ of an entire organism.

    Getting Over the Code Delusion (Epigenetics) – Talbott – November 2010
    Excerpt: The standard doctrine has it that functionally important sequences, precisely because they are important to the organism, will generally be conserved across considerable evolutionary distances. But the emerging point of view holds that architecture can matter as much as sequence. As bioinformatics researcher Elliott Margulies and his team at the National Human Genome Research Institute put it, “the molecular shape of DNA is under selection” — a shape that can be maintained in its decisive aspects despite changes in the underlying sequence. It’s not enough, they write, to analyze “the order of A’s, C’s, G’s, and T’s,” because “DNA is a molecule with a three-dimensional structure.”[14] Elementary as the point may seem, it’s leading to a considerable reallocation of investigative resources.

    The Gene Myth, Part II – August 2010
    Excerpt: “It was long believed that a protein molecule’s three-dimensional shape, on which its function depends, is uniquely determined by its amino acid sequence. But we now know that this is not always true – the rate at which a protein is synthesized, which depends on factors internal and external to the cell, affects the order in which its different portions fold. So even with the same sequence a given protein can have different shapes and functions. Furthermore, many proteins have no intrinsic shape, (intrinsically disoredered proteins), taking on different roles in different molecular contexts. So even though genes specify protein sequences they have only a tenuous (very weak or slight) influence over their functions.
    ,,,,So, to reiterate, the genes do not uniquely determine what is in the cell, but what is in the cell determines how the genes get used. Only if the pie were to rise up, take hold of the recipe book and rewrite the instructions for its own production, would this popular analogy for the role of genes be pertinent.
    Stuart A. Newman, Ph.D. – Professor of Cell Biology and Anatomy

    Biology’s Quiet Revolution – Jonathan Wells – September 8, 2014
    Excerpt: In 1996, biologists discovered a protein that does not fold into a unique shape but can assume different shapes when it interacts with other molecules. Since then, many such proteins have been found; they are called “intrinsically disordered proteins,” or IDPs. IDPs are surprisingly common, and their disordered regions play important functional roles.,,,
    So it is not true that biologists know all the basic features of living cells and are merely filling in the details. Nor is it true that Darwinian evolution is a settled scientific “fact,” as its defenders claim. Huge unanswered questions remain, and they will only be answered by going beyond the discredited myth that “DNA makes RNA makes protein makes us.”

    podcast – Dr. Jonathan Wells: Biology’s Quiet Revolution – September 17, 2014
    “We are talking about 1/3 of the proteins in our body, (could be Intrinsically Disordered Proteins)” – Jonathan Wells

    supplemental notes:

    The face of a frog: Time-lapse video reveals never-before-seen bioelectric pattern – July 2011
    Excerpt: For the first time, Tufts University biologists have reported that bioelectrical signals are necessary for normal head and facial formation in an organism and have captured that process in a time-lapse video that reveals never-before-seen patterns of visible bioelectrical signals outlining where eyes, nose, mouth, and other features will appear in an embryonic tadpole.,,, “When a frog embryo is just developing, before it gets a face, a pattern for that face lights up on the surface of the embryo,”,,, “We believe this is the first time such patterning has been reported for an entire structure, not just for a single organ. I would never have predicted anything like it. It’s a jaw dropper.”,,,
    per Physorg

    podcast – Jonathan Wells: Is There Biological Information Outside of the DNA?, pt. 3 – Bioelectric code

    What Do Organisms Mean? Stephen L. Talbott – Winter 2011
    Excerpt: Harvard biologist Richard Lewontin once described how you can excise the developing limb bud from an amphibian embryo, shake the cells loose from each other, allow them to reaggregate into a random lump, and then replace the lump in the embryo. A normal leg develops. Somehow the form of the limb as a whole is the ruling factor, redefining the parts according to the larger pattern. Lewontin went on to remark: “Unlike a machine whose totality is created by the juxtaposition of bits and pieces with different functions and properties, the bits and pieces of a developing organism seem to come into existence as a consequence of their spatial position at critical moments in the embryo’s development. Such an object is less like a machine than it is like a language whose elements… take unique meaning from their context.[3]”,,,

  25. 25
    AVS says:

    Oh BA.

    Firstly, never say “always” or “never” in biology. There are exceptions to just about every rule in biology.
    Also it took me about five seconds to find a minireview that contradicts everything your unreliable sources said.
    Regulatory regions in many cases are actually more tolerant to change than coding regions. This makes sense because the regulatory regions most often function by recruitment of protein factors. This means the sequence can run in either direction on the DNA strand, there is no required maintenance of an open-reading frame like that of coding genes, the regulatory sequences can be located anywhere within a wide range of basepair distances from the gene it effects, slightly altering the binding affinity of the regulatory element does not necessarily abolish function, instead inducing just slight changes. In fact, a number of important transcription factors have very relaxed binding specificities, allowing room for evolution while not destroying regulation mechanisms already in place.

    Carroll SB. 2000. Endless Forms: The Evolution of gene regulation and morphological diversity.

    Secondly, I’m not really sure what your point was about the pre-existing regulatory mechanisms in embryos. The largest portion of these “spatial anisotropies” is transcription factors, or morphogens, which are present in the embryo, have been expressed from the maternal genome. This creates a gradient across the early embryo that drives early differentiation events in the embryo. As for membrane patterns they are certainly not “completely independent of DNA.” The paper by Wells is just a giant review article about some of the basic processes that occur during development. The ability of the membrane to hold ontogenetic information is not a problem for evolution because the composition of the membrane is controlled by the genome. Transport to the membrane is controlled by specific signal sequences, addition of sugar molecules is initially dependent on certain sequences, etc. The paper just presents a blinding amount of information and when he actually tries to support his ideas, he typically cites papers over 20 years old.

    Thirdly, the “form” of DNA? You mean its structure as chromatin, which relies on histones and is under the control of a variety of other proteins?
    And so we’ve come to find that under different conditions, proteins can fold in different ways?
    As we have already seen, these are mechanisms of controlling gene expression, which has a huge hand in the role of evolution. We may currently not be able to explain how these systems came about, but we’re working on it, don’t you worry.

    In the meantime, Bio-complexity has published nothing of meaning. Good work.

    Also BA, you could up your credibility by actually writing comments in your own words and using primary articles as sources, maybe even from legitimate refereed journals. But that may actually require you to “think.”

  26. 26
    bornagain77 says:

    AVS, as usual you are all bluff, bluster and insult, with no actual substantive empirical support.
    As to the claim that dGRN’s are not flexible, Marshall and Meyer had a debate on this very point and Marshall did fair too well at all in the debate,,

    “Meyer noted that there is no empirical support for the idea that dGRNs could have been labile (flexible) in the past. Meyer made this same point in his response to Marshall review. In support of this claim, Meyer cited the work of Eric Davidson, whom Marshall had earlier accused Meyer of neglecting in his discussion of how body plans are built.
    In fact, Meyer discussed the importance of Davidson’s work extensively in Chapter 13 of Darwin’s Doubt, which makes it odd that Marshall charged during the debate that Meyer “completely missed” this literature. As Meyer wrote:
    Indeed, there are no examples of these deeply entrenched, functionally critical circuits varying at all. At the periphery of the hierarchy are gene regulatory networks that specify the arrangements for smaller-scale features that can sometimes vary. Yet, to produce a new body plan requires altering the axis and global form of the animal. This requires mutating the very circuits that do not vary without catastrophic effects. As Davidson emphasizes, mutations affecting the dGRNs that regulate body-plan development lead to “catastrophic loss of the body part or loss of viability altogether.” He explains in more detail:
    “There is always an observable consequence if a dGRN subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.”
    Thus, contra Marshall, Meyer didn’t “miss” the arguments of Davidson and others about dGRNs and hypotheses about rewiring preexisting networks of genes, nor did he critique a model of animal evolution that’s stuck “in the 1980s.” Rather, he discussed them, he confronted them, and he critiqued them.”

    Davidson was also cited here:

    Gene Regulatory Networks in Embryos Depend on Pre-existing Spatial Coordinates – Jonathan Wells – July 2011
    Excerpt: The development of metazoan embryos requires the precise spatial deployment of specific cellular functions. This deployment depends on gene regulatory networks (GRNs), which operate downstream of initial spatial inputs (E. H. Davidson, Nature 468 [2010]: 911). Those initial inputs depend, in turn, on pre-existing spatial coordinate systems. In Drosophila oocytes, for example, spatial localization of the earliest-acting elements of the maternal GRN depends on the prior establishment of an anteroposterior body axis by antecedent asymmetries in the ovary. Those asymmetries appear to depend on cytoskeletal and membrane patterns rather than on DNA sequences,,,

    I highly recommend listening to the entire debate:

    “Darwin’s Doubt” – Stephen Meyer vs. Charles Marshall – audio

    also of note, here is a 4-part responce, with references, to Marshall’s peer-reviewed critique of Darwin’s Doubt:

    Stephen Meyer Answers Charles Marshall (Peer Reviewed Paper) on Darwin’s Doubt – October 2013 (4 part response)

    Also of note is the stunning lack of empirical evidence for the Darwinian claim that DNA controls morphology:

    “Viable mutations with major morphological or physiological effects are exceedingly rare and usually infertile; the chance of two identical rare mutant individuals arising in sufficient propinquity to produce offspring seems too small to consider as a significant evolutionary event. These problems of viable “hopeful monsters” render these explanations untenable.”
    Paleobiologists Douglas Erwin and James Valentine

    …Advantageous anatomical mutations are never observed. The four-winged fruit fly is a case in point: The second set of wings lacks flight muscles, so the useless appendages interfere with flying and mating, and the mutant fly cannot survive long outside the laboratory. Similar mutations in other genes also produce various anatomical deformations, but they are harmful, too. In 1963, Harvard evolutionary biologist Ernst Mayr wrote that the resulting mutants “are such evident freaks that these monsters can be designated only as ‘hopeless.’ They are so utterly unbalanced that they would not have the slightest chance of escaping elimination through natural selection.” –
    Jonathan Wells

    ‘No matter what we do to a fruit fly embryo there are only three possible outcomes, a normal fruit fly, a defective fruit fly, or a dead fruit fly. What we never see is primary speciation much less macro-evolution’ –
    Jonathan Wells Darwin’s Theory – Fruit Flies and Morphology – video

    50 million year old Fruit Fly fossil compared to modern Fruit Fly – picture

    Response to John Wise – October 2010
    Excerpt: A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.

    also of note is the ‘to the limits of perfection’ optimality found in fruit fly embryogenesis, which is hardly something you would expect from some ‘cobbled together’ Darwinian accident:

    Seeing the Natural World With a Physicist’s Lens – November 2010
    Excerpt: Scientists have identified and mathematically anatomized an array of cases where optimization has left its fastidious mark, among them;,, the precision response in a fruit fly embryo to contouring molecules that help distinguish tail from head;,,, In each instance, biophysicists have calculated, the system couldn’t get faster, more sensitive or more efficient without first relocating to an alternate universe with alternate physical constants.

    Also of note, is the Drosophila genome is far more complex than previously suspected, which is also something one wouldn’t expect of a ‘cobbled together’ Darwinian accident:

    Study of complete RNA collection of fruit fly uncovers unprecedented complexity – March 17, 2014
    Excerpt: Scientists from Indiana University are part of a consortium that has described the transcriptome of the fruit fly Drosophila melanogaster in unprecedented detail, identifying thousands of new genes, transcripts and proteins.,,,
    The paper shows that the Drosophila genome is far more complex than previously suspected and suggests that the same will be true of the genomes of other higher organisms.

  27. 27
    bornagain77 says:

    Richard Sternberg PhD – podcast – On Human Origins: Is Our Genome Full of Junk DNA? Part 2. (Major Differences in higher level chromosome spatial organization)
    5:30 minute mark: “Basically the dolphin genome is almost wholly identical to the human genome,, yet no one would argue that bottlenose dolphins are our sister species”
    here is part 1 of the podcast:

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