'Junk DNA' News

Anyone remember ENCODE? Not much junk DNA? Still not much.

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Still not much junk DNA (open access):

Conclusion

In contrast to evolutionary and genetic evidence, biochemical data offer clues about both the molecular function served by underlying DNA elements and the cell types in which they act, thus providing a launching point to study differentiation and development, cellular circuitry, and human disease (14, 35, 69, 111, 112). The major contribution of ENCODE to date has been high-resolution, highly-reproducible maps of DNA segments with biochemical signatures associated with diverse molecular functions. We believe that this public resource is far more important than any interim estimate of the fraction of the human genome that is functional. By identifying candidate genomic elements and placing them into classes with shared molecular characteristics, the biochemical maps provide a starting point for testing how these signatures relate to molecular, cellular, and organismal function. The data identify very large numbers of sequence elements of differing sizes and signal strengths. Emerging genome-editing methods (113, 114) should considerably increase the throughput and resolution with which these candidate elements can be evaluated by genetic criteria. Given the limitations of our current understanding of genome function, future work should seek to better define genome elements by integrating all three methods to gain insight into the roles they play in human biology and disease.

They seem to want to say that their bookkeeping is more important than the fact that they can’t really identify much junk DNA. (“We believe that this public resource is far more important than any interim estimate of the fraction of the human genome that is functional.”)

If they say so.

Anti-ENCODE rants from Darwin’s faithful here and here. Response.

Watching a movement self-destruct intellectually is curious. No one asked Darwin’s followers to insist that most of the human genome is junk. They could come down from the trees any time and no one will even notice maybe …

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78 Replies to “Anyone remember ENCODE? Not much junk DNA? Still not much.

  1. 1
    kevnick says:

    You guys must really like Larry Moran’s state of blood pressure. It goes up each time you post a JUNK DNA post. He loves his junk but it looks like most of us, sooner or later, forget about are “junk” especially if more, and more evidence shows that more, and more function for it… We just don’t to tend to go back and rediscover something we had doomed as junk in the first place.

  2. 2
    Jehu says:

    Larry Moran is a function denier.

  3. 3
    Dionisio says:

    I have a question about something I don’t quite understand.
    In the bio classes I’ve taken, they said most somatic cells in the human body have the same DNA. If that’s the case, then how come they behave differently depending on the tissue the are in?
    Or is it the protein coding regions that are the same, but the non-coding areas different between different cell types.

  4. 4
    Mung says:

    Hi Dionisio,

    DNA is an inert molecule. It does not cause anything to take place. There are many biological processes that change depending upon context, including tissue differentiation.

    It’s not that the coding areas are different or that the non-coding areas are different. It’s that the context has changed and some how some way cells “know” this and act accordingly.

  5. 5
    AVS says:

    You obviously didn’t pay much attention in your bio classes Dio. And you haven’t been doing much reading nowadays in your studies apparently. I’m not really surprised I guess.

  6. 6
    scordova says:

    By the way, this latest PNAS paper supports my claim that Designs can be functional but selectively neutral or deleterious

    Loss-of-function tests can also be buffered by functional redundancy, such that double or triple disruptions are required for a phenotypic consequence.

    Have said this since 2006 where I gave an examples where a double disruption would have to occur for a serious problem to emerge:
    Airplane Magnetos, contingency designs

  7. 7
    AVS says:

    You sure about that Mungy? That “DNA doesn’t cause anything to take place”?
    Maybe a bunch of scientifically illiterate fools are not the people to rely on for education on biology, Dio.
    Just a thought.

  8. 8
    Mung says:

    Well, I look forward to the day that AVS posts whatever it is that AVS thinks DNA is the cause of.

    But I am not going to hold my breath.

  9. 9
    AVS says:

    Well maybe I don’t fully understand your argument Mungy, but I’d say that DNA sequences play a very important role in the expression of a downstream gene. In fact the initiation of transcription is highly dependent on DNA sequence.
    What do I know though?

  10. 10
    Mung says:

    Salvador:

    By the way, this latest PNAS paper supports my claim…

    Link to the PNAS paper, please.

  11. 11
    scordova says:

    Link to the PNAS paper, please.

    It’s in the OP. 🙄

  12. 12
    Mung says:

    AVS:

    Well maybe I don’t fully understand your argument Mungy, but I’d say that DNA sequences play a very important role in the expression of a downstream gene. In fact the initiation of transcription is highly dependent on DNA sequence.

    Well, perhaps you just don’t understand cell biology, much like you don’t understand how cells came to be in the first place.

    What, precisely, initiates transcription? Do you know?

    If you don’t know what initiates transcription, how can you asset that “the initiation of transcription is highly dependent on DNA sequence.”

    If you actually know what you are talking about, and you aren’t just yet another internet troll, please tell us how you know that “the initiation of transcription is highly dependent on DNA sequence.”

    please

  13. 13
    Dionisio says:

    AVS @ 5

    You obviously didn’t pay much attention in your bio classes Dio. And you haven’t been doing much reading nowadays in your studies apparently. I’m not really surprised I guess.

    AVS @ 7

    You sure about that Mungy? That “DNA doesn’t cause anything to take place”?
    Maybe a bunch of scientifically illiterate fools are not the people to rely on for education on biology, Dio.
    Just a thought.

    What’s wrong with you, buddy?

    I specially quoted your comments, so everyone reading this can realize how you write so many offensive statements, but don’t add any valuable information to answer my questions correctly. Try to be more positive, more helpful, more friendly. I mean, what in the world makes you so unfriendly. Can’t you just answer the questions, instead of telling others that they are stupid or ignorant? If you know so much, then go ahead and answer my questions. I’m sure they’re very simple questions to you. So explain, what makes a cardiac tissue cell behave different than a liver tissue cell, or a kidney tissue cell, if they all have the same DNA? Please, stick to the questions, don’t keep digressing into name-calling and offensive mocking. Just try to behave like a real scientist, gracious and willing to share knowledge.
    C’mon, I know you can, because you’re a very talented guy, with a very strong educational background. Just be nice. Thank you.
    P.S. you may provide links to videos, or to written material where the questions are answered correctly. I’m sure you know what ‘correctly’ means in this case.
    Remember that being nice to others is a virtue. C’mon, show us that you possess that virtue too.
    Here’s a happy face for you to cheer up! 🙂
    Remember I’m a stupid ignorant guy who is struggling to learn some easy biological stuff, so I can develop the simulation software I’m working on. See how important your help will be. So go ahead and write an impressive clear explanation, like the ones you wrote in other threads before. We know you can. Go for it! Thank you.
    Also, please, remember I need this information in order to write the programming tech specs. Hence details are very important.

  14. 14
    Mung says:

    Salvador, you claim that this paper Defining functional DNA elements in the human genome supports your claim that “Designs can be functional but selectively neutral or deleterious.”

    But you don’t say how this paper supports your claim.

    You make the same claim in this post:

    By the way, the latest PNAS paper supports my claim:

    But again, you fail to mention how that paper supports your claim.

    Specifically, what claim did you make, and how does that paper support your claim?

  15. 15
    AVS says:

    Ohhohhhohoooooo Mungy, now we’re talking. I certainly do have a good grasp on cell biology and in fact I do know a thing or two about the initiation of transcription. That is exactly why I asserted that “initiation is highly dependent on DNA sequence.”
    Now let me explain myself…something you guys never bother to do when making your BS claims.

    First of all, DNA’s ability to melt (or separate for you laymen) is largely effected by the nucleotide sequence. The sequence T,A is more flexible due to less hydrogen bonding an this is why the TATA box is a well known site for transcription initiation. There is also a site called the “initiation region” in DNA, that activates transcription. The DNA helix winding is also an important factor in activation/repression, effecting protein binding on different faces of the helix.
    I could go on for days about this stuff, Mungy.
    Now the next time Joe tries to tell me I don’t know what I’m talking about you’re gonna have to step in and correct him. Thanks!

  16. 16
    Dionisio says:

    Mung,
    I appreciate your explanations. Can you provide a link to where my questions get answered in details? For the project I’m working on, step-by-step details are very important. Can’t do my work without those details. Just point to some video or written material where that is explained. Thank you.

    I’ve looked around and searched the internet. Found some information, but not all I’m looking for.

  17. 17
    AVS says:

    Dio, if you were serious about learning biology, then you wouldn’t be on this site. This is the last place to learn biology.

    The last time I talked to you, I gave you a number of hints about things to research. You obviously weren’t ready for most of them, but that’s alright. I’ll give you a brief explanation.
    Genes express proteins. Regulation of many of these genes is specific to cell type. During development there are many different signaling factors that alter the transcription of genes. These factors bind cells and activate signal transduction pathways which alter transcription. These pathways can act on things like histones, promoter regions, enhancers, silencers, etc. This alters protein expression and cell type. All cells (except sex cells) have virtually the same genome.
    For the last time, buy some books or take some classes at a local university. Do NOT get your scientific information here.

  18. 18
    Mung says:

    AVS,

    There is also a site called the “initiation region” in DNA, that activates transcription.

    Just how is it that this site activates transcription?

  19. 19
    AVS says:

    The initiator region controls protein binding through sequence specific interactions. It recruits initiation factors through these protein interactions, which then recruit the pre-initiation RNA polymerase complex.
    Any other questions?

  20. 20
    scordova says:

    Dionisio,

    AVS wrote:

    All cells (except sex cells) have virtually the same genome.

    See:

    http://9e.devbio.com/article.php?id=253

  21. 21
    AVS says:

    Do you really think any of that is going to make sense to Dio?
    That some roundworm species and copepods get rid of some of their genome? Good work scordova.
    You’re just going to confuse the kid even more. He already has a loose grip on biology as it is.

  22. 22
    Dionisio says:

    AVS @ 17

    During development there are many different signaling factors that alter the transcription of genes.

    During what development? embryonic development?

    Ok, so during development, let’s follow two specific cells, and let’s say one cell becomes a liver cell and the other cell becomes a cardiac cell. Let’s simplify this so we don’t get lost. At that point, can you say their corresponding DNA are still the same, as they were in the zygote, or have been altered?

    Let’s go slowly, one step at a tome, so I don’t get lost.

    BTW, I can’t afford to buy books or take formal classes, because have no funds for that. Can take online classes, but they don’t seem to be so detailed. Most are sorta-kinda general. However, if you know of any source that explains this in details, let me know. Thanks.

    Now, back to the class by professor AVS.

  23. 23
    Dionisio says:

    Correction:

    Let’s go slowly, one step at a time, so I don’t get lost.

  24. 24
    AVS says:

    Yes, embryonic development, and also throughout the organisms life this occurs in many cases.
    Yes, a liver cell and cardiac cell have virtually the same genome and it is the same as the organisms original zygote cell.
    And I thought you were making six figures as a computer programmer or something? Yeah. ok. But anyways I’ll play along.

  25. 25
    scordova says:

    Good work scordova.

    Here is more good work, the Lamprey loses 20% of its genome in somatic cells:

    http://www.sciencedirect.com/s.....2212006732

    You’re just going to confuse the kid even more

    What? You want me to unconfuse him with this falsified claim:

    All cells (except sex cells) have virtually the same genome.

    And for humans:

    Extensive genetic variation in somatic human tissues

    Genetic variation between individuals has been extensively investigated, but differences between tissues within individuals are far less understood. It is commonly assumed that all healthy cells that arise from the samezygote possess the same genomic content, with a few known exceptions in the immune system and germ line. However, a growing body of evidence shows that genomic variation exists between differentiated tissues. We investigated the scope of somatic genomic variation between tissues within humans. Analysis of copy number variation by high-resolution array-comparative genomic hybridization in diverse tissues from six unrelated subjects
    reveals a significant number of intraindividual genomic changes between tissues. Many (79%) of these events affect genes.

    And you said:

    . Do NOT get your scientific information here.

    I agree. For example, if he got his biology learning from UD, he might be thinking:

    All cells (except sex cells) have virtually the same genome.

  26. 26
    Dionisio says:

    AVS @ 17 [Dionisio @ 22]

    Ok, so during development, let’s follow two specific cells, and let’s say one cell becomes a liver cell and the other cell becomes a cardiac cell. Let’s simplify this so we don’t get lost. At that point, can you say their corresponding DNA are still the same, as they were in the zygote, or have been altered?

    If the DNA in the liver cell is the same as the DNA in the cardiac cell, but the factors (enzymes proteins) that act on those DNA are different, does that mean that at the differentiation point these factors entered the cells?

    Please, explain.

  27. 27
    Dionisio says:

    AVS @ 24

    And I thought you were making six figures as a computer programmer or something? Yeah. ok. But anyways I’ll play along.

    Buddy, unfortunately they pay a lot more in engineering software development than in biology. Much more. But it’s not as exciting and fascinating as biology. I can live with what I have. God provides.

    Anyway, let’s not get distracted. Let’s focus in on the excellent class you’re teaching here.

  28. 28
    AVS says:

    Scordy, I understand where you are coming from, there are always exceptions to the rules in biology. I know. But if you are trying to teach the basics to someone, you can’t hit them with everything at once. They need to get the basics down and then you can tell them about the minute details.
    And anyways like I said, all cells have VIRTUALLY the same genome.
    From a brief skim of that paper it looks like the small differences that rarely occur are extra copies of gene segments or lacking copies anyways. Not much a difference.
    Pump the brakes bud.

  29. 29
    Dionisio says:

    AVS @ 24

    Yes, a liver cell and cardiac cell have virtually the same genome and it is the same as the organisms original zygote cell.

    Ok, so the difference is in the factors (protein enzymes).

    Does the liver cell contain some factors and the cardiac cell other different factors? How did they get there?

  30. 30
    Dionisio says:

    AVS @ 28

    if you are trying to teach the basics to someone, you can’t hit them with everything at once. They need to get the basics down and then you can tell them about the minute details.

    Agree 100%

    And anyways like I said, all cells have VIRTUALLY the same genome.

    Ok, so is there any difference between these two cells by now? When you say their genome is the same, are you referring to the entire DNA molecules, or to the so-called ‘coding’ region only? Just to make sure I’m following your lecture well.

  31. 31
    AVS says:

    So if you were making all this money as a computer guy, where’d it all go? Like i said, I’m calling bullshit.

    Anywho…
    First off, were not really talking about enzymes.
    Second, to talk about the process of development, you should start at the very beginning because many of the important initial events take place very early in development.

  32. 32
    Dionisio says:

    AVS @ 24

    Yes, a liver cell and cardiac cell have virtually the same genome and it is the same as the organisms original zygote cell.

    Ok, so the difference is in the factors (protein enzymes).

    Does the liver cell contain some factors and the cardiac cell other different factors? How did they get there? At what point did those different factors get into those cells?

  33. 33
    AVS says:

    For now, ignore scordy and just assume that all human cells (except sex cells) have the exact same genome. This means they have the same sequence in all 6 billion or so base pairs, both coding and non-coding regions.

  34. 34
    AVS says:

    Factors do not necessarily need to get into cells. They can bind receptors on the cells, which activate signaling pathways within the cell. Like I said, this is a very complicated topic that you are going to find difficult to understand. You should research the early stages in animal development once you get a better idea of how basic biology works.

  35. 35
    Dionisio says:

    AVS @ 31

    So if you were making all this money as a computer guy, where’d it all go? Like i said, I’m calling bullshit.

    My friend, the money went to raise a family, two kids who went to graduate schools, with zero debts, my home mortgage paid off, their weddings, annual traveling (part of the year in Europe and part in USA). I’m not a kid, my friend. I’m over 60. I don’t know your age, but by the way you express yourself, it seems like you’re very young.
    But you seem to know quite a bit of this biology stuff.

    Ok, we are digressing again, let’s stick to the subject of your lecture. Thanks.

    Second, to talk about the process of development, you should start at the very beginning because many of the important initial events take place very early in development.

    Ok, no problem. So, where do we start, at the telomeres within the zygote?

    What happens there with the factors and all that?

    At one point we have what they call cell fate determination and differentiation with migration. That seems to be quite a mechanism in itself, right?

    We could come back to that on another occasion, because that process by itself requires a separate program in my project.

    So cells start to form 3 main groups. Do we have some differences already here? Are the cells in the group 1 different than the cells in groups 2 and 3? What difference?

    Ok, maybe now you’re starting to get an idea why they pay more in engineering software development, right? 😉

    And we’re just starting… the best is still ahead ;-)+

  36. 36
    Dionisio says:

    AVS @ 34

    Factors do not necessarily need to get into cells. They can bind receptors on the cells, which activate signaling pathways within the cell.

    Ok, got that too. Thanks.

    So at the time of the forming of the first three layers, do the cells in each group have some factors attached to the cell receptors on the membrane? Or not yet? Or that happened earlier?

  37. 37
    AVS says:

    Well it would seem you are pretty bad at budgeting your money and planning ahead if you are currently unable to buy books in order to pursue your interests at age 60+. And you obviously haven’t put much effort in because I guarantee that I can go on amazon right now and get some not-latest-edition books on developmental biology/gene expression/general biology that would all serve there purpose just fine.
    Like I said, I’m calling bullshit. Or maybe you really are a 60+ year-old that is completely out of touch with reality.

    Anyways…
    You start at fertilization. Were not ready for fate determination yet, we haven’t even gone through the first round of cell division. So forget about the ecto/meso/endoderm layers for now too.

    They can pay software developers all the money they want, but if people like you are up and quitting….well that doesn’t say much for software development.

  38. 38
    gpuccio says:

    Dionisio:

    You may like to look at the just published papers with the results of the FANTOM5 project. They are exactly about that.

    There are a lot of data there, and I think we all need some time to understand part of them. I believe it is a fascinating step in knowledge. At last, we have some quantitative data about different human transcriptomes.

    Regarding your fundamental and recurring question, I think that what happens is probably something like that (in very gross terms):

    a) The original zygote is one cell. For a few cellular divisions, the new cells remain probably identical. Same genome, same totipotential transcriptome.

    b) Then something happens. the cells are no more identical, they take separate, ordered pathways which will lead to the separate differentiation of future specialized cells. That happens in a very ordered pattern, which generates the body plan and detailed body forms. The genome remains the same in all cells, but individual transcriptomes arise.

    c) How does that happen? We (with the singular exception of AVS) really don’t know but I suggest that what we need to explain that is a couple of things:

    1) Procedures. Software instructions, IOWs information, written somewhere in some way, that include the general plan of development, the successive steps to be realized, and all individual transcriptomes for each step. That’s a lot of functional information, and we don’t know where it is. It is not in protein coding genes, apparently. It is not in non coding DNS, according to Moran (can he be wrong?). Maybe it’s just a transmittable miracle! 🙂

    2) Tools to implement the above procedures. Here we can be more specific. Wherever the procedures are written, the tools to implement them must be epigenetic. IOWs, the procedure at some time must “mark” different cells for different results, and that can be done by epigenetic tools, like for example DNA methylation.

    d) In this way, a totipotent cell or group of cells can at some time activate an intelligent procedure, which marks epigenetically the daughter cells so that they implement different transcriptomes, because their DNA has been differently methylated, or epigenetically modified in other ways.

    e) So, we can understand in very general terms how similar genomes (for example, humans and chimps) can give very different functional results with similar protein effectors if the procedures (wherever they are written) are very different.

  39. 39
    gpuccio says:

    News:

    Thank you for pointing to that very interesting paper. Figure 1 really summarizes the present status of knowledge.

    So. let’s say that even if we consider only the intersection of the dark blue, green and read sets in that figure, there is already, at present, strong evidence for function for something like 20% of non coding DNA. That is really something, especially if we consider that the evidence is daily growing.

    I hope that Larry Moran is taking care of his blood pressure… 🙂

  40. 40
    gpuccio says:

    Sal:

    The concept of genetic differences in somatic cells, other than the classic ones in germ cells and immune system cells, is very interesting. We must certainly give great attention to these new perspectives.

    However, in a general sense, I think that the concept that most somatic cells share the same genome remains valid. That genome is the functional information which was originally transmitted to the individual, and from it we must explain everything functional which happens after that transmission.

  41. 41
    AVS says:

    We actually do know a fair amount about cell differentiation in early development (and it’s certainly not just me poochy).
    Cytoplasmic determinants are present in the oocyte even before fertilization and later dictate cell fate. These cytoplasmic determinants are distributed asymmetrically in the oocyte and are involved in decreasing cell potency. As cells of the embryo divide, the presence of zygotic determinants effect expression of other proteins according to a threshold. Cytoplasmic determinants can be mRNA themselves, actually. Protein half-lives are important in the function of some factors, keeping their distribution near their site of expression. I think gap gene transcription factors are an example of some of these processes, controlling gene expression patterns. Where the sperm enters the egg is also important in determining certain regions of the zygote. It brings about the formation of the dorsal-ventral axis and is associated with determining gastrulation. Other poles of the blastula and the fate of certain cell regions are decided in the early and late blastula stages. The location of the germ layers and the factors they secrete begins to signal cell fate determination, again using gradients of these factors to alter transcription of cells in the late blastula. As the blastula develops, the cells it consists of lose their potency. Successive rounds of differentiation and replication lead to the formation of different cells in different regions of the embryo which in turn begin to develop more specialized structures and in the process these cells become determined.
    There’s a whole slew of protein factors involved in all this, with many studies being combined in a umber of model systems.

  42. 42
    bornagain77 says:

    The concept of ‘Junk’ DNA is a prime example of how Darwinian presuppositions hinder science. For the Darwinists ‘Junk DNA’ serves two functions. Firstly, and most importantly for the Darwinist, it serves the very important Theological purpose of showing ‘no reasonable God would have done it that way’:

    “The human genome is littered with pseudogenes, gene fragments, “orphaned” genes, “junk” DNA, and so many repeated copies of pointless DNA sequences that it cannot be attributed to anything that resembles intelligent design. . . . In fact, the genome resembles nothing so much as a hodgepodge of borrowed, copied, mutated, and discarded sequences and commands that has been cobbled together by millions of years of trial and error against the relentless test of survival. It works, and it works brilliantly; not because of intelligent design, but because of the great blind power of natural selection.”
    – Ken Miller

    “Perfect design would truly be the sign of a skilled and intelligent designer. Imperfect design is the mark of evolution … we expect to find, in the genomes of many species, silenced, or ‘dead,’ genes: genes that once were useful but are no longer intact or expressed … the evolutionary prediction that we’ll find pseudogenes has been fulfilled—amply … our genome—and that of other species—are truly well populated graveyards of dead genes”
    – Jerry Coyne

    “We have to wonder why the Intelligent Designer added to our genome junk DNA, repeated copies of useless DNA, orphan genes, gene fragments, tandem repeats, and pseudo¬genes, none of which are involved directly in the making of a human being. In fact, of the entire human genome, it appears that only a tiny percentage is actively involved in useful protein production. Rather than being intelligently designed, the human genome looks more and more like a mosaic of mutations, fragment copies, borrowed sequences, and discarded strings of DNA that were jerry-built over millions of years of evolution.”
    – Michael Shermer

    Second, for the Darwinist, ‘Junk’ DNA serves the purpose of showing that neo-Darwinism can be ‘scientific’ in that the mathematics of ‘neutral’ theory, in so far as anyone can make out what neutral theory predicts,,,

    Majestic Ascent: Berlinski on Darwin on Trial – David Berlinski – November 2011
    Excerpt: The publication in 1983 of Motoo Kimura’s The Neutral Theory of Molecular Evolution consolidated ideas that Kimura had introduced in the late 1960s. On the molecular level, evolution is entirely stochastic, and if it proceeds at all, it proceeds by drift along a leaves-and-current model. Kimura’s theories left the emergence of complex biological structures an enigma, but they played an important role in the local economy of belief. They allowed biologists to affirm that they welcomed responsible criticism. “A critique of neo-Darwinism,” the Dutch biologist Gert Korthof boasted, “can be incorporated into neo-Darwinism if there is evidence and a good theory, which contributes to the progress of science.”
    By this standard, if the Archangel Gabriel were to accept personal responsibility for the Cambrian explosion, his views would be widely described as neo-Darwinian.
    http://www.evolutionnews.org/2.....53171.html

    Here is a Completely Different Way of Doing Science – Cornelius Hunter PhD. – April 2012
    Excerpt: But how then could evolution proceed if mutations were just neutral? The idea was that neutral mutations would accrue until finally an earthquake, comet, volcano or some such would cause a major environmental shift which suddenly could make use of all those neutral mutations. Suddenly, those old mutations went from goat-to-hero, providing just the designs that were needed to cope with the new environmental challenge. It was another example of the incredible serendipity that evolutionists call upon.
    Too good to be true? Not for evolutionists. The neutral theory became quite popular in the literature. The idea that mutations were not brimming with cool innovations but were mostly bad or at best neutral, for some, went from an anathema to orthodoxy. And the idea that those neutral mutations would later magically provide the needed innovations became another evolutionary just-so story, told with conviction as though it was a scientific finding.
    Another problem with the theory of neutral molecular evolution is that it made even more obvious the awkward question of where these genes came from in the first place.
    http://darwins-god.blogspot.co.....ay-of.html

    Ann Gauger on genetic drift – August 2012
    Excerpt: The idea that evolution is driven by drift has led to a way of retrospectively estimating past genetic lineages. Called coalescent theory, it is based on one very simple assumption — that the vast majority of mutations are neutral and have no effect on an organism’s survival. (For a review go here.) According to this theory, actual genetic history is presumed not to matter. Our genomes are full of randomly accumulating neutral changes. When generating a genealogy for those changes, their order of appearance doesn’t matter. Trees can be drawn and mutations assigned to them without regard to an evolutionary sequence of genotypes, since genotypes don’t matter.
    http://www.uncommondescent.com.....tic-drift/

    ,,, in that, in so far as anyone can make out what neutral theory predicts, neutral theory ‘predicts’ that most of the genome will be junk:

    Carter: Why Evolutionists Need Junk DNA – Robert W. Carter – 2009
    Excerpt: Junk DNA is not just a label that was tacked on to some DNA that seemed to have no function, but it is something that is required by evolutionary theory. Mathematically, there is too much variation, too much DNA to mutate, and too few generations in which to get it all done. This was the essence of Haldane’s work. Without junk DNA, evolutionary theory cannot currently explain how everything works mathematically. Think about it; in the evolutionary model there have only been 3-6 million years since humans and chimps diverged. With average human generation times of 20-30 years, this gives them only 100,000 to 300,000 generations to fix the millions of mutations that separate humans and chimps. This includes at least 35 million single letter differences, over 90 million base pairs of non-shared DNA, nearly 700 extra genes in humans (about 6% not shared with chimpanzees), and tens of thousands of chromosomal rearrangements. Also, the chimp genome is about 13% larger than that of humans, but mostly due to the heterochromatin that caps the chromosome telomeres. All this has to happen in a very short amount of evolutionary time. They don’t have enough time, even after discounting the functionality of over 95% of the genome–but their position becomes grave if junk DNA turns out to be functional. Every new function found for junk DNA makes the evolutionists’ case that much more difficult.
    Robert W. Carter – biologist
    http://creation.com/junk-dna-slow-death

    Kimura (1968) developed the idea of “Neutral Evolution”. If “Haldane’s Dilemma” is correct, the majority of DNA must be non-functional.

    At the 2:45 minute mark of the following video, the mathematical roots of the junk DNA argument, that is still used by Darwinists, is traced through Haldane, Kimura, and Ohno’s work, in the 1950’s, 60’s and 70’s, in population genetics:

    What Is The Genome? It’s Not Junk! – Dr. Robert Carter – video – (Notes in video description)
    http://www.metacafe.com/w/8905583

    Here is a short history of the Junk DNA argument from leading Darwinists
    http://docs.google.com/View?id=dc8z67wz_24c5f7czgm

    The problem with all this supposed mathematical rigor for Darwinism that neutral theory supplies,

    “On the other hand, I disagree that Darwin’s theory is as `solid as any explanation in science.; Disagree? I regard the claim as preposterous. Quantum electrodynamics is accurate to thirteen or so decimal places; so, too, general relativity. A leaf trembling in the wrong way would suffice to shatter either theory. What can Darwinian theory offer in comparison?”
    (Berlinski, D., “A Scientific Scandal?: David Berlinski & Critics,” Commentary, July 8, 2003)

    ,,, the problem with the supposed mathematical rigor for Darwinist that neutral theory supposedly supplies for Darwinism, which predicts that vast swaths of ‘junk’ DNA in the genome will be functionless (and ID proponents agree with this mathematical prediction for ‘vast swaths of junk’ if Darwinism were true),

    Using Computer Simulation to Understand Mutation Accumulation Dynamics and Genetic Load:
    Excerpt: We apply a biologically realistic forward-time population genetics program to study human mutation accumulation under a wide-range of circumstances.,, Our numerical simulations consistently show that deleterious mutations accumulate linearly across a large portion of the relevant parameter space.
    http://bioinformatics.cau.edu......aproof.pdf

  43. 43
    bornagain77 says:

    ,,,the problem with all this is that this mathematical prediction for ‘junk’, (which is NOT a prediction for functionality in the genome mind you but is only a prediction for junk), is that the ‘prediction’ is currently running head first into empirical evidence which is falsifying that ‘prediction’ in spectacular fashion. In terms of what is currently being revealed, DNA is simply ‘out of this world’ in terms of the undreamt levels of functional complexity being revealed. For instance:

    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.
    http://news.indiana.edu/releas.....ered.shtml

    The Extreme Complexity Of Genes – Dr. Raymond G. Bohlin – video
    http://www.metacafe.com/watch/8593991/

    DNA – Replication, Wrapping & Mitosis – video
    https://vimeo.com/33882804

    3-D Structure Of Human Genome: Fractal Globule Architecture Packs Two Meters Of DNA Into Each Cell – Oct. 2009
    Excerpt: the information density in the nucleus is trillions of times higher than on a computer chip — while avoiding the knots and tangles that might interfere with the cell’s ability to read its own genome. Moreover, the DNA can easily unfold and refold during gene activation, gene repression, and cell replication.
    http://www.sciencedaily.com/re.....142957.htm

    Multidimensional Genome – Dr. Robert Carter – video
    http://www.metacafe.com/watch/8905048/

    Scientists’ 3-D View of Genes-at-Work Is Paradigm Shift in Genetics – Dec. 2009
    Excerpt: Highly coordinated chromosomal choreography leads genes and the sequences controlling them, which are often positioned huge distances apart on chromosomes, to these ‘hot spots’. Once close together within the same transcription factory, genes get switched on (a process called transcription) at an appropriate level at the right time in a specific cell type. This is the first demonstration that genes encoding proteins with related physiological role visit the same factory.
    http://www.sciencedaily.com/re.....160649.htm

    Of particular note:

    Quantum Dots Spotlight DNA-Repair Proteins in Motion – March 2010
    Excerpt: “How this system works is an important unanswered question in this field,” he said. “It has to be able to identify very small mistakes in a 3-dimensional morass of gene strands. It’s akin to spotting potholes on every street all over the country and getting them fixed before the next rush hour.” Dr. Bennett Van Houten – of note: A bacterium has about 40 team members on its pothole crew. That allows its entire genome to be scanned for errors in 20 minutes, the typical doubling time.,, These smart machines can apparently also interact with other damage control teams if they cannot fix the problem on the spot.
    http://www.sciencedaily.com/re.....123522.htm

    Of note: DNA repair machines ‘Fixing every pothole in America before the next rush hour’ is analogous to the traveling salesman problem. The traveling salesman problem is a NP-hard (read: very hard) problem in computer science; The problem involves finding the shortest possible route between cities, visiting each city only once. ‘Traveling salesman problems’ are notorious for keeping supercomputers busy for days.

    NP-hard problem – Examples
    http://en.wikipedia.org/wiki/NP-hard#Examples

  44. 44
    bornagain77 says:

    Yet such traveling salesmen problems are shown to be amendable to ‘quantum computation’

    Speed Test of Quantum Versus Conventional Computing: Quantum Computer Wins – May 8, 2013
    Excerpt: quantum computing is, “in some cases, really, really fast.”
    McGeoch says the calculations the D-Wave excels at involve a specific combinatorial optimization problem, comparable in difficulty to the more famous “travelling salesperson” problem that’s been a foundation of theoretical computing for decades.,,,
    “This type of computer is not intended for surfing the internet, but it does solve this narrow but important type of problem really, really fast,” McGeoch says. “There are degrees of what it can do. If you want it to solve the exact problem it’s built to solve, at the problem sizes I tested, it’s thousands of times faster than anything I’m aware of. If you want it to solve more general problems of that size, I would say it competes — it does as well as some of the best things I’ve looked at. At this point it’s merely above average but shows a promising scaling trajectory.”
    http://www.sciencedaily.com/re.....122828.htm

    Since it is obvious that there is not a material CPU (central processing unit) in the DNA, or cell, busily computing answers to this monster logistic problem, in a purely ‘material’ fashion, by crunching bits, then it is readily apparent that this monster ‘traveling salesman problem’, for DNA repair, is somehow being computed by ‘non-local’ quantum computation within the cell and/or within DNA;

    Quantum Information/Entanglement In DNA – short video
    https://vimeo.com/92405752

    Quantum Entanglement and Information
    Quantum entanglement is a physical resource, like energy, associated with the peculiar nonclassical correlations that are possible between separated quantum systems. Entanglement can be measured, transformed, and purified. A pair of quantum systems in an entangled state can be used as a quantum information channel to perform computational and cryptographic tasks that are impossible for classical systems. The general study of the information-processing capabilities of quantum systems is the subject of quantum information theory.
    http://plato.stanford.edu/entries/qt-entangle/

    Is DNA a quantum computer? Stuart Hameroff
    Excerpt: DNA could function as a quantum computers with superpositions of base pair dipoles acting as qubits. Entanglement among the qubits, necessary in quantum computation is accounted for through quantum coherence in the pi stack where the quantum information is shared,,,
    http://www.quantumconsciousnes.....puter1.htm

    This finding simply was not on the radar screen of Darwinists. In fact I hold that this finding falsifies neo-Darwinism:

    It is very interesting to note that quantum entanglement, which conclusively demonstrates that ‘information’ in its pure ‘quantum form’ is completely transcendent of any time and space constraints, should be found in molecular biology on such a massive scale, for how can the quantum entanglement ‘effect’ in biology possibly be explained by a material (matter/energy) ’cause’ when the quantum entanglement ‘effect’ falsified material particles as its own ‘causation’ in the first place? (J. Bell, A. Aspect, A. Zeilinger) Appealing to the probability of various configurations of material particles, as Darwinism does, simply will not help since a timeless/spaceless cause must be supplied which is beyond the capacity of the material particles themselves to supply! To give a coherent explanation for an effect that is shown to be completely independent of any time and space constraints one is forced to appeal to a cause that is itself not limited to time and space! i.e. Put more simply, you cannot explain a effect by a cause that has been falsified by the very same effect you are seeking to explain! Improbability arguments of various ‘special’ configurations of material particles, which have been a staple of the arguments against neo-Darwinism, simply do not apply since the cause is not within the material particles in the first place!

    supplemental note:

    Does Quantum Biology Support A Quantum Soul? – Stuart Hameroff – video (notes in description)
    http://vimeo.com/29895068

    Verse and Music:

    Genesis 2:7
    “And the LORD God formed man of the dust of the ground, and breathed into his nostrils the breath of life; and man became a living soul.”

    Blues Brothers “Soul Man” Live
    https://www.youtube.com/watch?v=y1ehMrK3itM

  45. 45
    Dionisio says:

    gpuccio @ 38

    c) How does that happen? We (with the singular exception of AVS) really don’t know

    Mio caro amico,

    thank you for the excellent explanations you always provide, and the friendly tone of your messages. Most of us, specially AVS, should learn from your example on how to write serious helpful comments. You write like a very experienced science professor, whose lectures most students enjoy with pleasure.
    However, regarding the above highlighted quote extracted from your highly appreciated comments, somehow I intuitively felt that AVS holds the keys to all the detailed information I’m looking for, which the rest of the world scientists apparently ignore. That’s why I’ve been patiently trying to get all that valuable information from him 😉
    But I will heed your sound advice and look into the sources you have pointed to.
    Mile grazie!!!

  46. 46
    Dionisio says:

    AVS @ 37

    You start at fertilization. Were not ready for fate determination yet, we haven’t even gone through the first round of cell division. So forget about the ecto/meso/endoderm layers for now too.

    Ok, so then… what’s next?

  47. 47
    Dionisio says:

    AVS @ 37

    You start at fertilization. Were not ready for fate determination yet, we haven’t even gone through the first round of cell division. So forget about the ecto/meso/endoderm layers for now too.

    Are you saying that at the first round of cell divisions, i.e. the zygote splits into two cells, those cells are already different somehow or they are still identical?

    Again, I’m referring to the first round, where the zygote splits.

    But you also mentioned that before that, on fertilization, that future differentiation can be seen? How does that work?

    Buddy, this is getting exciting… can’t wait to see what’s coming next 🙂

    I’m looking for the first time when those divided cells are for the first time different, even if just slightly. Are we there yet? 😉

  48. 48
    Dionisio says:

    AVS @ 41

    We actually do know a fair amount about cell differentiation in early development (and it’s certainly not just me poochy).

    We appreciate your visible modesty, but you know that no one else knows as much as you do about this subject you’re trying to describe to me.
    That’s why I’m looking forward with great anticipation to reading all that interesting information you’re about to reveal to us here. I’m sure others here in this thread feel the same way. So let’s keep moving. Without further distractions, go ahead and continue explaining. Thanks.

  49. 49
    gpuccio says:

    Dionisio:

    This paper is highly tentative, but interesting:

    http://www.dimet.org/courses/S.....illon1.pdf

  50. 50
    gpuccio says:

    Dionisio:

    And this one is about the possible role of transposons:

    http://download.springer.com/s.....8;ext=.pdf

  51. 51
    gpuccio says:

    Dionisio:

    As you can see, while something is known, or hypothesized, about the epigenetic tools of cellular differentiation (but still we are at the very beginning of understanding), practically nothing is known about where the procedures are written that allow a cell to know exactly what epigenetic tools are to be activated at each step. Those procedures are probably written somewhere in the genome or elsewhere, and they must include verifications, maps and lists, and many other intelligent and functional informations. The procedural information remains still completely elusive. And it must be entirely present in the original zygote.

    You can also look at this wiki page for an introduction to some aspects specification. As you can see, not much is known or the real causes, and the modalities differ in different species (for example, between drosophila, where the longitudinal axis is partially determined in the oocyte) and mammals (in which that seems to happen much later).

  52. 52
    gpuccio says:

    Dionisio:

    I forgot the Wiki link. Here it is:

    http://en.wikipedia.org/wiki/R.....cification

  53. 53
    scordova says:

    However, in a general sense, I think that the concept that most somatic cells share the same genome remains valid.

    I was just giving AVS a hard time. 🙂

  54. 54
    Dionisio says:

    AVS @ 41

    Cytoplasmic determinants are present in the oocyte even before fertilization and later dictate cell fate. These cytoplasmic determinants are distributed asymmetrically in the oocyte and are involved in decreasing cell potency.

    Ok, that’s quite interesting. Later we’ll look at this in details. But we’re not there yet, so let’s hold on this for now.

    As cells of the embryo divide, the presence of zygotic determinants effect affect expression of other proteins according to a threshold.

    Are ‘cytoplasmic determinants’ the same as ‘zygotic determinants’ in the above highlighted quotes? Just double checking. Thanks.

    Cytoplasmic determinants can be mRNA themselves, actually. Protein half-lives are important in the function of some factors, keeping their distribution near their site of expression.

    Ok, we can keep that in mind. Thanks. Let’s move on.

    I think gap gene transcription factors are an example of some of these processes, controlling gene expression patterns.

    Ok, we can keep that in mind. Thanks. Let’s move on.

    Where the sperm enters the egg is also important in determining certain regions of the zygote. It brings about the formation of the dorsal-ventral axis and is associated with determining gastrulation.

    Ok, we have to look at how the above highlighted actions occur. But that’s later. Let’s keep moving.

    Other poles of the blastula and the fate of certain cell regions are decided in the early and late blastula stages.

    Ok, show me how that highlighted (bold) action happens. Or provide a link where that’s shown. Thanks.

    However, your explanation seems to have jumped ahead to the blastula, and has lost some granularity (details) and certain order. But hopefully we’ll recover it shortly.

    The location of the germ layers and the factors they secrete begins to signal cell fate determination, again using gradients of these factors to alter transcription of cells in the late blastula.

    Ok, the explanation lacks details and order, but let’s move on.

    As the blastula develops, the cells it consists of lose their potency.

    How? In simple steps, just show how that happens. Thanks.
    The explanation lacks step by step details.

    Successive rounds of differentiation and replication lead to the formation of different cells in different regions of the embryo which in turn begin to develop more specialized structures and in the process these cells become determined.

    How? Your explanation lacks a great deal of step by step details. Just point to the material where the required level of step by step details is described well.

    When writing programming tech specs docs I can’t simply pack a bunch of steps into a couple of general statements. They’ll fire me if I do that.

    There’s a whole slew of protein factors involved in all this, with many studies being combined in a number of model systems.

    Same problem as before. Step by step details missing from the description. This is totally unacceptable in a modeling/simulation software development project.

    You’re fired!

  55. 55
    Dionisio says:

    gpuccio @ 49, 50, 52

    Excellent! Mile grazie!

    Looking into those links next.

  56. 56
    Dionisio says:

    AVS @ 41

    Apparently I had too high expectations about your promised explanations. At the end you have disappointed me. Did not provide the step by step detailed descriptions you said you were going to produce. Apparently you changed your mind about revealing the detailed information that only you seem to know? Oh, well.
    Your cheap marketing skills have sorta-kinda deceived me.
    Ok, we’ll let you try again another time. But now, just go and take a brake. We’re busy trying to get some real work done here.
    Have a good day buddy.

  57. 57
    Dionisio says:

    gpuccio @ 38

    Mio caro amico, mile grazie! (I don’t know Italian)

    Thank you so much my friend!

    dzi?kuj? ci? bardzo, mój przyjaciel!

    Muchas gracias mi amigo!

    ??????? ??????? ??? ????!

    Danke schön meine Freunde! (I don’t know this language)

    Merci beaucoup mon ami! (don’t know this language either, but wanted to repeat my thanks in several languages)

    I don’t forget you told me ‘stick to biology’ in another thread, in response to someone else who suggested that I get out of this blog.

    Today you have provided me with a substantial amount of information for me to review and study. That’s very appreciated.

    Everyday I learn a little more. I thank God for allowing me to interact with nice friendly people like you and other folks in this blog, always so willing to share knowledge and help others who just start this ‘long and winding road’ of learning in the most fascinating area of science these days (in my opinion).

    May God bless you abundantly.

  58. 58
    Dionisio says:

    scordova @ 20 and @ 25

    Thank you for the comments and the links.

  59. 59
    Dionisio says:

    gpuccio @ 51

    That’s a remarkably insightful commentary you wrote that basically summarizes what I’ve started to learn in this thread. Thank you again.

    However, please allow me to disagree with you on one issue: apparently our buddy AVS knows a good part of what you and other science lovers don’t know yet. But unfortunately he does not seem willing to share that valuable information with the rest of us here. So I guess we’ll remain ignorant for some time ahead. 😉

  60. 60
    gpuccio says:

    Sal:

    I was just giving AVS a hard time.

    That’s always a noble endeavour! 🙂

  61. 61
    AVS says:

    Are you kidding me Dio? I took the time to write that long post and the best you can do is say I didn’t explain the details?
    Oh but when Poochy here copys and pastes a couple things you go into full “praise the almigthy” mode. What a joke. I’m not going to write a damn book for you. I gave you a basic outline of some of the most basic events that occur in development. Now it’s your turn. There’s plenty of information out their that goes into further detail about what I said. You have to do some of the work too buddy. Or is that how you work, pushing of your work on everyone else. Or are you making up this whole computer science-biology story? I wouldn’t be surprised.

    Anyways at this rate you’ll have the necessary information to write your program when you’re about 3000 years old. So, like I said, stick to computer science. Or get your information from reliable sources….you know these things called “books,” I don’t know if you’re familiar with them.

  62. 62
    gpuccio says:

    Dionisio:

    May God bless you abundantly.

    And you.

    So I guess we’ll remain ignorant for some time ahead. 😉

    We will probably survive… 🙂

  63. 63
    gpuccio says:

    Dionisio:

    AVS says:

    you know these things called “books,” I don’t know if you’re familiar with them.

    Maybe you only read e-books? 🙂

  64. 64
    AVS says:

    I think you guys only read picture books. =)

  65. 65
    Dionisio says:

    gpuccio @ 63

    Maybe you only read e-books? 🙂

    That’s exactly right!

    Thus I help to save the world forests, to help maintain ecological balance, so that nice guys like our buddy AVS can breathe clean air and provide us with so much detailed step by step information about fascinating biological processes that only he understands so well. Isn’t it wonderful? 😉

  66. 66
    Dionisio says:

    AVS @ 61

    Chill out buddy. You definitely need it. 😉

  67. 67
    AVS says:

    Oh I’m as chill as they come. I’m just in disbelief as to your idiocy.

  68. 68
    Dionisio says:

    AVS @ 61

    gpuccio humbly admits what he doesn’t know, but still provides much information and advice on what he knows, always in a very respectful way. That’s the main difference. Try to imitate him. He’s a very passionate biology researcher. He explains difficult subjects like a professor. His friendliness is contagious.
    Can’t find many people like him out there. Unfortunately.

    You may want to appear less arrogant next time, so you can get along with others.

    But most importantly, you should know that God loves you. I know it for sure, because God loves me, and I’m worse than you.

  69. 69
    AVS says:

    Poochy doesn’t know much of anything about biology. Do you really think his “explanations” are reliable, especially on difficult topics, if he doesn’t have a good grasp of the basics?
    No.
    I really don’t care how I appear on this site because this site is a joke. I come here specifically to make fun of you guys and maybe talk a bit about biology if somebody actually starts making sense. That rarely happens though.

  70. 70
    gpuccio says:

    AVS:

    Poochy doesn’t know much of anything about biology.

    Thank you, AVS. Coming from you, this is one of the best compliments I ever received.

  71. 71
    AVS says:

    Well good for you poochy. I’m not sure why you are so proud of your lack of knowledge, especially on a topic that you constantly try to talk about. But maybe that’s a quality that is revered here at UD; “the ability to talk about something you know nothing about.”
    Yeah, sounds about right.

  72. 72
    TZ says:

    AVS,

    I read the information you wrote for Dionisio, and liked what you described. However, maybe the guy was a little disappointed because you did not answer his initial most basic questions. Let me see if I can rewrite them better:

    0. fertilization
    1. zygote: Number of cells = 1
    2. first division: Number of cells = 2
    3. are they identical?
    4. NO – ok, so what is the difference? respond and done.
    5. Yes – identical, go to next round of division
    6. Second Division: Number of cells = 4
    7. are they still identical?
    8. NO – ok, so what’s the difference? respond and done.
    9. Yes – identical, go to next division round
    10. Third Division: Number of cells = 8
    11. still identical?
    12. NO – ok, so what’s the difference? respond and done
    13. Yes – identical, go to next division iteration

    Can you follow the above steps?

    I think that will make it easier for Dionisio to understand your description. Don’t overwhelm the poor guy with so much information packed into one sentence or one paragraph.
    Go step by step, building up gradually from simple to complex, like we know evolution works, right?
    Thank you.

  73. 73
    Dionisio says:

    AVS,
    Considering the explanation you provided earlier, please clarify this detail that I did not see well described in your comments:
    As far as you’re aware of, regarding the first two cells that result from the zygote first division iteration: are they identical or different?
    If identical, then apply the same question to the second, third, etc. division iterations, until the first known differences appear. Thank you for your kindness to provide this information, which only you know in this thread.

  74. 74
    Dionisio says:

    AVS,

    You see, that was the kind of simple step by step info I was expecting from your lecture earlier today. You definitely made reference to a number of interesting events that take place before, during and immediately after fertilization, which seem to have implications in the cell fate determination and posterior differentiation and migration. but apparently you did not indicate at which iteration the differences appeared among the telomeres. Just mentioned some stages where some of that might occur, but left the details out. What I’m doing requires specific details, not general ideas. Can’t write a program based solely on generalities.
    I’m currently reviewing the information gpuccio provided, which seems very good for what I’m looking for.
    Most textbooks out there lack the detail level I’m looking for. Also, part of the information written in most biology books is not confirmed yet.
    When I get this program running, i’ll let you know about it, so you can look at it and give me your feedback.
    If you’re familiar with Java or .NET C# XML XNA or Xamarin programming techniques, you could give me a hand with the actual coding too! But I’d rather take advantage of your expertise in the biology area, and deal with the programming issues alone. The hardest part for me is what seems like the easiest to you 😉
    I’ll write in the program credentials some note thanking all who in some way collaborated with the project.
    But first we have to make it work. We’re not there yet.
    All this time I’m spending here is time I’m taking away from the project, but I wanted to take a break too. Can’t sit in front of the computer all day. I can access this blog on a tablet, away from my computer.

  75. 75
    Box says:

    Dionisio, this article, about bioelectrical signals that are essential for the proper formation of the head and face in frog embryos, may interest you.
    Another article of interest may be the one by Stephen Talbott on context dependency. I found his commentary on a study concerning mouse hair follicles very interesting.

  76. 76
    AVS says:

    That’s a lovely story, but look Dio, I gave you a brief overview. If you want to talk about details then I’m sorry to say it, but you are going to need to sit down and do some serious researching on your own. To understand developmental biology you need a good background in general biology, something you simply do not have. The difficulties in studying developmental biology are compounded by the limits of our experimental model systems.
    Learn the basics, then you can study the detailed information that has come from studies in various species.

  77. 77
    Dionisio says:

    Box @ 74

    Thanks.

  78. 78
    Dionisio says:

    AVS,

    Ok, thanks.

    Have a good weekend.

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