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The amazing placenta: A reply to Dr. Ann Gauger


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.

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 bornagain77
More evidence of common descent: On the Diversification of Fur, Feathers, and Scales Mung
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. vaccine
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/pdfs/tj/j27_3/j27_3_105-112.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. bill cole
bill cole @64 Thank you for sharing the reference to that interesting paper! Dionisio
BA77 Posted references to the original papers behind the article on proteins target searching in crowded environments: https://uncommondescent.com/intelligent-design/mystery-at-the-heart-of-life/#comment-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. 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 bill cole
BA77 Good point. Also thank you for the interesting links. Dionisio
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/txt/st/org/comm/ar/2015/genes_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-proteins-roar-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
"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/pdfs/tj/j27_3/j27_3_105-112.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. Peer
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. Dionisio
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! Dionisio
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? :) Dionisio
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/pdfs/tj/j27_3/j27_3_105-112.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 Peer
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. vaccine
Naturalism absolutely requires magic to work. I don't think I have enough faith. Andre
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. bill cole
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. tjguy
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.net/C228303755/E20060821202417/
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.com/2010/08/gene-myth-part-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.org/refereed-scientific-article-on-dna-argues-for-irreducibly-complexity/
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/publications/what-do-organisms-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
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. mk
Pretty interesting old world artwork of synapsids? http://s8int.com/images4/pompeii-4.jpg http://creationwiki.org/pool/images/1/1d/Killing_dragons_by_Collaert_after_Stradanus_c1640.jpg http://s8int.com/images4/nile-extinct-4a.jpg http://s8int.com/images4/nile-extinct-4c.jpg http://creationwiki.org/File:Dinosaur_in_nile_mosaic.JPG butifnot
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-like-reptiles-major-trait-reversals-and-discontinuities "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:" butifnot
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. butifnot
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? vjtorley
jerry asks about mammal-like reptiles (now known as synapsids) in the fossil record. The following sites might be of interest: http://morgana249.blogspot.jp/2014/08/5-ancient-mammal-like-reptiles.html http://www.tor.com/2014/02/05/nine-of-your-relatives-that-ruled-before-dinosaurs/ https://www.sciencedaily.com/releases/2016/04/160425112655.htm Regarding the evolution of mammals, please see the following links: http://www.talkorigins.org/faqs/comdesc/section1.html#morphological_intermediates_ex2 https://en.wikipedia.org/wiki/Evolution_of_mammals http://naturalhistory.si.edu/mammals/pages/how/ Enjoy! vjtorley
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. vjtorley
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. Mung
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. jerry
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. jerry
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/2016/05/in_arguments_fo102847.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. mk
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