The amazing placenta: A reply to Dr. Ann Gauger

_{Vincent Torley

June 30, 2016

Evolution, Intelligent Design}

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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.

Comments

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).mk_{July 2, 2016
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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/?articles.view%2FarticleNo%2F33782%2Ftitle%2FEvolution-by-Splicing%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/publications/Yang_Cell_OMIM_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/2015/01/kenneth_miller_1092771.html
bornagain77_{July 2, 2016
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Let's discuss: http://jvi.asm.org/content/77/7/3893Dr JDD_{July 2, 2016
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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.snelldl_{July 2, 2016
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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? :)PaV_{July 2, 2016
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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?REW_{July 2, 2016
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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?PaV_{July 2, 2016
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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/2015/11/it_really_isnt100911.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/publications/the-unbearable-wholeness-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/2011-03-quantum-no-hiding-theorem-experimentally.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/Quantum_no-deleting_theorem#Consequence
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?
bornagain77_{July 2, 2016
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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.bill cole_{July 2, 2016
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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.Dionisio_{July 2, 2016
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To Whom This May Concern: you may want to see the papers referenced @1019-1021 here: https://uncommondescent.com/evolution/a-third-way-of-evolution/#comment-612074Dionisio_{July 2, 2016
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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. :)Dionisio_{July 2, 2016
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"viruses make placentas"
Just when you think things couldn't get more ridiculous ...Origenes_{July 2, 2016
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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.com/2014/02/richard-dawkins-how-could-anyone.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/2016/01/reviewing_the_e102281.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.com/2010/05/new-model-for-evolution-rhizome.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.com/2014/06/more-fossil-molecule-contradictions-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/2014/02/the_ghost_of_te081981.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/articles/salvo27/logged-out.php
bornagain77_{July 2, 2016
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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.Dionisio_{July 2, 2016
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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)Anaxagoras_{July 2, 2016
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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.Anaxagoras_{July 2, 2016
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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?Andre_{July 2, 2016
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@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.Prof. S. Joshua Swamidass_{July 1, 2016
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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/science/article/pii/S0143400409004135caleb_{July 1, 2016
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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/hgTracks?org=Human&db=hg38&position=chr7:92468380-92477986 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.bill cole_{July 1, 2016
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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...drc466_{July 1, 2016
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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.thegospelandevolution.com/StoryInOurGenes/audio-slides/2of2/ http://www.thegospelandevolution.com/about-this-blog/ http://biologos.org/blogs/archive/evolution-and-the-gospel-from-enemy-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.Prof. S. Joshua Swamidass_{July 1, 2016
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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/biology/professors/srenn/pages/teaching/BIO431S05_2008/431S05_readings/431s05_examples/king_wilson_1975(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/?articles.view%2FarticleNo%2F33782%2Ftitle%2FEvolution-by-Splicing%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/pmc/articles/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/publications/Yang_Cell_OMIM_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)bornagain77_{July 1, 2016
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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
bornagain77_{July 1, 2016
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How do you know viruses didn't evolve from existing mammalian sequences?Dr JDD_{July 1, 2016
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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?Robert Sheldon_{July 1, 2016
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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.Dionisio_{July 1, 2016
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....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.butifnot_{July 1, 2016
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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.mw_{July 1, 2016
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Stages in the evolution of the mammalian placenta

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

Is the placenta likely to have been designed?

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

What singular predictions does the hypothesis of common descent make?

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

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