Evolution Intelligent Design

The amazing placenta: A reply to Dr. Ann Gauger

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Dr. Ann Gauger argues that the hypothesis of common descent fails to account for the origin of the mammalian placenta, in an ENV article titled, The Placenta Problem (June 17, 2016). As we’ll see, the evidence she puts forward proves precisely the opposite: common descent is the only hypothesis which explains the facts, without resorting to ad hoc suppositions.

I’d like to begin with a confession. When I read Dr. Gauger’s article on the origin of the placenta, my first reaction was: “Whoa.” It appeared that Dr. Gauger had made a very strong case against the hypothesis of common descent. But then I did some more reading, and after looking at the evidence which Professor Joshua Swamidass kindly forwarded to me, I came to realize that my initial impression was mistaken. For laypeople like myself, Carl Zimmer’s highly readable and refreshingly jargon-free article, Mammals made by viruses (Discover magazine, February 14, 2012) provides an excellent overview of the evidence, from an evolutionary standpoint. Readers with a background in biology may find this 2015 article by Imakawa et al. more interesting.

But first of all, let’s examine what Dr. Gauger has to say:

According to the theory of common descent, all true mammals are supposed to have descended from a common ancestor with a placenta. This is a trait common to all mammals. However, it has been a puzzle for some time that placentas differ in the form they take among different mammalian clades.

As an Australian, I feel bound to point out that Dr. Gauger’s description of placental mammals as “true mammals” is biologically incorrect. For example, monotremes (such as the Australian platypus) are mammals that lay eggs, and they don’t have a placenta. Marsupials (such as the kangaroo, the koala and the North American opossum) are mammals that carry their young in a pouch. They also do not have a placenta. Nevertheless, they are true mammals.

I’m also mystified by Dr. Gauger’s assertion, later on in her article, that “in 2015 a functional syncytin was found in several marsupials, extending the presence and essential function of the protein to all placental mammals examined.” I’m quite sure Dr. Gauger is perfectly well aware that marsupials are not placental mammals.

But let us continue with Dr. Gauger’s case against common descent (bolding is mine – VJT):

In the year 2000, French researcher Thierry Heidmann and coworkers found that genes derived from endogenous retroviruses (ERVs) appear to have been coopted to perform an essential role in placental formation. These genes, which resemble the ERV envelope gene env, make a protein that originally promoted fusion of the virus with its host cell’s membrane, but now acts to promote fusion of membranes between the embryo and the lining of the uterus. These “repurposed” proteins are called syncytins. They are essential for placental formation, yet are of independent origin in different kinds of mammals — primates have one kind, mice another, rabbits, cows, and carnivores yet others. They are clade-specific. In fact, in 2015 a functional syncytin was found in several marsupials, extending the presence and essential function of the protein to all placental mammals examined. All syncytins are lineage-specific, meaning that each mammalian clade has its own syncytin, with a unique sequence and location in the genome. They must have inserted themselves (or been placed there) after the separation of the mammals into different clades! This means there must have been multiple independent acquisitions of these syncytins to participate in an essential process that is common to all mammals. Why should there be unique syncytins in each clade?

What we have to explain is the unique and independent group-specific cooption of syncytins for a function that is essential for placental development, a feature common to all mammalian groups. Six independent origins for the placenta! There is no evidence of a grand ancestral syncytin shared by all groups that was later replaced by other syncytins, so the common descent explanation of the placenta in mammals fails…

Rather than postulating six independent, random capture events in placental development, they [Lavialle et al., the authors of a review paper on syncytins] are now postulating at least one more, a founding syncytin leading to a primitive placenta, then the other syncytins to replace that one in each lineage. Each replacement must have had a clear selective advantage as time went on to make the replacement possible, and each must be the outcome of a random series of events. To say it again, the common descent prediction is that there must have been a founding syncytin in the first mammal with a placenta, or something else that functioned in syncytin’s place, in order for the primitive placenta to arise and subsequently be passed to all mammalian clades. For which there is no evidence, and may never be.

Can common descent explain the unexpected observation of six independent origins for the placenta? No. Could it predict it? No….

In considering these alternative explanations, ask yourself, how likely is it that a retrovirus would infect, invade the germ line (the cells that make eggs and sperm), then insert itself at random in locations in the genome that are expressed in the developing embryo or primitive uterus at the proper time, then promote fusion of membranes to permit the formation of a placenta, with all this happening at least six separate times in the six lineages tested so far? We should also make clear, expressing a syncytin by itself is unlikely to be enough to make a placenta, which is a complex organ requiring interactions between mother and embryo, and the ability to exchange nutrients and oxygen.

Dr. Gauger has put together what appears to be a very powerful case. So how would a proponent of common descent answer it?

Stages in the evolution of the mammalian placenta

What we need to keep in mind is that the evolution of the mammalian placenta would have required a large number of steps. At the present time, we do not know precisely how these steps would have been implemented, on a genetic or anatomical level. Nor do we know exactly how many steps would have been required. However, Professor Swamidass has outlined the major changes that would have taken place.

In the ancestors of today’s mammals, egg-laying in a wet environment would have been replaced by the appearance of parchment-shelled eggs. Next, egg wetting (or the supply of water to parchment-shelled eggs, which can rapidly lose moisture in a hot, dry environment) would have evolved, followed by the appearance of an early placenta. After that, the placenta would have undergone further refinement, with better separation between fetal/maternal cells so as to enable longer gestation, leading finally to a modern placenta.

Of the changes listed above, the first three are the most critical. Professor Swamidass suggests that the early steps in mammalian evolution, shared by all mammals, were either low probability or highly contingent on the exact genetic, functional, and environment of earliest mammals. For example, parchment eggs that required egg wetting might have been the low probability event that enabled the whole sequence.

Syncytins, on the other hand, relate to the penultimate phase (better separation between fetal/maternal cells), which is one of the easiest steps in the evolution of the placenta. Syncytins are just one of many ways of accomplishing better separation between fetal and maternal cells, so as to enable longer gestation. There are many ways of doing this, but acquiring a gene from a syncytal virus is a particularly easy way. It is not at all surprising that this happened several times, in different lineages of mammals.

Would the insertion of a retrovirus in a mammal’s genome have been an extremely unlikely event?

Dr. Ann Gauger contends that the capture of a retrovirus containing a gene capable of encoding a protein required for the formation of a placenta, coupled with the insertion of this retrovirus into an appropriate location in a mammal’s genome, where it can be expressed at the right time, would have been a staggeringly unlikely event:

In considering these alternative explanations, ask yourself, how likely is it that a retrovirus would infect, invade the germ line (the cells that make eggs and sperm), then insert itself at random in locations in the genome that are expressed in the developing embryo or primitive uterus at the proper time, then promote fusion of membranes to permit the formation of a placenta, with all this happening at least six separate times in the six lineages tested so far?

However, Professor Swamidass has informed me that it is actually very common for mammals to be infected by viruses with syncytins, and that it is also very common for them to insert themselves into the genome. The only rare part would inserting into the right place in the genome, so that the genetic expression is right. Given that we only need to have this happen once every several million years, Swamidass sees no difficulty here.

Now, perhaps some readers may disagree with Professor Swamidass’s reasoning here. Fine. But if you disagree, then please, let us see your calculations – even if they are merely calculations of the “back-of-the-envelope” variety.

While we’re on the topic of syncytin genes, allow me to quote from a perspicacious remark by a commenter named Evolve, in a recent thread on Uncommon Descent (bolding is mine – VJT):

Ann Gauger thinks she has nailed the case against common descent through the example of syncytins because they were not inherited by all placental mammals from their supposed common ancestor. She says that different syncytins, with no common origin, were inserted by a designer into specific mammalian lineages at different time points. But her logic is utterly flawed because syncytins did not pop into existence from nowhere one fine morning. They are viral proteins and viral infections are very common in all vertebrates including mammals. It is also common for viral genes to integrate into the host organism’s genome (all mammalian genomes sequenced thus far are littered with tons of viral gene remnants, which emphatically prove this point). Occasionally, some viruses infect the germline too and, when this happens, viral genes can get passed down to the next generation. Different syncytins were inherited by different mammalian lineages from such infections.

Syncytins perform two main functions for the virus – they suppress the host’s immune response and they facilitate fusion of the viral envelope with the host cell. When syncytins were acquired by the host organism, both these functions were co-opted for different purposes. The immune suppressing role was used to prevent rejection of the foetus by the mother, while the fusogenic (fusion-promoting) role was used to form the placenta – a tissue that results from the fusion of maternal and fetal cells.

Syncytins are not mysterious, magic genes Ann Gauger’s designer pulled out of thin air. Their origin and co-option for different purposes by mammals occurred through well-understood processes. As such, a designer is not the most parsimonious explanation, and it is unnecessary and redundant.

Is the placenta likely to have been designed?

So, was the mammalian placenta designed? My own answer to this question would be: “Yes, but design is not an all-or-nothing affair.” I would guess that Intelligent Design was required during the first three phases in the evolution of the placenta (discussed above), but not during subsequent phases. I may of course be wrong here; but if you think I am wrong, please provide me with some solid reasons. The capture of a founding retroviral env gene, and its subsequent replacement by new env-derived syncytin genes, doesn’t sound like an intelligently designed process to me. Still, I might be mistaken.

Do advocates of common descent postulate six different origins of the placenta?

No. Advocates of common descent do NOT postulate “six independent origins for the placenta,” as Dr. Gauger claims in her article. That is a misunderstanding. Taken by itself, the hypothesis of common descent is completely agnostic as to whether the different placentas we find in mammals have a single, unified origin in the ancestor of modern-day placentals, or multiple, independent origins in different lineages of placental mammals.

Professor Swamidass points out that there are two hypotheses that could explain the data. On the one hand, it could be a case of convergent evolution, where syncytin is acquired independently by different lineages of placental mammals. Alternatively, there may have been only one origin of the placenta, followed by six independent capture events. In order for this to happen, there would have to be a “baton pass” mechanism, enabling each lineage to replace the original syncytin that would have been present in the ancestor of modern placentals. However, the key point, as we’ll see below, is that while the genes required for the formation of a placenta differ across various lineages of mammals, they follow a lineage-specific pattern, which is consistent with common descent. It is very easy to imagine patterns in the data that would contradict common descent, but we do not see these patterns.

Readers may be wondering how a “baton pass” mechanism would work. That’s a reasonable question. Professor Swamidass has kindly forwarded me a copy of a 2015 paper titled, Baton pass hypothesis: successive incorporation of unconserved endogenous retroviral genes for placentation during mammalian evolution, by Kazuhiko Imakawa, So Nakagawa, and Takayuki Miyazawa (Genes to Cells, Volume 20, Issue 10, October 2015, pages 771–788). The paper’s abstract puts forward the authors’ hypothesis:

The syncytin genes so far characterized are known to be endogenized to the host genome only within the past 12–80 million years, more recently than the appearance of mammalian placentas, estimated to be 160–180 million years ago. We speculate that ERVs [endogenous retroviruses – VJT] including syncytin-like gene variants integrated into mammalian genomes in a locus-specific manner have replaced the genes previously responsible for cell fusion. We therefore propose the ‘baton pass’ hypothesis, in which multiple successive ERV variants ‘take over’ cell-fusion roles, resulting in increased trophoblast cell fusion, morphological variations in placental structures, and enhanced reproductive success in placental mammals.

The authors also propose a highly specific mechanism for how this baton pass might work:

As in an actual baton pass, the two (or more) genes briefly share the same function in the genome of a given host species. Eventually however, the newly acquired gene ‘takes over’, becoming more prominent as the previous gene’s relative importance subsides. The previous gene may be lost or co-opted for another function such as an immunosuppressive property, also essential for mammalian pregnancy (Esnault et al. 2013; Lavialle et al. 2013). In this hypothesis, gene evolution through ERV integration could proceed more quickly than in more conventional models of gene evolution, because the transcription of tissue-specific and/or neighboring genes may regulate ERV gene expression (Yu et al. 2002; Muroi et al. 2009; Nakaya et al. 2013). For the ERVs that function in reproductive processes, the integration of ERVs must be locus-specific because they could be transcribed with their own LTRs or along with placenta-specific genes (Dewannieux & Heidmann 2013; Nakaya et al. 2013). In the baton pass hypothesis, acquisition of ERVs still requires changes in chromosome/genome structures, as it takes over and modifies the preexisting function such as trophoblast cell fusion among mammalian species, enabling novel evolutionary changes.

Under this model, the original placental would have had a syncytin, but the “baton pass” mechanism would have subsequently enabled different lineages of placental mammals to genetically drift to using new and different syncytins.

Now, Dr. Gauger is perfectly entitled to point out that there is, at the present time, no evidence for a founding syncytin in the first mammal with a placenta. Fair enough. But as we’ll see below, the hypothesis of common descent makes a singular prediction about the genes that play a key role in the formation of placentas, which no other hypothesis makes. This bold prediction makes the hypothesis of a founding syncytin a reasonable one. Whether it should prove to be true or false, the “baton pass” theory is more than mere speculation: it is a plausible hypothesis.

What singular predictions does the hypothesis of common descent make?

As Professor Swamidass has pointed out above, the hypothesis of common descent does not predict a single, common origin for placentas, or for the genes involved in their development. What it does predict is that the genes that play a key role in the formation of placentas should always be in the same location, in the genomes of genetically similar mammals (e.g. primates). Of course, the genes that play a key role in the formation of the placenta may be located in totally different positions in the genomes of different lines of mammals (e.g. Old World primates vs. rats and mice). And this is precisely what we find. Even though they all originated from a similar biochemical mechanism, being derived from endogenous retroviruses that became embedded in mammals’ genomes, the specific DNA insertion sites for these placental genes are different, in different lines of mammals, and they line up by clade. Dr. Gauger herself acknowledges as much:

In the year 2000, French researcher Thierry Heidmann and coworkers found that genes derived from endogenous retroviruses (ERVs) appear to have been coopted to perform an essential role in placental formation. These genes, which resemble the ERV envelope gene env, make a protein that originally promoted fusion of the virus with its host cell’s membrane, but now acts to promote fusion of membranes between the embryo and the lining of the uterus. These “repurposed” proteins are called syncytins. They are essential for placental formation, yet are of independent origin in different kinds of mammals — primates have one kind, mice another, rabbits, cows, and carnivores yet others. They are clade-specific. (Bolding mine – VJT.)

Precisely. This is just what the hypothesis of common descent would predict.

Professor Swamidass expresses the point very succinctly:

CD [Common descent] does not predict that syncytin arises only once. CD itself just predicts that each specific event will fit into the tree.

Likewise, CD does not predict one common origin for placentas. It predicts that the genetics will be well nested in clades, which it is.… (Bolding mine – VJT.)

What would really upset proponents of common descent is if we were to find that a few species of primates (e.g. human beings) possessed the version of syncytin found in rats and mice, instead of the version found in most Old World primates. Alternatively, if the genes involved in the formation of the placenta in human beings were in a different location from the corresponding genes in other Old World primates, that would also tell heavily against the theory of common descent.

As Professor Swamidass has pointed out, the reason why these results lend such solid support to the theory of common descent is that they demonstrate that on a genetic level, there are even more types of placentals than scientists had previously believed, on the basis of purely anatomical comparisons. What’s more, these genetic types cluster perfectly, just as the hypothesis of common descent would predict.

I should add that from a common design (as opposed to common descent) perspective, it would have been very easy for the Designer to have given evidence against common descent in our genomes. For instance, the Designer could have given human beings placentas a genetically different placenta. He could have inserted our syncytins in a location in our genome which is inconsistent with the hypothesis of common descent. Alternatively, He could have given us entirely different syncytins. There’s no biological constraint which prevents the Designer from doing either of these things. But He didn’t.

Carl Zimmer summarizes the evidence that humans and other primates share a common ancestry in his article, Mammals made by viruses (Discover magazine, Februaey 14, 2012):

It turned out that syncytin was not unique to humans. Chimpanzees had the same virus gene at the same spot in their genome. So did gorillas. So did monkeys. What’s more, the gene was strikingly similar from one species to the next. The best way to explain this pattern was that the virus that gave us syncytin infected a common ancestor of primates, and it carried out an important function that has been favored ever since by natural selection. Later, the French virologist Thierry Heidmann and his colleagues discovered a second version of syncytin in humans and other primates, and dubbed them syncytin 1 and syncytin 2.

There is no known principle that explains all of the anatomical and genetic features of human placentas, except common ancestry with apes. That’s why the strong genetic similarity between chimps and humans is evidence for common descent.

Finally, Professor Swamidass explains why the genetic evidence for common descent from the study of placentas is much stronger than the anatomical evidence. When you look at anatomy, he says, you can see similar patterns in animals belonging to the same group, but this often requires very careful study, and anatomical comparisons between animals invariably involve an element of subjectivity. Genetic comparisons, however, are not subjective. They are very clear. The genetic data is 100% consistent with common descent. It could have contradicted it, but it didn’t. Only common descent explains why the genetic data has to cluster in clades. On a common design hypothesis, it might, but it doesn’t have to.

At this point, I’d like to invoke an explanatory principle commonly used by scientists:

If hypothesis A predicts that X must occur, and no other known hypothesis makes that prediction, and X occurs, then hypothesis A is a better explanation of X than other hypotheses, and (ceteris paribus) more likely to be true.

Common design doesn’t explain why the genetic data has to cluster in clades. It only says that it might – but then again, it might not. That’s not a prediction. Only common descent unambiguously predicts that it will cluster in clades. That’s what makes it a better hypothesis.

It may also be objected that a theory of common descent, taken by itself, supplies no mechanism for evolutionary change. However, common descent is best regarded as an explanatory framework. It is a foundation, to which we can append more precise claims about mechanisms, in order to form a testable hypothesis. Adding the neutral theory of evolution generates a hypothesis with a good track record of correctly predicting/modeling the data.

Finally, I should add that in very rare cases, the theory of common descent may need to be supplemented by a theory of Intelligent Design, to help it surmount any probabilistic hurdles involved in the evolution of the placenta that would have been insuperable via unguided natural processes. However, the existence of these hurdles has yet to be demonstrated, so we should all keep an open mind.

Does Ann Gauger’s hypothesis of convergent design account for the origin of the placenta?

At this point, critics of Dr. Gauger may be wondering what her alternative to common descent is. Dr. Gauger has a ready response to this question:

Common design has an explanation, but not one that will be palatable to my interlocutors. The designer used the same idea six different times to produce the same outcome in six different “designs” (clades). That’s another way of saying all these clades have the same outcome, the placenta, but achieved by independent uses of the same idea…

Convergent design is to be expected under the design hypothesis because the designer is not constrained by an evolutionary tree. He can reuse ideas that work in one setting in a different place. In fact, he can mix and match his methods to get to any outcome he wants. I am thinking of echinoderms (sea stars and sea urchins) that look alike as adults but get there by very different developmental paths, or two very different animal groups that come up with similar molecular solutions to create a new function, echolocation

However, Professor Swamidass finds this line of reasoning inconsistent. On the one hand, Dr. Gauger appears to be arguing that homology and synteny constitutes evidence that the Designer is copying from a common design to make new organisms. In other words, when similar DNA does very different things, this counts as evidence of design. But on the other hand, Dr. Gauger also argues that multiple DNA coding solutions that do similar things are designed, too. In other words, when totally different DNA blueprints are used to generate very similar solutions, somehow this also counts as evidence of design. There’s a name for this kind of logic: heads, I win; tails, you lose.

Unfortunately, Dr. Gauger makes no attempt to explain why the Designer sometimes uses repeated DNA blueprints for different purposes, and why He sometimes uses different DNA blueprints for the same purpose. What design principle is at work here? And why don’t the platypus and the opossum have a placenta? No answer is provided.

By contrast, the hypothesis of common descent explains:

(i) the full range of genetic and anatomical differences and similarities we see in placental mammals;
(ii) why syncytins could have arisen multiple times (it’s a high-probability way to solve one step in the path to a modern mammalian placenta); and
(iii) why the genetically related placentals group into nested clades (this is an automatic prediction of common descent, if we assume that the process generating nested hierarchies of classification in placental mammals is a memoryless Markov chain).

Taken together, all of this data constitutes very powerful evidence for common descent.

To sum up: we see several patterns that are easily explained by the hypothesis of common descent. None of them are explained by a consistent design principle.

71 Replies to “The amazing placenta: A reply to Dr. Ann Gauger

  1. 1
    Mung says:

    Why isn’t the appeal to magical viruses ad hoc?

  2. 2
    bill cole says:

    Hi VJT
    Very interesting post and glad you and Joshua were able to create a counter argument.

    However, Professor Swamidass has informed me that it is actually very common for mammals to be infected by viruses with syncytins, and that it is also very common for them to insert themselves into the genome. The only rare part would inserting into the right place in the genome, so that the genetic expression is right. Given that we only need to have this happen once every several million years, Swamidass sees no difficulty here.

    Can you quantify here what very common means? How many of these viruses are inserted in a typical genome.

    If we are to look at several chicken genomes would we expect to see this gene? What if we inserted it into an area where it will be expressed? What changes would the chicken experience after insemination?

    During fetal development the placenta cells need to be differentiated. We know this gene is part of those cells. If this is the only change a different differentiation step had to be added to the development process otherwise we would see this protein in another cell type.

    Assuming that the gene that allows fetuses to grow inside animals did come from viruses then where did this original sequence inside the virus come from?

  3. 3
    Mung says:

    From the OP:

    By contrast, the hypothesis of common descent explains:

    (i) the full range of genetic and anatomical differences and similarities we see in placental mammals;

    I can understand how common descent can explain anatomical similarities. Yet there are anatomical differences which are clearly not explained by common descent.

    Most biologists would be willing to admit that there do in fact exist anatomical differences that are not explicable under the hypothesis of common descent. I would wager that Darwin himself considered such exceptions.

  4. 4
    Dionisio says:

    Interesting debate that has produced several OPs in a relatively short time here in this site.

    Can any of the two sides really explain the “delta dev” issue that was posted in previous threads?

    Dev(d1) = Dev(ca) + Delta(d1)
    Dev(d2) = Dev(ca) + Delta(d2)

    Where

    Dev(x) is the developmental process of any given biological system x

    Delta(x) is the whole set of spatiotemporal procedural differences required to produce Dev(x).

    d1 and d2 are two descendants of their common ancestor (ca).

    For example: d1 = gekko; d2 = python; (gpuccio’s example in another thread)

    Just point to the literature that explains this in details.
    The explanation must be comprehensive, coherent and it must hold water under any kind of thorough examination.
    Thank you.

  5. 5
    butifnot says:

    This series is hard to take seriously. Common descent doesn’t ‘explain’ a placenta. Or anything. The origin of placentas is … what? Nothing can be built by anything yet offered. That building a placenta is being attributed to viral infection and some unguided forces is amusing yet annoying.

    Here’s a hypothesis

    Transposable and transposed elements are present in all genomes and contribute to generate variation in offspring. Hence, they qualify as variation-inducing genetic elements (VIGEs). Here, I will discuss the ‘VIGE-first hypothesis’—which holds that RNA viruses originate in the genomes from genetic elements commonly known as endogenous retroviruses—in the context of the origin and evolution of the syncytin gene locus. I will argue that the most parsimonious explanation for understanding the syncytin locus involves the assumption of only two integrations of derailed VIGEs. The ‘VIGE-first hypothesis’ implies that the functional syncytin gene present in the human genome was not derived from the envelope gene of an ancient RNA virus. Rather, the mobile genetic elements that contain a syncytin-like gene are secondary and originated after uptake of the syncytin gene from the genome. Importantly, this vision also indicates that HERV-W may
    be on its way to becoming a full-blown RNA virus.

    http://creation.com/images/pdf.....05-112.pdf

  6. 6
    Dionisio says:

    butifnot @5

    “In a fallen world we might expect all sorts of unpleasant things to happen, including the recombination of novel RNA viruses from previously harmless VIGEs.”

    Interesting article, though technically it’s too far above my pay grade. 🙂

    Thank you for sharing it here.

    BTW, any thoughts on the “delta dev” conundrum posted @4?

  7. 7
    Dionisio says:

    Here’s an undeniable fact that could serve as a strong argument for either CD or UD (you pick):

    The F-35 is a descendant of the F-25 and the X-35.

    🙂

  8. 8
    Anaxagoras says:

    In my opinion it is a big mistake to oppose common descent to common design. Common descent is about mechanisms whereas ID is about causes. The question about retroviruses intervening by cooption in the formation of a placenta through an hypothetical process in different stages as reported in this post is whether the process can be seen as a fortuitous event or as a teleological one. In my opinion the process should be considered completely teleological, oriented to a goal. I wonder if VJT is not proposing a fully evolutionist (naturalistic mechanicist and reduccionist bottom-up) explanation. In fact it makes little sense to talk of a full process where all the stages are necessary but only the first three steps are “designed”.
    Teleology and effective design (order) are the hallmark of an intelligent cause.
    An evolutionary biologist told me once:
    “If I were a proponent of ID I would consider viruses as true messengers of life”
    I answered:
    “It is because you have showed me that viruses are in fact messengers of life that I have become a proponent of ID”.

  9. 9
    Robert Byers says:

    Wait a minute.
    I think it is said all mammals come from a placental mammal and then marsupials went another way. Otherwise one has many mammals coming from a creature neither placental or marsupial.
    Further who says there are mammals? Why not they simply have some common traits?! Who says marsupials are not placentals who adapted upon migration to a marsupial mode.
    I wrote an essay called “Post Flood marsupial migration Explained” By Robert Byers. Just google.

    Yes to quick change of placental to marsupial. NO to the whole thing coming from step by step with vacation time.
    Its just guessing to see placental evolving at any point.
    Right or wrong its still guessing.

  10. 10
    mahuna says:

    Dionisio @ 7

    “The F-35 is a descendant of the F-25 and the X-35.”

    Are you suggesting that some unthinking USAF official allowed a naughty F-25 (which doesn’t appear to have existed), um, “make babies” with the single X-35 in a hangar someplace?

    Otherwise, using aeroplane examples of “evolving DESIGNS” is exactly the same as using automobile designs: intelligent designers modified an existing design. This “re-design” is VERY well documented, and everyone agrees that’s how the changes occurred.

    There may of course have been other influences on the new design, but I don’t know of anyone who’s suggesting that ANY of the influence was random bio-chemistry.

  11. 11
    Origenes says:

    VJT: Dr. Ann Gauger contends that the capture of a retrovirus containing a gene capable of encoding a protein required for the formation of a placenta, coupled with the insertion of this retrovirus into an appropriate location in a mammal’s genome, where it can be expressed at the right time, would have been a staggeringly unlikely event.

    I agree with Dr.Gauger. I would also like to get some sort of overview of all the other staggeringly unlikely events which have to happen simultaneously in order for the new system to be functional. Or is it Swamidass’ idea that only one gene is responsible for innumerable coordinated adaptations (nutritional, blood stream, thermo-regulation, waste elimination, gas exchange via the mother’s blood supply, fight against internal infection and hormone production to name but a few) by the mother and also by the embryo?

  12. 12
    mw says:

    Hi Vjt:

    “What we need to keep in mind is that the evolution of the mammalian placenta would have required a large number of steps. At the present time, we do not know precisely how these steps would have been implemented, on a genetic or anatomical level. Nor do we know exactly how many steps would have been required.”
    ________________________________________________

    As for “precisely,” “exactly how many steps”? One miraculous step surely remains a distinct possibility under the preciseness of divine law and God’s chiselling, and when God spoke “clearly” to Moses (Num 12:3-9).

    A belief, sure. Either that or the Judaeo-Christian God at Sinai was on moonshine with Moses.

    Judaeo-Christians must respect the theological implications of divine law. Darwinism is not a law, and doesn’t not even come close.

    Jesus/God, backed up the Father at Sinai. It is clear, too many Judaeo-Christians are not taking a blind bit of notice, and do not back Jesus in His fulfilling. Straining at placenta similarities between animals, while smashing two stone tablets over their brains as did Darwin from Down. Sorry, could not resist that outburst.

    Still, Darwinism is an imaginary irrefutable theory, that is why we can go on chasing genetic shadows endlessly.

    A point is; if by chance and mutations, arranged was some form of a subhuman/female placental system; then, at the very same time chance and mutations ‘arranged’ for a corresponding subhuman/male sperm to be able to implant as the fittest to beget by chance and mutations a subhuman offspring – all without intelligence – then there must be evidence of gross deformation that we would expect from mutational wrong reading of codes, under the terms of no intelligence allowed.

    In other words, a trial and error creationism, with the brains of God suspended, if you wish to include Him. Certainly suspended at Sinai if evolutionism is the case.

    There are not even stacks upon stacks of perfect transitional forms, let alone placental transitional fossils. Surely we are dealing with a fully operational belief system in its own right.

    Still, never mind, convergent methods of evolution combined with stacks of imaginary natural selection will produce mammalian placental arrangement and precision pathways from non-mammals, because Darwin’s system and methodology works every time.

    Number of steps? Surely vjt, with respect, such is a mirage of Darwin’s brains.

  13. 13
    butifnot says:

    ….And the bar lowers

    VJ you’ve jumped the shark

    The ‘hypothesis’ that placentas were created-formed-originated-explained by a virus infecting a placenta-less mammal is a spurious, unsubstantiated, ‘impossible’, mystical, ad hoc after-the-fact application of a zany religious doctrine.

  14. 14
    Dionisio says:

    mahuna @10

    Thank you for the thought-provoking comment:

    Are you suggesting that some unthinking USAF official allowed a naughty F-25 (which doesn’t appear to have existed), um, “make babies” with the single X-35 in a hangar someplace?

    Didn’t think of that possibility, but I kind of like your interesting suggestion. Hey, why not? 🙂

    My references to the controversial military jet projects were intended to parodying some of the apparently ‘serious’ (but really vacuous nonsense) comments some folks (even with PhD degrees) post in the discussion threads these days. 🙂

    Now, jokes aside, any serious thoughts on the “delta dev” conundrum posted @4? That’s the real deal. Other arguments may easily fall into the category of what the beloved Italian singer Mina used to call ‘parole, parole, parole’.

    One of the reasons for asking about this ‘delta-dev’ issue is that the project I’m currently working on substantially depends on the resolution or at least clarification of that problem. I’m searching the most recent publications on the subject, mostly the so called ‘evo-devo’ papers to no avail so far. I don’t expect to find the solution here in this site, but perhaps someone has seen something seriously related to it and could point to the source of such information.
    While I search for information that could be useful to my project, sometimes I may encounter interesting articles that I think others here would like to read too. That’s why I’ve posted a few references to some papers in this site.
    Since I lack the required biology background and have been working in a low budget project, I have borrowed textbooks from libraries and/or taken free online biology courses before looking at the peer-review publications. Also some friends who are biologists have helped me, but I’ve tried not to abuse their generosity because they’re very busy working in academic/scientific research in addition to caring for their families, hence they lack spare time. They don’t have time to look at blogs like this.

    Also some nice folks here in this site have explained interesting concepts I didn’t know or knew very little about. Besides, some of the discussions here have been helpful for learning various important terminology and concepts or seeing them from a different perspective.

    I’ve also been trying to learn more English (which is not my first language) and enrich my limited vocabulary, while improving my poor communication style and acquiring at least some minimal writing skills. Perhaps participating in some discussions here have been helpful in those mentioned aspects too.

    I don’t consider myself an ID proponent, though I like some of their main concepts. I don’t count myself among the YEC or OEC folks either, though I may agree with some of their fundamental beliefs. I don’t like to tag myself with any acronyms.

    I want my identity to be solely in Christ, to Whom I owe everything that is right. I believe He is the Creator and foundation of everything that is right. Anything that is not right is simply because it’s against Him and He temporarily allows it for the purpose of His sovereign will, revealed to us in the sacred Scriptures compiled in the Christian Bible. All glory and praises belong to Him only.
    I’m a worthless sinful creature that has been eternally forgiven and reconciled with God through the saving faith in the redemptive power of Christ’s death on the cross and His supernatural resurrection. He is the true source of life.

    Now, let’s go back to the discussion topics here: CD vs. UD?
    At this point I’m looking for concrete comprehensive logically coherent explanations for the “delta-dev” issue posted @4, regardless of whether it comes from CD or UD proponents. Keep in mind that the provided information must be useful to writing 4D graphical interactive animation software for educational and/or presentation purposes.

    We can talk about the Euro2016 football quarterfinals and semifinals or something else another time. 🙂

    Have a good weekend.

  15. 15

    VJ,
    I hope I can be a mediating voice here, though my hope is rather faint. If you, VJ, argue that viruses brought the syncytins, through a process more generally known as Horizontal Gene Transfer (HGT), is this not a case of an admitting an alternative to Common Descent? In which case, why not suppose that all the different stages of the placental development are likewise so mediated by HGT?

    From a Bayesian standpoint, the only criteria to deny such a hypothesis is if HGT is less likely than CD. But as Gauger (and Doug Axe) argue, 6 mutations are about the maximum one can ever observe in RM/NT CD. So if two variants in gene expression vary by more the 6 mutations, invoke HGT, but if less than 6 invoke CD.

    Now you may rightly ask, “where does the virus vector for HGT get the gene from?” It’s a very fine question, though I will repeat your own words when you defended CD, “HGT is agnostic about the source of the information,” since viruses are just the vector.

    If you are like most CD advocates, you will find this a very weasily answer, suitable for defending CD, but unsuitable for defending HGT. So I will attempt a better reply.

    Carbonaceous chondrites are water-soluble meteorites with large amounts of carbon and water. They have a numerical classification determined by the highest temperature sustained by the meteorite. CI is the lowest temperature, the meteorite never having been above 100C. All 26 or so named CI meteorites possess microfossils–casts of cyanobacteria made out of water-soluble minerals like MgSO4 encased in a carbonized “keratogenous” sheath. All of the fossils have nitrogen content less than 0.5%, indicating extreme age–frozen mammoth hair some 25,000 years old still has 15% nitrogen, while dino bones do not. Some of the microfossils resemble “acritarchs”, which are eukaryotic spores last seen on Earth 400 million years ago. Several of the fossilized diatoms have never been seen before on Earth.

    What does all this evidence suggest? Simply that Earth is not a closed system, but living organisms rain down on Earth from above. Then HGT is not completely agnostic about the origin of novel genes, but has some basis in believing that it was transported to Earth. Once again, the Bayesian criterion is whether extra-terrestrial transport is more or less likely than in situ evolution. I argue that this calculation is so obvious it hardly needs proving–chances are <1 in 10^150 that random mutations create new genes, whereas we have 26/26 meteorites with fossilized life on them.

    If this answer still does not satisfy you, and you still insist that transport has to come from "somewhere", then let me make two, obvious points. First, comets access the galaxy, so "somewhere" has been multiplied by not just 10^10 stars, or 10^11 planets, but by 10^18 comets in our galaxy. This hardly makes a dent in the 10^150 probability of RM/NT creation of de novo genes, but at least it does a better job on the statistics than Darwin, so I really can't understand objections from Darwinists about this point.

    Second, CD assumes a constant location but uspecified time. HGT replaces that with a constant time (a veritable rain of bacteria), but an unspecified place. Surely you will grant me the 20th century privilege of swapping time with space, otherwise how can you reconcile modern physics with biology? Do really believe (despite evidence to the contrary) that the Earth is the center of the (biological) universe?

  16. 16
    Dr JDD says:

    How do you know viruses didn’t evolve from existing mammalian sequences?

  17. 17
    bornagain77 says:

    as to:

    Carl Zimmer’s highly readable and refreshingly jargon-free article, Mammals made by viruses (Discover magazine, February 14, 2012)

    Well if it were proper to invoke agent causality to viruses, I would say those are some pretty damn smart viruses. But then again, seeing as Carl Zimmer wrote the article, I can rest assured that he is using the now falsified reductive materialistic framework as the basis for his reasoning. And thus, I can safely ignore his paper just as I can safely ignore the musings of astrologers, since they both, scientifically speaking, carry the same weight.

    I sent the following video to Zimmer, whether he watched it or not, since it refutes a article that he wrote,

    Molecular Biology – 19th Century Materialism meets 21st Century Quantum Mechanics – video
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1141908409155424/?type=2&theater

  18. 18
    bornagain77 says:

    As to common descent, it seems that Darwinists, and Theistic evolutionists such as Torley, are going about this the wrong way. Most of the time they point to the similarity of DNA, and basically hand wave off difference, and says that this proves common descent. But it is not the similarities between chimps and humans that need explaining, it is the differences.

    Even King and Wilson themselves noted the deficiencies in such reasoning that Darwinists and Theistic evolutionists are using

    In “Science,” 1975, M-C King and A.C. Wilson were the first to publish a paper estimating the degree of similarity between the human and the chimpanzee genome. This documented the degree of genetic similarity between the two (approx. 99% amino acid similarity) ! The study, using a limited data set, found that we were far more similar than was thought possible at the time. Hence, we must be one with apes mustn’t we? But…in the second section of their paper King and Wilson honestly describe the deficiencies of such reasoning:
    “The molecular similarity between chimpanzees and humans is extraordinary because they differ far more than sibling species in anatomy and way of life. Although humans and chimpanzees are rather similar in the structure of the thorax and arms, they differ substantially not only in brain size but also in the anatomy of the pelvis, foot, and jaws, as well as in relative lengths of limbs and digits (38).
    Humans and chimpanzees also differ significantly in many other anatomical respects, to the extent that nearly every bone in the body of a chimpanzee is readily distinguishable in shape or size from its human counterpart (38).
    Associated with these anatomical differences there are, of course, major differences in posture (see cover picture), mode of locomotion, methods of procuring food, and means of communication. Because of these major differences in anatomy and way of life, biologists place the two species not just in separate genera but in separate families (39). So it appears that molecular and organismal methods of evaluating the chimpanzee human difference yield quite different conclusions (40).”
    King and Wilson went on to suggest that the morphological and behavioral differences between humans and apes,, must be due to variations in their genomic regulatory systems.
    David Berlinski – The Devil’s Delusion – Page 162&163
    Evolution at Two Levels in Humans and Chimpanzees Mary-Claire King; A. C. Wilson – 1975
    http://academic.reed.edu/biolo.....5(classic).pdf

    And it is indeed in the genomic regulatory regions where we find tremendous differences. For instance, alternative splicing, which is part of the genetic regulatory network, is very different between chimps and humans:

    Evolution by Splicing – Comparing gene transcripts from different species reveals surprising splicing diversity. – Ruth Williams – December 20, 2012
    Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,,
    A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species.
    On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,,
    http://www.the-scientist.com/?.....plicing%2F

    Moreover, Alternative splicing can produce up to a million variant proteins and expression patterns as different as the products of different genes. As well, ‘Alternatively spliced isoforms of proteins exhibit strikingly different interaction profiles’.

    Frequent Alternative Splicing of Human Genes – 1999
    Excerpt: Alternative splicing can produce variant proteins and expression patterns as different as the products of different genes.
    http://www.ncbi.nlm.nih.gov/pm.....PMC310997/

    Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing – 2016
    In Brief
    Alternatively spliced isoforms of proteins exhibit strikingly different interaction profiles and thus, in the context of global interactome networks, appear to behave as if encoded by distinct genes rather than as minor variants of each other.,,,
    Page 806 excerpt: As many as 100,000 distinct isoform transcripts could be produced from the 20,000 human protein-coding genes (Pan et al., 2008), collectively leading to perhaps over a million distinct polypeptides obtained by post-translational modification of products of all possible transcript isoforms (Smith and Kelleher, 2013).
    http://iakouchevalab.ucsd.edu/.....M_2016.pdf

    In what should be needless to say, A plethora of unique proteins, (which are wrought by very different alternative splicing patterns in chimps and humans and yet having ‘strikingly different interaction profiles’ than the isoforms of proteins encoded by the same gene), is impossible for common descent to explain. (Axe, Gauger, Behe)

  19. 19

    Traveling now so, unfortunately, please do not expect may comments for me

    VJ, excellent article.

    To be clear, CD does not explain how placenta’s arose. Rather, it explains (and predicts) that the genetics of placentas (including horizontal gene transfer) will fall neatly in nested clades (with some rare exceptions, for provable reasons). This is the prediction of CD, which could easily be invalidated here. Yet, placental genetics falls in nested clades (i.e. lineage specific). This is evidence for common descent.

    Those curious about how the full pattern of viral insertions (including SINEs and ERVs) follows the CD pattern in the genome might also look here:

    http://www.thegospelandevoluti.....ides/2of2/

    http://www.thegospelandevoluti.....this-blog/

    http://biologos.org/blogs/arch.....to-harmony

    To be clear, this is to a BioLogos friendly author. I hope that does not offend anyone. Of course, you will disagree with him about ID, but his science is correct and easy to understand.

    And, I am 100% sure, that VJ would disagree with both that author and me about the ID scientific case. So, once again, do not punish him for my indiscretion.

  20. 20
    drc466 says:

    Sorry, vjt, but I’m with bin @13 – you’ve jumped the shark on this one. This “response” would fit nicely in the “just-so-story” section filled to bursting already by professional evolutionists.

    Without fisking every line, let me simply offer this critique: remove every “may”, “could”, “hypothesis”, and other evidence-free argument made in your response, and see what you are left with.

    A few of your more egregrious magical thinking moments:
    1) Syncytins appear late in placental evolution? Nice assertion, given that there is no empirical evidence that placentas “evolved”, let alone in what order. Pure speculation.
    2) Common descent “predicts” clade-specific syncytins? So, let me get this straight, CD predicts that all mammals will be the same (placenta), all mammals will differ at the clade level (syncytins), and all mammals will differ at the species level (c.f. the x% genetic difference separating species from each other). So, basically, CD doesn’t “predict” a darn thing, does it? It just accommodates absolutely everything – isn’t that a truer statement? Come on, tell the truth – if there had only been one universal syncytin, wouldn’t you have said that confirmed CD? and that CD “predicted” it?

    For your next “I sold my soul for CD” post, I suggest you explain to us (with Dr. Swamidass’ assistance) how CD “predicts” live birth in snakes and lizards…

  21. 21
    bill cole says:

    VJT
    I have read the posts and see very little support for CD based on Ann’s argument. Joshua has tried here but the hand he is playing with is a pair of 2s vs Ann’s full house.

    The biggest probability problem is the emergence of different syncytin genes with different sequences.

    http://genome.ucsc.edu/cgi-bin.....0-92477986

    This sequence takes up 10000 nucleotides in the genome. 4^10000 of possible ways to arrange these nucleotides. Given Art hunts numbers a 1/10^320 of finding function through random change. This is functionally designed to support embryo development. Its sequence cannot be formed by an unguided process. The emergence of 6 new sequences is highly problematic. The CD process of isolated populations cannot create this gene or modify it.

    It appears that Ann has created serious doubt in CD, you and Joshua have your work cut out for you on this one.

  22. 22
    caleb says:

    Hi everyone–
    Needless to say, I disagree with much of what Torley (and Swamidass) have said, but I don’t have time to respond now. In fact, I haven’t got time to read the whole post. But for starters, use Google Scholar to search on marsupial placenta. And read the Brawand paper carefully.

    Ann

    http://www.sciencedirect.com/s.....0409004135

  23. 23

    @21

    Why is the evolution of different syncytins a problem exactly?

    As a design proponent, you have several ways to explain this:

    1. God Himself added this new gene into the evolutionary history of mammals at several distinct times. And they passed on these genes to their descendents.

    2. Several different viral infection events (involving different syncytial from viruses) introduced these genes into into mammalian line.

    Either way, both mechanisms (God’s action and viral infection) produces the exact same common descent predicted genetics. While I certainly do not think that God had to directly intervene by first cause in this case (knowing what I know of biology), even if you think He did, this does not affect the evidence for CD in any way. CD predicts that the genetics fall in nested clades (with rare exceptions). Syncytin genes entirely fall in nested clades, fitting the CD prediction.

    To be clear, you are just making an argument for design. But design and CD are totally independent notions.

  24. 24
    Andre says:

    So I will bite, viruses make placenta’s. The obvious question apart from where does viruses come from? Two other questions. Luck or design? How do we test it?

  25. 25
    Anaxagoras says:

    Says Prof Swamidass in #19:

    “To be clear, CD does not explain how placenta’s arose. Rather, it explains (and predicts) that the genetics of placentas (including horizontal gene transfer) will fall neatly in nested clades”

    Ok, we got it: Common Descent DOES NOT explain how placentas arose.
    If this is so, if there is no evolutionary naturalistic explanation for how placentas arose, then common descent among different kinds of placentals is, to a big extent, irrelevant.

    Common descent is commonly understood as the hypothesis that all living organisms are descended from a Last Universal Ancestor. But there are big leaps in the history of life on Earth than can not be accounted for by common descent.

    But if some specific (and critical )feature like the reproductive system of a kind, (a family, a genus…) can not be explained by simply assuming common descent, and if we can reasonably presume that an input of design and formal order must have intervened as part of the causal explanation for the emergence of such feature, then, “placental genetics falling in nested clades” can preferably be presented as “COMMON DESIGN” regardless of the mechanism and process by which the diversity of placentals took place.

  26. 26
    Anaxagoras says:

    Prof Swamidass very explicit intervention in #23 makes clear his big mistake in understanding what the theory of Intelligent Design is all about.
    He seems to beleive thet ID purports that GOD is presented as a mechanism for making new genes.
    Let ´s start again from the begining.

    Naturalistic evolution is a theory that claims that all living organisms are formed by natural events (mechanisms) that are driven by only natural causes (chance and necessity). The concept of COMMON DESCENT makes part of the theory.

    ID is the theory that claims that natural events produced by natural forces can not sufficiently explain the increasing complexity and organization in living organisms, and that integrative complexity, finalism, teleological agency, regulatory cybernetic mechanisms, natural genetic engineering, intelligent responses to challenges in the environment, purposeful arrangement of parts to the whole, means arranged to acheive ends, having its own “goog”, evident top-down causation like in embryo development, etc. etc can not be explaines without invoking an intelligent cause. (an intelligent cause conceived as a philosophical intuition of a transcendent entity, not exactly GOD)

  27. 27
    Dionisio says:

    Andre @24

    “So I will bite, viruses make placenta”

    Why not?

    It’s widely known how much change viruses can make.

    Haven’t you heard of Zika lately?

    Well, that’s a virus that has been associated with major developmental changes.

    There you have a clear example showing that the virus argument is worth serious consideration.

  28. 28
    bornagain77 says:

    as to:

    CD predicts that the genetics fall in nested clades (with rare exceptions).

    That claim is falsified:

    Richard Dawkins: How Could Anyone “Possibly Doubt the Fact of Evolution” – Cornelius Hunter – February 27, 2014
    Excerpt: there is “no known mechanism or function that would account for this level of conservation at the observed evolutionary distances.”,,,
    the many examples of nearly identical molecular sequences of totally unrelated animals are “astonishing.”,,,
    “data are routinely filtered in order to satisfy stringent criteria so as to eliminate the possibility of incongruence.”,,,
    he has not found “a single example that would support the traditional tree.” It is, another evolutionist admitted, “a very serious incongruence.”
    “the more molecular data is analysed, the more difficult it is to interpret straightforwardly the evolutionary histories of those molecules.”
    And yet in public presentations of their theory, evolutionists present a very different story. As Dawkins explained, gene comparisons “fall in a perfect hierarchy, a perfect family tree.” This statement is so false it isn’t even wrong—it is absurd. And then Dawkins chastises anyone who “could possibly doubt the fact of evolution.” Unfortunately this sentiment is typical. Evolutionists have no credibility.
    http://darwins-god.blogspot.co.....nyone.html

    Reviewing The Evolution Revolution, the NCSE Offers Uninformed Criticism that Misses the Point – Lee M. Spetner – January 13, 2016
    Excerpt: Some researchers in the life sciences, who are not necessarily knowledgeable about evolution (including Levin), think that the various trees based on different biological systems or on protein- and DNA-sequence data yield the same tree. Life scientists once thought that trees based on anatomy and on the molecular sequences of proteins and DNA would be the same, but they were wrong (Nichols 2001; Degnan and Rosenberg 2006; Degnan and Rosenberg 2009; Heled and Drummond 2010; Rosenberg and Degnan 2010). They thought at least there would be consistency among the trees based on the DNA sequences of different genes, but again they were wrong. They then hoped that if they used the whole genome instead of individual genes, the data might average out and things would be better. In fact, it only made matters worse (Jeffroy et al. 2006; Dávalos et al. 2012). All this is discussed in my book. Levin is mistaken about what he calls the “cornerstone” of the evidence for common descent.
    He criticizes my rejection of common descent. I reject common descent because it is based on only circumstantial evidence. The drawback to circumstantial evidence is that it needs a valid theory to connect the evidence with the conclusion, and evolutionary theory is invalid, as I explain at length in my first chapter. There is thus no valid evidence for common descent — and certainly not what Levin calls its “cornerstone.”
    http://www.evolutionnews.org/2.....02281.html

    “The genomic revolution did more than simply allow credible reconstruction of the gene sets of ancestral life forms. Much more dramatically, it effectively overturned the central metaphor of evolutionary biology (and, arguably, of all biology), the Tree of Life (TOL), by showing that evolutionary trajectories of individual genes are irreconcilably different. Whether the TOL can or should be salvaged—and, if so, in what form—remains a matter of intense debate that is one of the important themes of this book.”
    Koonin, Eugene V. (2011-06-23). The Logic of Chance: The Nature and Origin of Biological Evolution (FT Press Science) (Kindle Locations 76-80). Pearson Education (USA). Kindle Edition.
    more studies

    A New Model for Evolution: A Rhizome – Didier Raoult – May 2010
    Excerpt: Thus we cannot currently identify a single common ancestor for the gene repertoire of any organism.,,, Overall, it is now thought that there are no two genes that have a similar history along the phylogenic tree.,,,Therefore the representation of the evolutionary pathway as a tree leading to a single common ancestor on the basis of the analysis of one or more genes provides an incorrect representation of the stability and hierarchy of evolution. Finally, genome analyses have revealed that a very high proportion of genes are likely to be newly created,,, and that some genes are only found in one organism (named ORFans). These genes do not belong to any phylogenic tree and represent new genetic creations.
    http://darwins-god.blogspot.co.....izome.html

    More Fossil-Molecule Contradictions: Now Even the Errors Have Errors – Cornelius Hunter – June 2014
    Excerpt: a new massive (phylogenetic) study shows that not only is the problem (for Darwinists) worse than previously thought, but the errors increase with those species that are supposed to have evolved more recently.,,,
    “Our results suggest that, for Aves (Birds), discord between molecular divergence estimates and the fossil record is pervasive across clades and of consistently higher magnitude for younger clades.”
    http://darwins-god.blogspot.co.....s-now.html

    Molecular Data Wreak Havoc on the Tree of Life – Casey Luskin – February 7, 2014
    Excerpt: Douglas Theobald claims in his “29+ Evidences for Macroevolution” that “well-determined phylogenetic trees inferred from the independent evidence of morphology and molecular sequences match with an extremely high degree of statistical significance.”
    In reality, however, the technical literature tells a different story. Studies of molecular homologies often fail to confirm evolutionary trees depicting the history of the animal phyla derived from studies of comparative anatomy. Instead, during the 1990s, early into the revolution in molecular genetics, many studies began to show that phylogenetic trees derived from anatomy and those derived from molecules often contradicted each other.
    Stephen Meyer – Darwin’s Doubt – (pp. 122-123)
    ,,,Moreover, when complex parts that are shared by different animals aren’t distributed in a treelike pattern, that wreaks havoc on the assumption of homology that’s used to build phylogenetic trees. In other words, this kind of extreme convergent evolution refutes the standard assumption that shared biological similarity (especially complex biological similarity like a brain and nervous system) implies inheritance from a common ancestor.
    If brains and nervous systems evolved multiple times, this undermines the main assumptions used in constructing phylogenetic trees, calling into question the very basis for inferring common ancestry.,,,
    http://www.evolutionnews.org/2.....81981.html

    Logged Out – Scientists Can’t Find Darwin’s “Tree of Life” Anywhere in Nature by Casey Luskin – Winter 2013
    Excerpt: the (fossil) record shows that major groups of animals appeared abruptly, without direct evolutionary precursors.
    Because biogeography and fossils have failed to bolster common descent, many evolutionary scientists have turned to molecules—the nucleotide and amino acid sequences of genes and proteins—to establish a phylogenetic tree of life showing the evolutionary relationships between all living organisms.,,,
    Many papers have noted the prevalence of contradictory molecule-based phylogenetic trees. For instance:
    • A 1998 paper in Genome Research observed that “different proteins generate different phylogenetic tree[s].”6
    • A 2009 paper in Trends in Ecology and Evolution acknowledged that “evolutionary trees from different genes often have conflicting branching patterns.”7
    • A 2013 paper in Trends in Genetics reported that “the more we learn about genomes the less tree-like we find their evolutionary history to be.”8
    Perhaps the most candid discussion of the problem came in a 2009 review article in New Scientist titled “Why Darwin Was Wrong about the Tree of Life.”9 The author quoted researcher Eric Bapteste explaining that “the holy grail was to build a tree of life,” but “today that project lies in tatters, torn to pieces by an onslaught of negative evidence.” According to the article, “many biologists now argue that the tree concept is obsolete and needs to be discarded.”,,,
    Syvanen succinctly summarized the problem: “We’ve just annihilated the tree of life. It’s not a tree any more, it’s a different topology entirely. What would Darwin have made of that?” ,,,
    “battles between molecules and morphology are being fought across the entire tree of life,” leaving readers with a stark assessment: “Evolutionary trees constructed by studying biological molecules often don’t resemble those drawn up from morphology.”10,,,
    A 2012 paper noted that “phylogenetic conflict is common, and [is] frequently the norm rather than the exception,” since “incongruence between phylogenies derived from morphological versus molecular analyses, and between trees based on different subsets of molecular sequences has become pervasive as datasets have expanded rapidly in both characters and species.”12,,,
    http://www.salvomag.com/new/ar.....ed-out.php

  29. 29
    Origenes says:

    “viruses make placentas”

    Just when you think things couldn’t get more ridiculous …

  30. 30
    Dionisio says:

    Origenes @29

    Just when you think things couldn’t get more ridiculous …

    Hey, why not?

    Weren’t most software apps running in the current smartphones and tablets made by bits and bytes?

    If you don’t agree, then just look deep into those well-documented gadgets and you’ll notice their complexity, but at the bottom they are just a bunch of tiny electronic impulses dancing around wildly. Apparently those are the bits, which are grouped into bytes (which in turn are grouped into Kb, Mb, Gb and so on) just for naming purposes (I guess). 🙂
    Well, the same principles apply to the ERV stuff discussed here. Perhaps the grouping does not apply to the ERV. But who knows? Maybe they also have Kilo-ERV, Mega-ERV, Giga-ERV? Dunno.
    Now we (the ignorant folks) know the rest of the story and can understand (at least partially) the comments posted here in this thread by the “all-knowing” scientists and their cousins with their PhD degrees and the whole nine yards.
    🙂

  31. 31
    Dionisio says:

    To Whom This May Concern:

    you may want to see the papers referenced @1019-1021 here:

    http://www.uncommondescent.com.....ent-612074

  32. 32
    Dionisio says:

    Please, let’s keep this in mind:

    […] the fundamental order of development is well conserved among mammals.

    At fertilization, sperm and egg unite to form the zygote, which undergoes successive cleavage divisions, yielding two-, four-, and eight-cell embryonic stages.

    Initially, the zygotic genome is transcriptionally inactive, with maternally inherited factors regulating embryonic metabolism and development.

    Embryonic genome activation occurs at around the eight-cell stage in humans and the two-cell stage in mice and is accompanied in each species by epigenome-wide remodeling.

    The zygote and its daughter cells are totipotent; that is, they have the potential to differentiate into all embryonic and extraembryonic cell types.

    During development, the differentiation potential of embryonic cells becomes progressively more restricted.

    At the blastocyst stage, the cells of the inner cell mass (ICM) are pluripotent, meaning that while they cannot give rise to extraembryonic tissues, they can generate all cell lineages and are able to self-renew.

    Hence, early development involves rapid cellular diversification driven by myriad, and largely still undefined, transcriptional and epigenetic programs.

    Transposable elements in the mammalian embryo: pioneers surviving through stealth and service
    Patricia Gerdes, Sandra R. Richardson, Dixie L. MagerEmail author and Geoffrey J. Faulkner
    Genome Biology 201617:100
    DOI: 10.1186/s13059-016-0965-5

    Did we get that clear?
    OK, let’s repeat it:
    early development involves rapid cellular diversification driven by myriad, and largely still undefined, transcriptional and epigenetic programs.

    That’s a gross oversimplification of the real stuff.
    But it’s fine for this particular discussion.

    Let’s say it again:
    early development involves rapid cellular diversification driven by myriad, and largely still undefined, transcriptional and epigenetic programs.

    Once more:

    early development involves rapid cellular diversification driven by myriad, and largely still undefined, transcriptional and epigenetic programs.

    What does “largely still undefined” mean?

    It probably means “work in progress”, hence we should “stay tuned”. Not there yet.
    The more we know, more is ahead for us to learn about this amazingly complex complexity.
    That’s why we look forward, with increasing anticipation, to reading newer research papers that could shed more light on the elaborate cellular and molecular choreographies operating within the biological systems.
    Unending revelation of the ultimate reality.
    Have a good weekend.

  33. 33
    bill cole says:

    Joshua
    Thanks you for working with VJT and providing a counter argument to this fascinating case.

    If I agree that your low probability event which is 6 viruses infecting zygotes in such a way that this gene can become part of a placenta complex to such precision that a fertilized egg can become a live mammal. I am still left with a major explanatory problem.

    What is the origin of the syncytin genes that can perform their function in a complex system. I need functional sequences that live in almost infinite mathematical space. Where did the viruses get these?

    The origin of the sequences is best explained by ID. CD has no explanatory power here. Without the sequences we don’t have a mammal.

  34. 34
    bornagain77 says:

    I would like to reiterate that neo-Darwinists and Theistic evolutionists are NOT even on the right theoretical foundation to begin with in order to explain ‘body plan morphogenesis’.

    Stephen Meyer puts the irreconcilable problem for neo-Darwinian explanations as such:

    “Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body-plan. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.”
    Stephen Meyer – Functional Proteins and Information for Body Plans – video
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1140536289292636/?type=2&theater

    As Dr. Meyer so eloquently put it in the preceding video, although Darwinists can’t even explain the origin of a single new protein, that is only the tip of the iceberg of the problem for Darwinists in regards to explaining how an organism gets its final form. The main question that is never honestly addressed by Darwinists and Theistic Evolutionists, even if they could explain the origin of proteins, is once you get a protein, how in blue blazes do random material processes figure out how to coordinate that new protein with all the other trillions of proteins?

    The human body is composed of something like a billion-trillion protein molecules.

    One Body – animation – video
    http://www.youtube.com/watch?v=pDMLq6eqEM4

    It is simply insane to think that the unguided, bottom up, random, material processes of Darwinian evolution can figure out how to coordinate all those billion-trillion protein molecules as a single cohesive whole for precisely a life time and not a moment longer:

    It’s Really Not Rocket Science – Granville Sewell – November 16, 2015
    Excerpt: In a 2005 American Spectator article, Jay Homnick wrote:
    “It is not enough to say that design is a more likely scenario to explain a world full of well-designed things. It strikes me as urgent to insist that you not allow your mind to surrender the absolute clarity that all complex and magnificent things were made that way. Once you allow the intellect to consider that an elaborate organism with trillions of microscopic interactive components can be an accident… you have essentially “lost your mind.””
    ,,, Max Planck biologist W.E. Loennig once commented that Darwinism was a sort of “mass psychosis” — then he asked me, is that the right English word? I knew psychosis was some kind of mental illness, but wasn’t sure exactly what it was, so I looked it up in my dictionary when I returned home: “psychosis — a loss of contact with reality.” I wrote him that, yes, that was the right word….
    Loennig and Homnick are still right. Once you seriously consider the possibility that all the magnificent species in the living world, and the human body and the human brain, could be entirely the products of unintelligent forces, you have been in academia too long and have lost contact with reality — you have lost your mind.
    http://www.evolutionnews.org/2.....00911.html

    Stephen Talbott asks a very profound question in the following article:

    The Unbearable Wholeness of Beings – Stephen L. Talbott – 2010
    Excerpt: Virtually the same collection of molecules exists in the canine cells during the moments immediately before and after death. But after the fateful transition no one will any longer think of genes as being regulated, nor will anyone refer to normal or proper chromosome functioning. No molecules will be said to guide other molecules to specific targets, and no molecules will be carrying signals, which is just as well because there will be no structures recognizing signals. Code, information, and communication, in their biological sense, will have disappeared from the scientist’s vocabulary.
    ,,, the question, rather, is why things don’t fall completely apart — as they do, in fact, at the moment of death. What power holds off that moment — precisely for a lifetime, and not a moment longer?
    Despite the countless processes going on in the cell, and despite the fact that each process might be expected to “go its own way” according to the myriad factors impinging on it from all directions, the actual result is quite different. Rather than becoming progressively disordered in their mutual relations (as indeed happens after death, when the whole dissolves into separate fragments), the processes hold together in a larger unity.
    http://www.thenewatlantis.com/.....-of-beings

    Talbott gave us a huge hint as to what the answer is to the question of, “What power holds off that moment — precisely for a lifetime, and not a moment longer?”, when he stated, “Code, information, and communication, in their biological sense, will have disappeared from the scientist’s vocabulary.”

    That is to say, the one thing that is ‘holding that power off for precisely a lifetime’ is information. Yet, as Talbott pointed out, the information that was faithfully keeping the organism alive for precisely a life time, suddenly goes missing from the body upon death.

    Where does the information go?

    Although materialists/Darwinists hold that the information that was ‘holding that power off for precisely a lifetime’ simply disappears from reality, since they falsely believe information to be ’emergent’ from a material basis’, the fact of the matter is that the information that was ‘holding that power off for precisely a lifetime’ does not simply disappear from reality.

    In fact, in quantum mechanics, information is held to be its own distinct entity. A distinct entity that is separate from matter and/or energy.

    In fact, many leading quantum physicists hold that matter-energy is emergent from a information basis, not the other way around as materialists/Darwinists falsely presuppose:

    “it from bit” Every “it”— every particle, every field of force, even the space-time continuum itself derives its function, its meaning, its very existence entirely—even if in some contexts indirectly—from the apparatus-elicited answers to yes-or-no questions, binary choices, bits. “It from bit” symbolizes the idea that every item of the physical world has a bottom—a very deep bottom, in most instances, an immaterial source and explanation, that which we call reality arises in the last analysis from the posing of yes-no questions and the registering of equipment—evoked responses, in short all matter and all things physical are information-theoretic in origin and this is a participatory universe.”
    – Princeton University physicist John Wheeler (1911–2008) (Wheeler, John A. (1990), “Information, physics, quantum: The search for links”, in W. Zurek, Complexity, Entropy, and the Physics of Information (Redwood City, California: Addison-Wesley))

    “In conclusion, it may very well be said that information is the irreducible kernel from which everything else flows. Thence the question why nature appears quantized is simply a consequence of the fact that information itself is quantized by necessity. It might even be fair to observe that the concept that information is fundamental is very old knowledge of humanity, witness for example the beginning of gospel according to John: “In the beginning was the Word.”
    Anton Zeilinger – Why the Quantum? It from Bit? A Participatory Universe?

    48:24 mark: “It is operationally impossible to separate Reality and Information”
    49:45 mark: “In the Beginning was the Word” John 1:1
    Prof Anton Zeilinger speaks on quantum physics. at UCT – video
    http://www.youtube.com/watch?v=s3ZPWW5NOrw

    “The most fundamental definition of reality is not matter or energy, but information–and it is the processing of information that lies at the root of all physical, biological, economic, and social phenomena.”
    Vlatko Vedral – Professor of Physics at the University of Oxford, and CQT (Centre for Quantum Technologies) at the National University of Singapore, and a Fellow of Wolfson College – a recognized leader in the field of quantum mechanics.

    Moreover, in quantum mechanics, it is information that is primarily conserved, not matter and/or energy.

    Quantum no-hiding theorem experimentally confirmed for first time
    Excerpt: In the classical world, information can be copied and deleted at will. In the quantum world, however, the conservation of quantum information means that information cannot be created nor destroyed. This concept stems from two fundamental theorems of quantum mechanics: the no-cloning theorem and the no-deleting theorem. A third and related theorem, called the no-hiding theorem, addresses information loss in the quantum world. According to the no-hiding theorem, if information is missing from one system (which may happen when the system interacts with the environment), then the information is simply residing somewhere else in the Universe; in other words, the missing information cannot be hidden in the correlations between a system and its environment.
    http://www.physorg.com/news/20.....tally.html

    Quantum no-deleting theorem
    Excerpt: A stronger version of the no-cloning theorem and the no-deleting theorem provide permanence to quantum information. To create a copy one must import the information from some part of the universe and to delete a state one needs to export it to another part of the universe where it will continue to exist.
    http://en.wikipedia.org/wiki/Q.....onsequence

    So where does this ‘conserved’ quantum information, that was holding that power off for precisely a lifetime, go upon death?

    Well, there are ‘theories’ as to where the ‘soul’ goes upon death?

    Special and General Relativity compared to Heavenly and Hellish Near Death Experiences – video (reworked May 2016)
    https://www.facebook.com/philip.cunningham.73/videos/1193118270701104/

    Supplemental note:

    Scientific (physical) evidence that we do indeed have an eternal soul (Quantum DNA and Proteins) – video
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1116313858381546/?type=2&theater

    Verse:

    Mark 8:37
    Or what can anyone give in exchange for their soul?

  35. 35
    PaV says:

    I noticed “butifnot”‘s contribution above, with a linked paper. The best way of understanding what’s going on here is via the work/presence of transposons, and the linked paper appears–at first blush–to help. We should pay attention to it.

    But, assuming transposons are the proximate cause of these differences, the more distal, or first, cause must involve, as I see it, a NGE interpretation of the workings of the transposons, which—in this case—would involve common descent.

    But we’re not necessarily talking about a major taxonomic event here. It is at the level of phyla that CD breaks down. It is also possible that CD breaks down at the level of sub-phyla and classes. Marsupials are an “infraclass” of mammals; that is, kind of a “sub-class.” Ho-hum.

    The reality is that the cell has all kinds of tricks available to it; and this flexibility makes organisms very adaptable: something that a Designer would, I believe, consider important for the cell/organism.

    Dr. Swamidass points out—as I have elsewhere—that one cannot tell the difference between an “act of God” and something completely brought about by NGE.

    Well, what is all this telling us? That we continue to beat a dead horse. My question is, Why?

  36. 36
    REW says:

    VJT
    Very interesting article! (and its interesting for several reasons) A few points:

    Its implied but never stated that all 6 syncytins are functionally equivalent. This could be demonstrated by replacing the mouse syn with the human or cow version(with the possibility that minor tweaking would be needed), but right now there’s every reason to believe that there could just as easily have been one syncytin for all placental mammals. This is not a case of ‘form follows function’

    The ancestral animal that the syn capture occurred in produced viable offspring without the syncytin genes help. But now knocking out the gene would render any placental mammal unable to produce offspring. In other words the syn gene in the context of placenta formation constitutes an irreducibly complex system. This demonstrates that IR systems can evolve from non-IR systems by natural processes.

    You do an excellent job of laying out the case of CD in this example. When an ID proponent is presented with evidence such as this there are 2 ways they can react. They can ignore/misunderstand the evidence and/or focus on irrelevancies. This is what the majority of commenters have done. The other way they can react is to accept the evidence for natural processes in this example but then insist that ID is still a viable explanation for other systems. This is what you’ve done but I’d like to ask you how reasonable this is considering the big picture. Would a designer go to the trouble of carefully crafting living things for a purpose and then passively stand back while random fortuitous events profoundly changed the physiology of those organisms? In all of the cases where you think ID is a viable explanation isn’t it more likely that we just haven’t yet found the evidence, or that the evidence has long since been erased by time?

  37. 37
    PaV says:

    Here, BTW, is the press release for a paper from 2007, and deals with the repercussions of the newly sequenced opposum genome.

    vjt: I think you might like the title of Nat’l Geo article:
    First Decoded Marsupial Genome Reveals “Junk DNA” Surprise

    But, of course, “junk-DNA” is junk, right? 🙂

  38. 38
    snelldl says:

    vjt OP:
    “As an Australian, I feel bound to point out that Dr. Gauger’s description of placental mammals as “true mammals” is biologically incorrect. For example, monotremes (such as the Australian platypus) are mammals that lay eggs, and they don’t have a placenta. Marsupials (such as the kangaroo, the koala and the North American opossum) are mammals that carry their young in a pouch. They also do not have a placenta. Nevertheless, they are true mammals.”

    I suspect that Dr. Gauger is referring to eutherians – “eu” meaning true. As opposed to metatherians and monotremes.

  39. 39
  40. 40
    bornagain77 says:

    Contrary to what Darwinists and Theistic Evolutionists would apparently prefer to believe in the preceding comments, The problem with CD is far, far, bigger than just syncytin genes

    Evolution by Splicing – Comparing gene transcripts from different species reveals surprising splicing diversity. – Ruth Williams – December 20, 2012
    Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,,
    A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species.
    On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,,
    http://www.the-scientist.com/?.....plicing%2F

    Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing – 2016
    In Brief
    Alternatively spliced isoforms of proteins exhibit strikingly different interaction profiles and thus, in the context of global interactome networks, appear to behave as if encoded by distinct genes rather than as minor variants of each other.,,,
    Page 806 excerpt: As many as 100,000 distinct isoform transcripts could be produced from the 20,000 human protein-coding genes (Pan et al., 2008), collectively leading to perhaps over a million distinct polypeptides obtained by post-translational modification of products of all possible transcript isoforms (Smith and Kelleher, 2013).
    http://iakouchevalab.ucsd.edu/.....M_2016.pdf

    Simply put, proteins simply can’t randomly find “strikingly different interaction profiles” for “perhaps over a million distinct polypeptides”:

    “The immediate, most important implication is that complexes with more than two different binding sites-ones that require three or more proteins-are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the last 4 billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable.”
    – Michael Behe – The Edge of Evolution – page 146

    And to remind, Behe’s ‘Edge’ is not just some theoretical musing, but his ‘Edge’ has now been confirmed in the laboratory:

    Michael Behe – Observed (1 in 10^20) Edge of Evolution – video – Lecture delivered in April 2015 at Colorado School of Mines
    25:56 minute quote – “This is not an argument anymore that Darwinism cannot make complex functional systems; it is an observation that it does not.”
    https://www.youtube.com/watch?v=9svV8wNUqvA

    Kenneth Miller Steps on Darwin’s Achilles Heel – Michael Behe – January 17, 2015
    Excerpt: Enter Achilles and his heel. It turns out that the odds are much better for atovaquone resistance because only one particular malaria mutation is required for resistance. The odds are astronomical for chloroquine because a minimum of two particular malaria mutations are required for resistance. Just one mutation won’t do it. For Darwinism, that is the troublesome significance of Summers et al.: “The findings presented here reveal that the minimum requirement for (low) CQ transport activity … is two mutations.”
    Darwinism is hounded relentlessly by an unshakeable limitation: if it has to skip even a single tiny step — that is, if an evolutionary pathway includes a deleterious or even neutral mutation — then the probability of finding the pathway by random mutation decreases exponentially. If even a few more unselected mutations are needed, the likelihood rapidly fades away.,,,
    So what should we conclude from all this? Miller grants for purposes of discussion that the likelihood of developing a new protein binding site is 1 in 10^20. Now, suppose that, in order to acquire some new, useful property, not just one but two new protein-binding sites had to develop. In that case the odds would be the multiple of the two separate events — about 1 in 10^40, which is somewhat more than the number of cells that have existed on earth in the history of life. That seems like a reasonable place to set the likely limit to Darwinism, to draw the edge of evolution.
    http://www.evolutionnews.org/2.....92771.html

  41. 41
    mk says:

    hi guys. here is several problems with this ervs argument:

    1)its a fact that retrovirus need a host and cant survive without it. all experiments so far support this conclusion. so its possible that those retrovirus evolved from the genome and not the other direction.
    2)we know that virus can steal genes (for example the rous sarcoma virus)
    3)we know that a lot of them functional. what is the chance that a virus infacted someone and it not just help him but also get fix in the entire population about 100,000 times for the about 100,000 ervs in the genome?. and if they functional- therefore its good evidence that those ervs are the product of design.
    4) we found ervs that contradict the animals phylogeny (for example the herv-k erv found in chmp and gorila but not human).

  42. 42
    mk says:

    hi vj. you said that :

    “Alternatively, if the genes involved in the formation of the placenta in human beings were in a different location from the corresponding genes in other Old World primates, that would also tell heavily against the theory of common descent.”

    not true. first: we know about counter examples of different locations with the same gene. one example will be the prk gene:

    http://www.biolbull.org/content/227/3/300.abstract

    2)we know about examples of different sine in the same locations(rat and mouse):

    http://www.evolutionnews.org/2.....02847.html

    3)the syncytin gene need for the placenta of the mouse that cant survive without it. so how its evolved in the first place?

    those examples alone falsified dr joshua claims.

  43. 43
    jerry says:

    Are we talking about

    UCD, all species descend from some original organism in the distant past.

    or are we talking about

    CD – that some species descend from other species

    a specific case is humans possibly descending from some ape like species 6-8 million years ago

    UCD and CD are very different things.

    Also

    In this particular OP it is the latter, mammals descending from some other species 160 million years ago. Then this raises several specific questions. For example, what else was added to the first pre mammal species besides a placenta and where are the non placenta species that are very similar to mammals except for a placenta? Because there had to be a gene population to which the virus was added but not all organisms in this gene pool would have received the virus. What happened to them?

    The Mammal class could not have received all its differentiating characteristics in one fell swoop naturally. It had to play out over millions of years and this would leave numerous trails in the fossil record of close but not really mammal species. Where are they? They had to exist for it to happen naturally. Isn’t this the Denton argument that these trails don’t exist in any of the phyla?

    I am looking for a simple explanation as to how this could have happened. Then it would be appropriate to look at specific biological changes that would have to have happened and the likelihood of them all happening naturally. The ID proposition is that this is incredibly improbable.

  44. 44
    jerry says:

    Would a designer go to the trouble of carefully crafting living things for a purpose and then passively stand back while random fortuitous events profoundly changed the physiology of those organisms? In all of the cases where you think ID is a viable explanation isn’t it more likely that we just haven’t yet found the evidence, or that the evidence has long since been erased by time?

    This is a theological argument. It is making a statement about how the designer thinks and assumes one knows the purpose that the designer has in mind. As such is it not an argument that is valid against ID.

    This has always been the defense of naturalistic evolution, since Darwin’s book. Why would the designer create or design a new species for the next island or geographical location. Or why would the designer have just created so many species in general and why the horrible way in which they live. In other words the defense of naturalistic evolution has always relied on theological arguments about the nature of the designer.

    ID makes the case that naturalistic evolution defies rational belief. Why because it is so probabilistically low that all the life form changes could have happen naturally. There must be another explanation. A designer is the most likely explanation. Some people then like to speculate on the motives of the designer(s) but that is not part of ID. Interesting but not ID.

  45. 45
    Mung says:

    VJ Torley:

    As we’ll see, the evidence she puts forward proves precisely the opposite: common descent is the only hypothesis which explains the facts, without resorting to ad hoc suppositions.

    VJ Torley:

    Taken by itself, the hypothesis of common descent is completely agnostic as to whether the different placentas we find in mammals have a single, unified origin in the ancestor of modern-day placentals, or multiple, independent origins in different lineages of placental mammals.

    Am I right to be confused? The second statement seems to directly contradict the first statement.

  46. 46
    vjtorley says:

    Hi everyone,

    In response to readers wondering whether I’ve “jumped the shark,” I’d like to distinguish between two events: the origin of a syncytin gene and its subsequent acquisition by a mammal, through viral transfer. It is the latter event, and not the former, which I hold to be a natural event, requiring no intelligent guidance.

  47. 47
  48. 48
    vjtorley says:

    Hi mk,

    I’m not sure I follow your comment about different locations for the same gene. You cite the example of the prk gene, and you mention this paper:

    http://www.biolbull.org/content/227/3/300.abstract

    Could you quote the relevant passage in the paper which you believe supports your case?

  49. 49
    butifnot says:

    As BA highlights above we are currently massively unaware of even what we don’t know. Much of what has been discovered looks like ingredients and we should be chasing the recipe. Meta-meta-meta-meta control. I wonder just what percent of this Swamidass et all believe we have wrapped up? Just about figured it out, work out a few details? I’m certain CD believers have just plowed by the massively assumptive, circular, preconceived, dismissive of any inconsistent evidence nature of the whole endeavor. Drawing pictures and putting things in charts with valid, yet subjective analyses of ‘data’ that is taken to be the result (and evidence of) of an undemonstrated (as well as impossible) process. UCD adherents commonly seem to caricature what others believe, and are unable to even conceive that there other explanations as consistent/not inconsistent with observation. Witness Swamidass – Your several (2) choices are: God… or several viral infection events… introduced into the mammilian line. Or Swamidass is a thousand miles from reality, fundamentally and foundationally in error. The viruses in question are degenerate products. The theory of ‘evolution’ is largely correct, yet going backwards! Viruses, physics or random events never created anything. Interestingly there should be quite a bit of overlap between even the opposite ends of YEC and materialis evolution with respect to everyone agreeing that living things are descended from previous living things, with a lot of modification, all the way back to the beginning of living things. One positing a single ancestor and the other a plurality.

  50. 50
    butifnot says:

    jerry asks about mammal-like reptiles (now known as synapsids) in the fossil record.

    With Talk Origins submitted I might as well toss out some Woodmorrappe

    http://creation.com/mammal-lik.....ntinuities

    “Evolutionists repeatedly claim that their assembled chain of mammal-like reptiles shows a step-by-step morphological progression to mammals. Despite this, a close and simultaneous examination of hundreds of anatomical character traits shows no such thing, even if one takes basic evolutionary suppositions as a given. Very many, if not most, of the pelycosaur and therapsid traits used in recent evolutionistic studies to construct cladograms actually show a contradictory pattern of progression towards, followed by reversion away from, the presumed eventual mammalian condition. Furthermore, gaps are systematic throughout the pelycosaur-therapsid-mammalian ‘sequence’, and these gaps are actually larger than the existing segments of the ‘chain’. These sobering facts demonstrate that, however the supposed evolutionary ‘lineage’ of mammal-like reptiles towards mammals is interpreted, it is divorced from reality.”

    (2001)
    “The highly-touted, alleged succession of mammal-like reptiles towards increasing ‘mammalness’ is not found at any one location on Earth. It can only be inferred through the correlation of fossiliferous beds from different continents. Judgments are made as to which stratum on one continent is older than another stratum on another continent. Moreover, intercontinental correlations are made even when the fossil genera do not correspond with each other. Instead, the correlations are based on the general similarity of specimens, as well as their assumed degree of evolutionary advancement.1 The circularity of such reasoning is obvious. Thus, despite the claims of some evolutionists, it is clear that such biostratigraphic correlations are not empirically self-evident:”

  51. 51
  52. 52
    mk says:

    hi vj. the prk gene was move from one species to another. so its in a different chromosome as far as i know. we also have another examples like this one:

    https://aeon.co/essays/genes-that-jump-species-does-this-shake-the-tree-of-life

    “They would find, for example, nearly identical sequences of DNA in mice and rats, but not in squirrels; and the same sequence would turn up in nocturnal primates known as bushbabies, but not in other primate species. It was highly unlikely that mice, rats and bushbabies had independently evolved the exact same chunk of DNA. Further complicating things, these puckish strings of DNA were not in the same position on the same chromosome in different species, as you would expect if they had been inherited the traditional way – rather, their locations were highly variable.”

    so according to evolution its possible to get the same gene in a different location without any problem for evolution. therefore evolution doesnt predict this. i also have other evidence against other dr joshua claims.

    have a nice day.

  53. 53
    bornagain77 says:

    as to:

    “I’d like to distinguish between two events: the origin of a syncytin gene and its subsequent acquisition by a mammal, through viral transfer. It is the latter event, and not the former, which I hold to be a natural event, requiring no intelligent guidance.”

    And, borrowing Torley’s hypothesis, I would also like to propose that while Shakespeare may have wrote the sentence “Methinks it is like a weasel” a natural event, instead of Shakespeare himself, randomly placed that sentence in Hamlet.

    But then again, I just may be mistaken about my hypothesis of natural events randomly inserting “Methinks it is like a weasel” into Hamlet since natural events can’t ‘see’ context (Eric Larson – What is a Mind? 2014).

    In other words, the context in which the weasel phrase finds its meaning in Hamlet is derived from several different levels of the play. i.e. The ENTIRE play, who said it, why was it said, where was it said, and even nuances of the Elizabethan culture, etc… are taken into consideration to provide proper context to the phrase.
    The Weasel phrase simply does not make sense without taking its proper context into consideration

    A Meaningful World: How the Arts and Sciences Reveal the Genius of Nature – Book Review
    Excerpt: They focus instead on what “Methinks it is like a weasel” really means. In isolation, in fact, it means almost nothing. Who said it? Why? What does the “it” refer to? What does it reveal about the characters? How does it advance the plot? In the context of the entire play, and of Elizabethan culture, this brief line takes on significance of surprising depth. The whole is required to give meaning to the part.
    http://www.thinkingchristian.n.....821202417/

    It is also interesting to note what the specific context is for the “Methinks it is like a weasel” phrase is.
    The context in which the phrase is used is to illustrate the spineless nature of one of the characters of the play. i.e. To illustrate just how easily the spineless character in the play can be led around by the nose to say anything that Hamlet wants him to say:

    Ham. Do you see yonder cloud that ’s almost in shape of a camel?
    Pol. By the mass, and ’t is like a camel, indeed.
    Ham. Methinks it is like a weasel.
    Pol. It is backed like a weasel.
    Ham. Or like a whale?
    Pol. Very like a whale.
    http://www.bartleby.com/100/138.32.147.html

    Though Dawkins infamously used this phrase to try to disprove Intelligent Design in an evolutionary algorithm, after I realized what the actual context of the ‘Methinks it is like a weasel’ phrase was, I remember thinking to myself that it was perhaps the worse possible phrase that Dawkins could have possibly chosen to use to try to illustrate his point.
    Especially since the phrase, when taken into proper context, reveals deliberate, nuanced, deception and manipulation of another person.
    I’m fairly sure that deception and manipulation of another person is hardly the overall point that Dawkins was wishing to convey with his ‘Weasel’ program.

    But is this ‘context dependency’ that is found in literature also found in life? Yes! Abundantly more so! Although Hamlet is Shakespeare’s longest play at 4024 lines,,,

    A complete list of all the plays in order, from longest to shortest. Shakespeare
    1. Hamlet – 4024 lines,,,
    https://www.playshakespeare.com/study/play-lengths

    4024 lines is literally nothing, (pun intended), compared to the up to a million unique polypeptides generated by our 20,000 genes that typify the billion-trillion protein molecules of a human body.

    Moreover, much like the words we use, many, if not all, of these up to a million unique polypeptides ‘take on different roles in different molecular contexts’

    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 Disordered 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
    http://darwins-god.blogspot.co.....rt-ii.html

    Genes Code For Many Layers of Information – They May Have Just Discovered Another – Cornelius Hunter – January 21, 2013
    Excerpt: “protein multifunctionality is more the rule than the exception.” In fact, “Perhaps all proteins perform many different functions,,,.”
    http://www.fasebj.org/content/23/7/2022.full

    Moreover, contrary to Darwinian thought, the position and organization of genes on the chromosome is not arbitrary

    Refereed scientific article on DNA argues for irreducible complexity – October 2, 2013
    Excerpt: This paper published online this summer is a true mind-blower showing the irreducible organizational complexity (author’s description) of DNA analog and digital information, that genes are not arbitrarily positioned on the chromosome etc.,,
    ,,,First, the digital information of individual genes (semantics) is dependent on the the intergenic regions (as we know) which is like analog information (syntax). Both types of information are co-dependent and self-referential but you can’t get syntax from semantics. As the authors state, “thus the holistic approach assumes self-referentiality (completeness of the contained information and full consistency of the different codes) as an irreducible organizational complexity of the genetic regulation system of any cell”. In short, the linear DNA sequence contains both types of information. Second, the paper links local DNA structure, to domains, to the overall chromosome configuration as a dynamic system keying off the metabolic signals of the cell. This implies that the position and organization of genes on the chromosome is not arbitrary,,,
    http://www.christianscientific.....omplexity/

    Also of note, the following excerpt provides a particularly lucid example that clearly illustrates the primacy of context over any material particulars of an organism:

    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]“,,,
    http://www.thenewatlantis.com/.....nisms-mean

    Perhaps Torley can forgive me for ‘unscientifically’ postulating a ‘soul’ so as to provide the adequate ‘context’ for the billion-trillion protein molecules of a human body to adhere to, as single cohesive whole, for precisely a lifetime and not a moment longer?

    Scientific (physical) evidence that we do indeed have an eternal soul (Quantum DNA and Proteins) – video
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1116313858381546/?type=2&theater

    Verse, Quote, and Music

    James 2:26
    For just as the body without the spirit is dead, so also faith without works is dead.

    “There are more things in heaven and earth, Horatio,
    Than are dreamt of in your philosophy.”
    – Hamlet (1.5.167-8), Hamlet to Horatio
    – Shakespeare

    Jewel – Who will save your soul
    https://www.youtube.com/watch?v=-LukEq643Mk

  54. 54
    tjguy says:

    Mung @3

    I can understand how common descent can explain anatomical similarities.

    Yes, common descent can explain SOME anatomical similarities, but the problem is, it cannot explain them all.

    So then you have to assume common descent to explain away the data that does not fit. Maybe that’s too simply a conclusion, but I would think if the hypothesis cannot explain all the data, perhaps it is not accurate.

  55. 55
    bill cole says:

    VJT
    Ok lets assume some how the gene poofed into existence and is available through HGT and common retro viruses.

    Lets start with the origin of the first mammal that used a placenta to carry their children prior to birth.

    The birthing system including the placenta needs to be built. This in itself is a very complex process that requires cell differentiation. The DNA needs to have specific parts turned off for the proper tissue to form.

    According to a paper I read yesterday this involves the coordinated expression of 762 micro RNA’s. If we want to go out on a limb:-) and assume that a complex system required design which involved the coordination of hundreds of thousands of nucleotides in the genome and the syncytin gene was part of that system design, why would that gene come about by HGT where all other parts of the system did not?

    I think Ann has created a land mark case for ID with this argument and should be congratulated. I am grateful that you and Joshua came up with a counter argument to test it.

    Based on this case, I think common decent is speculative at best and creates confusion for the science.

    What we are observing is common biochemical mechanisms and different biochemical mechanisms.

  56. 56
    Andre says:

    Naturalism absolutely requires magic to work. I don’t think I have enough faith.

  57. 57
    vaccine says:

    Dr. Ann Gauger basically said she finds the arguments for common ancestry compelling but find the ways it fails more convincing. She said if common ancestry were true we should expect ABC but observe XYZ.
    VJ Torley basically said, it evolved, it appeared, it just happened.
    I find Dr Gauger made a more convincing case.

    Also, what kind of doubletalk is this:
    “What we need to keep in mind is that the evolution of the mammalian placenta would have required a large number of steps.”
    “Nor do we know exactly how many steps would have been required.”
    So, you don’t know how many were required, but it would have required a large number.

  58. 58
    Peer says:

    The capture and integration of “viruses”, the cocommitant precise excision of regulatory sequences to account for the syncytin loci in mammals is highly unlikely and far less parsimonous as the scenario proposed here:

    http://creation.com/images/pdf.....05-112.pdf

    In other words, the evolutionists still have cause and effect up-side-down. We are not dealing with remnants of viruses, rather we are dealing with regulatory and structurla elements of the genome, which can easily mutate into viruses.

    PT

  59. 59
    Dionisio says:

    tjguy @54

    Yes, common descent can explain SOME anatomical similarities, but the problem is, it cannot explain them all.

    Can it explain the “delta dev” issue posted @4? 🙂

  60. 60
    Dionisio says:

    bill cole @55

    According to a paper I read yesterday […]

    Please, can you write the title, DOI code or another reference to that paper, so I can read it too?
    You may post it in the thread “Mystery at the heart of life”.
    Thank you!

  61. 61
    Dionisio says:

    bornagain77 @53

    But is this ‘context dependency’ that is found in literature also found in life? Yes! Abundantly more so!

    Aren’t there many examples of pleiotropic entities in biology? Same DNA segments being used to express different proteins or ncRNAs through post-transcriptional splicing or post-translational modifications?
    Same proteins or ncRNA used by the biological systems differently depending on the context?
    Isn’t that often seen in the recent research papers?
    What are the mechanisms behind that pleiotropic activity?
    What are the mechanisms behind those contextual decisions?
    What are the mechanisms behind the contextual pleiotropic mechanisms?
    What’s behind all those interwoven spatiotemporally precise and robust signaling pathways and regulatory networks with myriad of feedback and feed-forward loops, oscillators, the whole nine yards, all masterfully choreographed to produce intended effects, operating within hostile stochastic environments saturated with different thermodynamic noise?
    How long can it take for a person to see all that and at least humbly admit that it’s so amazingly fascinating?
    Well, it could take forever if the person doesn’t want to admit it. After all, humility is not included in our birth package. It’s not a natural attribute.
    That’s why even their own reductionist mechanistic approaches to research could lead to those same conclusions too, if only one is open-minded and think out of the established (and sometimes imposed?) box.
    It doesn’t matter how one looks at this, the same logical conclusion can be drawn.

  62. 62
    Peer says:

    “Precisely. This is just what the hypothesis of common descent would predict.”

    The issue is not common descent perse, but whether life is monophyletic or polyphyletic. And whether or not ERVs are remnants of viruses. The latter can be dismissed for biological (gene regulatory) reasons. So, it must be the other way around. RNA viruses originate in the genome by recombining and taking up pieces of genes. This is a non-random phenomenon on LTRs, which are better described as eukaroytic promoters for global gene transcription. By picking up the syncytine gene, which yields fusing capacities to tranposbale elements, RNA viruses in different primates can arise independently. The other scenario, RNA viruses integrating in and providing the syncytine gene is so highly unlikely, it will never happen. It involves at least 6 very unlikely genetic events including precision cut-paste mechanisms of which we do not find any evidence in the genomes. I recommend to read this:

    http://creation.com/images/pdf.....05-112.pdf

    The paper is for free and may open your eyes. I have linked this paper several times before, but nobody seems to be reading it. People who are interested in how genomes work, and want to know what has been mixed up by main stream science, should read it.

    If ERVs are not remnants of viruses, but rather provirus stages, as I demonstrate, life is most likely polyphyletic with many independent origins of similar genetic structures, and we also have a scientific understanding of the origin of RNA viruses.

  63. 63
    bornagain77 says:

    Dionisio, along that line of thought,,,

    Genes and Organisms: Improvising the Dance of Life – Stephen L. Talbott – Nov. 10, 2015
    Excerpt: The performances of countless cells in your body are redirected and coordinated as part of a global narrative for which no localized controller exists. This redirection and coordination includes a unique choreography of gene expression in each individual cell. Hundreds or thousands of DNA sequences move (or are moved) within vast numbers of cell nuclei, and are subjected to extraordinarily nuanced, locally modulated chemical activity so as to contribute appropriately to bodily requirements that are nowhere codified — least of all in those DNA sequences.,,,
    DNA in its larger matrix
    You may recall from my earlier article, “Getting Over the Code Delusion” (Talbott 2010), that packing DNA into a typical cell nucleus is like packing about 24 miles of very thin, double-stranded string into a tennis ball, with the string cut up (in the normal human case) into 46 pieces, corresponding to our 46 chromosomes.
    To locate a protein-coding gene of typical size within all that DNA is like homing in on a one-half-inch stretch within those 24 miles. Or, rather, two relevant half-inch stretches located on different pieces of string, since we typically have two copies of any given gene. Except that sometimes one copy differs from the other and one version is not supposed to be expressed, or one version needs to be expressed more than the other, or the product of one needs to be modified relative to the other. So part of the job may be to distinguish one of those half-inch stretches from the other. “Decisions” everywhere, it seems.
    But no such decisions are made in a vacuum. As it happens, the chromosome does not consist of a naked DNA double helix. Our DNA, rather, is bound up with a massive, intricate, and dynamic protein-RNA-small molecule complex (called chromatin) that is as fully “informative” for the cell as the DNA sequence itself — and, you might say, much more active and directive.,,,
    the cell, by managing the shifting patterns of the chromatin infrastructure within which DNA is embedded, brings our chromosomes into movement on widely varying scales. These include large looping movements that put particular genes into connection with essential regulatory sequences and with other, related genes (that is, with other one-half inch stretches of our “24 miles of string in a tennis ball”).,,,
    A gene is not in any case the kind of rigidly defined entity one might hope to calculate with. As a functional unit appropriate to current circumstances, it must be cobbled together by the cell according to the needs of the moment. There is no neatly predefined path to follow once the cell has located the “right” half inch or so of string, or once it has done whatever is necessary to bring that locus into proper relation with other chromosomal loci participating in the same “dance”.
    One issue has to do with the fact that there are two strands in the DNA double helix and, starting from any particular point, it is possible to transcibe either of two DNA sequences in either of two directions: “forward” along one strand, or “backward” along the other. This yields two completely different products. One of them is very likely not even a protein-coding RNA, and yet it may still play a vital role in gene expression and in cellular processes more generally.
    And even when the cell would proceed in one particular direction, it must “choose” the exact point in the genetic sequence at which to begin. Different starting points can yield functionally distinct results. “Many studies focusing on single genes have shown that the choice of a specific transcription start site has critical roles during development and cell differentiation, and aberrations in . . . transcription start site use lead to various diseases including cancer, neuropsychiatric disorders, and developmental disorders”.8,,,
    The (protein) enzyme that transcribes DNA into RNA is RNA polymerase12. The enzyme certainly does not work alone, however, and its task is by no means cut-and-dried. To begin with, its critical interactions with various elements of the pre-initiation complex help determine whether and exactly where transcription will begin, if it is to begin at all. Then, after those “decisions” have been made, RNA polymerase moves along the double helix transcribing the sequence of genetic “letters” into the complementary sequence of an RNA.
    Throughout this productive journey, which is called elongation, the RNA polymerase still keeps good and necessary company. Certain co-activators modify it during its transit of a genetic locus, and these modifications not only enable transcription elongation to begin, but also provide binding sites for yet other proteins that will cooperate throughout the transcription journey.,,,
    Finally — and mirroring all the possibilities surrounding initiation of gene transcription — there are the issues relating to its termination. Again, they are far too many to mention here. Transcription may conclude at a more or less canonical terminus, or at an alternative terminus, or it may proceed altogether past the gene locus, even to the point of overlapping what, by usual definitions, would be regarded as a separate gene farther “downstream”. The cell has great flexibility in determining what, on any given occasion, counts as a gene, or transcriptional unit.
    The last part of the transcribed gene is generally non-protein-coding, but nevertheless contains great significance. Examining this region in a single gene, a research team recently identified “at least 35 distinct regulatory elements” to which other molecules can bind.13 Further regulatory potentials arise from yet more binding sites on the customized “tail” that the cell adds to the RNA immediately upon conclusion of its transcription.
    Proteins and other molecules that bind to the various regulatory elements of the non-protein-coding portion of the transcript do so in a context-sensitive manner, where cell and tissue type, phase of the cell cycle, developmental stage, location of the RNA within the cell, and environmental factors, both intra- and extra-cellular, may all play a role. These converging influences can change the stability of the RNA, change its localization within the cell, and change the efficiency of its translation into protein, among other possibilities.,,,
    What is generally considered the post-transcriptional modulation of gene expression actually begins during transcription proper. A prime example has to do with what happens partly as a result of the pauses during elongation.
    Cells don’t just passively accept the RNAs that emerge from the transcription process, but rather “snip and stitch” them via an elaborate procedure known as RNA splicing. It happens that the cutting out and knitting together of selected pieces typically begins before the RNA is fully transcribed, and the rhythm of pauses during elongation has an important influence upon which pieces form the mature transcript.
    This splicing operation, which is applied to nearly all human RNAs, is performed by the spliceosome, consisting of a few non-protein-coding RNAs and over 300 cooperating proteins, and is hardly less exacting in its requirements than, say, brain surgery.
    For the vast majority of human genes the operation can be performed in different ways, yielding distinct proteins (called isoforms) from a single RNA derived from a single DNA sequence. This is called alternative splicing, and it would be hard to find anything in human development, disease etiology, or normal functioning that is not dependent in one way or another on the effectiveness of this liberty the cell takes with its gene products.
    But RNA splicing is hardly the end of it. Through RNA editing the cell can add, delete, or substitute individual “letters” of the RNA sequence.15 Or, leaving the letters in place, the cell can chemically modify them in any of over one hundred different ways.16 ,,,
    Eventually, a protein-coding RNA needs to be translated into protein. This happens by means of large molecular complexes called “ribosomes”. Just as with gene transcription, there are many associated factors that must work together to bring about the initiation of translation, many that cooperate with the ribosome during translation, and yet others that play a role in modifying, localizing, or otherwise regulating the newly produced protein.
    The overall picture of gene expression is one of unsurveyable complexity in the service of remarkably effective living processes.,,,
    A decisive problem for the classical view of DNA is that “as cells differentiate and respond to stimuli in the human body, over one million different proteins are likely to be produced from less than 25,000 genes”.30 Functionally, in other words, you might say that we have over a million genes.,,,
    http://www.natureinstitute.org.....nes_29.htm

    And despite all that mind blowing, overlapping, integrated complexity being found in life, we still read that finding a lack of ‘random’ collisions in a crowded cell is a ‘counterintuitive surprise’ for researchers:

    Proteins put up with the roar of the crowd – June 23, 2016
    Excerpt: It gets mighty crowded around your DNA, but don’t worry: According to Rice University researchers, your proteins are nimble enough to find what they need.
    Rice theoretical scientists studying the mechanisms of protein-DNA interactions in live cells showed that crowding in cells doesn’t hamper protein binding as much as they thought it did.,,,
    If DNA can be likened to a library, it surely is a busy one. Molecules roam everywhere, floating in the cytoplasm and sticking to the tightly wound double helix. “People know that almost 90 percent of DNA is covered with proteins, such as polymerases, nucleosomes that compact two meters into one micron, and other protein molecules,” Kolomeisky said.,,,
    That makes it seem that proteins sliding along the strand would have a tough time binding, and it’s possible they sometimes get blocked. But the Rice team’s theory and simulations indicated that crowding agents usually move just as rapidly, sprinting out of the way.
    “If they move at the same speed, the molecules don’t bother each other,” Kolomeisky said. “Even if they’re covering a region, the blockers move away quickly so your protein can bind.”
    In previous research, the team determined that stationary obstacles sometimes help quicken a protein’s search for its target by limiting options. This time, the researchers sought to define how crowding both along DNA and in the cytoplasm influenced the process.
    “We may think everything’s fixed and frozen in cells, but it’s not,” Kolomeisky said. “Everything is moving.”,,,
    Floating proteins appear to find their targets quickly as well. “This was a surprise,” he said. “It’s counterintuitive, because one would think collisions between a protein and other molecules on DNA would slow it down. But the system is so dynamic (and so well designed?), it doesn’t appear to be an issue.”
    http://phys.org/news/2016-06-p.....crowd.html

    And exactly why should researchers find such a lack of random collisions in the cell to be “counterintuitive”? Short answer is because of late 19th, early twentieth, century materialism:

    Molecular Biology – 19th Century Materialism meets 21st Century Quantum Mechanics – video
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1141908409155424/?type=2&theater

  64. 64
    Dionisio says:

    BA77

    Good point.
    Also thank you for the interesting links.

  65. 65
    bill cole says:

    Dionisio

    . A PubMed search for the keywords “miRNA” and “trophoblast” or “placenta,” yields 137 results, the first paper having been published in 2006. One seminal study that set the de novo landscape of miRNA-regulation in cells of the trophoblast lineage, was published in 2012 by Morales-Prieto et al. (2012). There, the authors screened 762 human miRNAs for their expression level in term and first trimester cytotrophoblasts, as well as in four cell lines:

    Front. Genet., 21 November 2013 | http://dx.doi.org/10.3389/fgene.2013.00248
    Trophoblasts, invasion, and microRNA

  66. 66
    Dionisio says:

    BA77

    Posted references to the original papers behind the article on proteins target searching in crowded environments:

    http://www.uncommondescent.com.....ent-612219

    Note that the same folks have published a few papers on the same subject.
    Sometimes it takes time and perseverance to get to the bottom of an issue.

    Thank you for posting the link to the interesting paper.

  67. 67
    Dionisio says:

    bill cole @64

    Thank you for sharing the reference to that interesting paper!

  68. 68
    bill cole says:

    Peer

    The paper is for free and may open your eyes. I have linked this paper several times before, but nobody seems to be reading it. People who are interested in how genomes work, and want to know what has been mixed up by main stream science, should read it.

    http://creation.com/images/pdf.....05-112.pdf

    I just read your paper for the first time and find it a very credible argument that the syncytine gene is in mammals proceeded the env version. I recommend everyone with some understanding of biochemistry read Peer’s paper.

  69. 69
    vaccine says:

    The genes line up by clade seems a good case, but as a skeptic I have to ask, how do you know an ERV didn’t just happen to put it in the same place in mice and rats, mimicking common ancestry? It could be said a virus insertion in the same place in two species is an extremely unlikely event, but you’ve already invoked an extremely unlikely event to explain the six independent origins. What, apart from presuming common ancestry, is there about the syncytin gene that allows you to distinguish whether it was put there by an ERV or inherited? This is just another case of common ancestry being invoked as evidence for common ancestry.

  70. 70
  71. 71
    bornagain77 says:

    Falsification of Natural Selection and Universal Common Descent Within Population Genetics – video
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1227292020617062/?type=2&theater

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