CharlieM, I am not quite sure how any of your post below is meant as a response to mine but I will try to figure out what you are trying to assert with your latest quotes.

CharlieM wrote:Do you consider transposons to be random mutations? Here is an excerpt from an article entitled, 'Invasion of Genomic Parasites Triggered Modern Mammalian Pregnancy, Study Finds' at http://www.sciencedaily.com/releases/2011/09/110925185434.htm

The Yale team studying the evolutionary history of pregnancy looked at cells found in the uterus associated with placental development. They compared the genetic make-up of these cells in opossums -- marsupials that give birth two weeks after conception -- to armadillos and humans, distantly related mammals with highly developed placentas that nurture developing fetuses for nine months.
They found more than 1500 genes that were expressed in the uterus solely in the placental mammals. Intriguingly, note the researchers, the expression of these genes in the uterus is coordinated by transposons -- essentially selfish pieces of genetic material that replicate within the host genome and used to be called junk DNA.
"Transposons grow like parasites that have invaded the body, multiplying and taking up space in the genome," said Vincent J. Lynch, research scientist in EEB and lead author of the paper.
But they also activate or repress genes related to pregnancy, he said.

1500 difference between placentals and other mammals in the uterine system, that's a fair bit of mutation going on.

So these lumps of parasitic waste have managed to pull themselves out of the rubbish tip and now have the important job of making sure pregnancy goes to plan. How do we know that these transposons started out as accidental insertions? Because they selfishly replicate themselves but perform no useful functions. But what about the ones found to have important regulatory functions? Well obviously they were co-opted into their present function. But how do we know that they haven't performed this function from the beginning? Because they are transposons and we know that transposons are parasitic selfish inserts. And how do we know this? Because they perform no useful function.....Stop the bus I want to get off.

The simple explanation is that the difference between placentals and marsupials had to come from somewhere. Mutations to the genome however they arise can be co-opted into service. If transpositions have been co-opted to have important regulatory functions so what.

As to your aspersions about circular reasoning I can see no indication in that quote that warrants your conclusion that any circular reasoning was employed to arrive at the understanding that transposons were in fact involved in gene expression.

I see no confirmation here that anything had to be guided in an way.

CharlieM wrote:Then there is the article below:
http://www.sciencedaily.com/releases/2011/07/110721121547.htm

"House mice not only have become resistant to rat poisons in the 'usual' way, but also in a very 'unusual' way, through interbreeding with a separate mouse species that is removed by 1.5 to 3 million years," said Michael Kohn of Rice University. "Our work is perhaps the first to catch this unusual process in the act."...

"Nature will respond to challenges in the most creative ways, even if challenges are human-made and presumably foolproof," Kohn said. On the other hand, he added, evolution might be more predictable in some ways than we had imagined. After all, the very same gene and gene pathway has evolved multiple times to confer resistance to warfarin in both mice and rats. "Understanding such constraints and the mechanisms by which evolution proceeds will be critical for our continued ability to stay one step ahead of evolved resistances in the animals, plants, and microbes that we wish to control," he said.

Random mutations were not so prevailent that they prevented different species of mice from interbreeding after 1.5 to 3 million years, but they have managed to alter the genome in several different species and even genera in the same way so as to confer resistance to warfarin. The evidence points to conservation of the kind and convergence rather than divergence.

Just because random mutations have built up after 1.5 to 3 million years between two different lineages does not mean to say that they are necessarily going to produce genetic incompatibilities. That genetic incompatibilities generally do arise is not a "rule" of evolutionary theory, it's just something that can and often does happen. The fact that several different species from different genera still have the same parts of the genome that can mutate and be selected in the same way to an environmental pressure is not in any way surprising either. The simple fact that random mutations take place and can take place in the same genes in different species to confer an extreme advantage in this case just means that it is more likely to happen because of these extreme conditions. Just because mutations are random does not mean that they cannot occur in the same place in the genome in different species, it may be unlikely but that does not mean to say that it would be impossible. Again I see no reason to conclude that anything requires to be guided in this scenario.

CharlieM wrote:More of the same at::
http://www.sciencedirect.com/science/article/pii/S0168952510001289

Convergent phenotypes provide extremely valuable systems for studying the genetics of new adaptations. Accumulating studies on this topic have reported surprising cases of convergent evolution at the molecular level, ranging from gene families being recurrently recruited to identical amino acid replacements in distant lineages. Together, these different examples of genetic convergence suggest that molecular evolution is in some cases strongly constrained by a combination of limited genetic material suitable for new functions and a restricted number of substitutions that can confer specific enzymatic properties. We discuss approaches for gaining further insights into the causes of genetic convergence and their potential contribution to our understanding of how the genetic background determines the evolvability of complex organismal traits.

More evidence that life is guided along a limited path.

Just because there is a limited path because of constraints on how beneficial random mutations can produce viable outcomes does not man that there is any guidance along that path. In fact these cases of constraints make it more likely that evolution will take these paths even if the mutations themselves are random. We know there are constraints on what changes are viable, we know that evolution is not entirely random but this does not show that there is any guidance to the process whatsoever.

What is it with these types of posters that makes them post seemingly random quotes to support their assertions that never appear to actually support their position?

You posted a video and then said:

Rumraket wrote:That was a video on this paper:

On the origin of the translation system and the genetic code in the RNA world by means of natural selection, exaptation, and subfunctionalization
http://www.biology-direct.com/content/2/1/14

I'm not sure why you linked to a paper by Koonin to make your case. He believes that a translation-replication system cannot appear by chance. That's why he goes with the multiverse theory. Working within this one given universe he makes a generous estimate that the probability of this system occuring would be P < 10^-1018.

As they say in the paper you linked to:

Although the individual ribozyme-catalyzed reactions involved in the postulated scheme are feasible, the succession of multiple evolutionary steps that appear to be required for the emergence of translation might be legitimately viewed as far fetched, particularly, considering the inevitably inefficient ribozyme-mediated replication that must have been prevalent in the RNA World. Be as it may, this is, at present, our best effort to develop a conceptual model for the origin of translation. Elsewhere, one of us (EVK) examines a radical alternative [17].

And here is Koonin from his link (http://www.biology-direct.com/content/2/1/15)

Hypothesis
Origin of life is a chicken and egg problem: for biological evolution that is governed, primarily, by natural selection, to take off, efficient systems for replication and translation are required, but even barebones cores of these systems appear to be products of extensive selection. The currently favored (partial) solution is an RNA world without proteins in which replication is catalyzed by ribozymes and which serves as the cradle for the translation system. However, the RNA world faces its own hard problems as ribozyme-catalyzed RNA replication remains a hypothesis and the selective pressures behind the origin of translation remain mysterious. Eternal inflation offers a viable alternative that is untenable in a finite universe, i.e., that a coupled system of translation and replication emerged by chance, and became the breakthrough stage from which biological evolution, centered around Darwinian selection, took off. A corollary of this hypothesis is that an RNA world, as a diverse population of replicating RNA molecules, might have never existed. In this model, the stage for Darwinian selection is set by anthropic selection of complex systems that rarely but inevitably emerge by chance in the infinite universe (multiverse).
Conclusion
The plausibility of different models for the origin of life on earth directly depends on the adopted cosmological scenario. In an infinite universe (multiverse), emergence of highly complex systems by chance is inevitable. Therefore, under this cosmology, an entity as complex as a coupled translation-replication system should be considered a viable breakthrough stage for the onset of biological evolution.

One reviewer, Eric Bapteste, thinks that he is opening the door to ID supporters. Obviously Koonin disagrees, he thinks that "the anthropic principle is a death knell to ID".

CharlieM wrote:Do you consider transposons to be random mutations?

Transposons qualify as mutations, yes. Many of them have no function, they are junk. It certainly wouldn't make sense for junk to be "guided" into taking place.
http://sandwalk.blogspot.com/2008/02/theme-genomes-junk-dna.html

Larry Moran wrote:Transposable Elements: (44% junk)
DNA transposons:
active (functional): <0.1% defective (nonfunctional): 3%
retrotransposons:
active (functional): <0.1% defective transposons (full-length, nonfunctional): 8% L1 LINES (fragments, nonfunctional): 16% other LINES: 4% SINES (small pseudogene fragments): 13% co-opted transposons/fragments: <0.1% a
aCo-opted transposons and transposon fragments are those that have secondarily acquired a new function.

CharlieM wrote:Here is an excerpt from an article entitled, 'Invasion of Genomic Parasites Triggered Modern Mammalian Pregnancy, Study Finds' at http://www.sciencedaily.com/releases/2011/09/110925185434.htm

...snipped for size...

1500 difference between placentals and other mammals in the uterine system, that's a fair bit of mutation going on.

Well the two groups diverged 150 million years ago

CharlieM wrote:So these lumps of parasitic waste have managed to pull themselves out of the rubbish tip and now have the important job of making sure pregnancy goes to plan. How do we know that these transposons started out as accidental insertions?

Strawman. Noone is claiming these transposons ever were "accidental insertions". Though you seem to be implying we are dealing with something like a giant lump of transposons who all suddenly got coopted into regulating pregnancy. That's not what the paper says. The differences we see between placentals and other mammals is the result of a 150 million year divergence.

CharlieM wrote:Because they selfishly replicate themselves but perform no useful functions. But what about the ones found to have important regulatory functions? Well obviously they were co-opted into their present function.But how do we know that they haven't performed this function from the beginning? Because they are transposons and we know that transposons are parasitic selfish inserts.And how do we know this? Because they perform no useful function.....Stop the bus I want to get off.

Weirdly, none of this reasoning is presented in the actual paper.

http://www.somosbacteriasyvirus.com/embarazo.pdf

Lynch et al wrote:There is a broad consensus that many of the genetic changes underlying the evolution of morphology occur by the stepwise modification of individual pre-existing cis-regulatory element modules5,6,29. However, it is questionable whether the origin of complex novelties—such as the origin of new cell types, which involves the recruitment of hundreds of genes—can be achieved by these small-scale changes7,29. Our findings indicate that the gene regulatory network of ESCs was rewired in placental mammals during the evolution of pregnancy, a reorganization partly mediated by the transposable element MER20. Furthermore, MER20s coopted specific signaling pathways essential for implantation and pregnancy into ESCs by acting as cell type–specific regulatory elements. These findings strongly support the existence of transposon-mediated gene regulatory innovation at the network level, a mechanism of gene regulation first suggested more than forty years ago by McClintock30 and Britten and Davidson31. Our data and those of other recent studies13,14,32 show that transposable elements are potent agents of gene regulatory network evolution and add to an increasing body of evidence indicating that the evolution of novel characters involves genetic mechanisms that are distinct from those involved in the modification of existing characters23,33

CharlieM wrote:Random mutations were not so prevailent that they prevented different species of mice from interbreeding after 1.5 to 3 million years, but they have managed to alter the genome in several different species and even genera in the same way so as to confer resistance to warfarin. The evidence points to conservation of the kind

Which could simply be a sign of persistent gene-flow between the different populations.

CharlieM wrote:and convergence rather than divergence.

If the selective pressures are the same(warfarin resistence), on already highly similar, closely related species(mice and rats), then it's only to be expected that similar solutions to the same problem will be found by evolution.

However, in the specific example of the article you link, resistance was transferred from one population to the other by interbreeding. Is this your evidence of "guided evolution" for the purpose of cosmic love?

CharlieM wrote:More of the same at:http://www.sciencedirect.com/science/article/pii/S0168952510001289
More evidence that life is guided along a limited path.

Man you just can't get over the teleology can you?

Actually, it's evidence that once a specific system is in place, it's constrained by it's inherent properties(degree of sequence divergence) and that of physics and biochemistry(A limited number of solutions exist to any given physicochemical problem).
And given this sequence divergence and the physicochemical constraints, some solutions are simply more easily evolvable than others.

Here's the full paper, very interesting stuff:
http://www.brown.edu/Research/Weinreich/WeinreichPublications/ChristinWeinreich&Besnard2010.pdf

Take the evolution of the shape of sharks and dolphins as an example. They are roughly very alike in their morphology, which is very well adapted to reduce drag in an aquatic environment. Do we need to postulate a "guiding force" to explain their 'converged' morphologies? Obviously not, we only need to include natural selection and the physical constraints of the environment: The friction and drag of water on the organisms physical body in relation to it's ability to catch prey while expending as little energy as possible. There is obviously a slope for selection to climb, and movement towards the shark/dolphin-morphology "peak" is almost inevitable. We don't need designers or "guidance", all we need is physics, chemistry, natural selection and genetic drift.

CharlieM wrote:You posted a video and then said:

Rumraket wrote:That was a video on this paper:

On the origin of the translation system and the genetic code in the RNA world by means of natural selection, exaptation, and subfunctionalization
http://www.biology-direct.com/content/2/1/14

I'm not sure why you linked to a paper by Koonin to make your case.

Because you claimed:

CharlieM wrote:But naturalistic forces have not explained how the genetic code came about.

Of course, you can always start moving your goalposts and wibble around what you meant by "naturalistic forces". I took it to mean you think there's no natural explanation.

CharlieM wrote:He believes that a translation-replication system cannot appear by chance.

Of course not, neither do I. that's why he explains it with evolution by natural selection, exaptation, and subfunctionalization.

I think it's strange how you first argue that there's no naturalistic explanation for the origin of the genetic code, and then go on to supply a second solution by Koonin, to the one I linked myself. In other words, Koonin has two solutions to the problem. One he considers far fetched, and another he considers inevitable.

Shagz wrote:after all, whales (which have evolved from land mammals, which had evolved from aquatic animals) have clearly returned to a previous stage, even if just partially.

Point of order: No they haven't. What they have done is to return to a previously occupied environment, which is nothing like the same thing. Dollo's law holds.

hackenslash wrote:

Shagz wrote:after all, whales (which have evolved from land mammals, which had evolved from aquatic animals) have clearly returned to a previous stage, even if just partially.

Point of order: No they haven't. What they have done is to return to a previously occupied environment, which is nothing like the same thing. Dollo's law holds.

According to wikipedia (which I know is sometimes wrong), Dollo said, "An organism is unable to return, even partially, to a previous stage already realized in the ranks of its ancestors."

Fish have fins and a tail. Whales have fins and a tail similar to a fish, and live in the water. Whales have fish or fish-like animals as very distant ancestors; thus, we could say that they have partially returned to a previous stage.

Unable means it will never happen. Yet, it appears to me that it has happened, at least slightly partially. Therefore, I feel pretty confident saying that Dollo was wrong. Unless he was misquoted in wikipedia. Admittedly, I have not read anything about him elsewhere, and am by no means an expert.

It doesn't feel right to say that organisms will never attain any form, though; even if it was a form that their distant ancestors had. How can we say never? Surely it is extremely improbable; but never? It smacks of a IDer's irreducible complexity argument. Are the odds so against it that it will never happen in the history of the earth? How does one go about calculating the exact odds when we only have this one planet with life to study?

The point is that whales didn't return to a previous stage already realised in the ranks of their ancestors, they merely returned to an environment previously occupied by their ancestors, which is not a violation of Dollo's Law. Dollo wasn't wrong, and you're misunderstanding what is actually meant by a return to a previous stage already realised in the ranks of its ancestors.

Fish swim using lateral undulations, all whales swim by using horizontal undulations. Whales gave not returned to the same form, if that's where this was headed.

RS

hackenslash wrote:The point is that whales didn't return to a previous stage already realised in the ranks of their ancestors, they merely returned to an environment previously occupied by their ancestors, which is not a violation of Dollo's Law. Dollo wasn't wrong, and you're misunderstanding what is actually meant by a return to a previous stage already realised in the ranks of its ancestors.

So did he say "even partially"? You can't see how whales are similar to fish, at least very partially?

How can we say they they will never return to a previous stage, anyway? Any form is just as likely to be evolved into as any other form; it doesn't matter if it happened to be a form that was previously realized in the past. Since there are so many possible forms, it seems incredibly unlikely that the same form will come about twice; maybe so incredibly unlikely, it will never happen in the history of the earth. But, how can we say for sure? How does one go about calculating those odds?

theropod wrote:Fish swim using lateral undulations, all whales swim by using horizontal undulations. Whales gave not returned to the same form, if that's where this was headed.

RS

True, their fins and tail are not identical. I never said that whales returned to the same form, only that they have partially returned in some ways. And Dollo apparently said "even partially".

Shagz wrote:

hackenslash wrote:The point is that whales didn't return to a previous stage already realised in the ranks of their ancestors, they merely returned to an environment previously occupied by their ancestors, which is not a violation of Dollo's Law. Dollo wasn't wrong, and you're misunderstanding what is actually meant by a return to a previous stage already realised in the ranks of its ancestors.

So did he say "even partially"? You can't see how whales are similar to fish, at least very partially?

Evolving features that bear a vague similarity to features held by an ancestor does not constitute even partially returning to a previous stage. Returning to a previous stage is wholesale reversal of mutations down a very specific path, which simply won't happen. This is what Dollo's Law is about. Although whales have fins, they are fundamentally different to fish. They are mammals, and they have to surface to breathe, among many other things. You are misunderstanding the applicability of Dollo's Law, and applying it to something that it doesn't apply to. This would be akin to suggesting that the loss of visual capacity in cave fish is a return to an ancestral stage, when it is merely the economy of evolution determining that eyes provide no survival or reproductive advantage.

How can we say they they will never return to a previous stage, anyway? Any form is just as likely to be evolved into as any other form; it doesn't matter if it happened to be a form that was previously realized in the past. Since there are so many possible forms, it seems incredibly unlikely that the same form will come about twice; maybe so incredibly unlikely, it will never happen in the history of the earth.

Again, you misunderstand. Dollo's Law applies to the precise reversal of mutations. It doesn't rule out similar forms, it rules out a reversal of genotype. Moreover, in this sentence you're overlooking convergent evolution, an observed principle. All one needs to do is to look at the way that marsupials diversified to occupy the environmental niches occupied by placental mammals elsewhere. What this would suggest, by the principle you are applying here, is that a thylacine and a dog are essentially the same, when they are clearly not. That the morphology is externally similar is only indicative of the success of the form in occupying a particular environmental niche, not of the forms actually being the same.

But, how can we say for sure? How does one go about calculating those odds?

Pretty easily, as it happens. The calculation would be based on mutation rates and the probability of a given mutation.

True, their fins and tail are not identical. I never said that whales returned to the same form, only that they have partially returned in some ways. And Dollo apparently said "even partially".

But they haven't even partially returned, they have merely returned to an environment, as has been explained to you.

I don't want to derail Charlie's thread, so I will stop here. But I'd like to start another thread, at some point, when I have time, as I remain unconvinced.

Shagz wrote:

hackenslash wrote:The point is that whales didn't return to a previous stage already realised in the ranks of their ancestors, they merely returned to an environment previously occupied by their ancestors, which is not a violation of Dollo's Law. Dollo wasn't wrong, and you're misunderstanding what is actually meant by a return to a previous stage already realised in the ranks of its ancestors.

So did he say "even partially"? You can't see how whales are similar to fish, at least very partially?

But they did not return to something that they were, in any way.

They evolved a characteristic similar to one that an ancient ancestor had.

Returning to a previous stage would require undoing the mutations and changes that have occurred. THAT is what Dollo said was impossible.

Guided by the dictates of physics.... well done Charlie!

Whales are like fish? What? You mean they're both adapted to live in water? That's about the end of that comparison!

Here's Larry Moran talking about transposons in the human genome specifically:
http://sandwalk.blogspot.com/2011/09/tr ... enome.html

Here's an interesting comment to Moran's thread:

Artificial Selection said...
I'm a researcher in one of the labs on the paper Larry is discussing in this post, and as a long-time Sandwalk reader, I just want to say how cool it is that a paper to which my labmates contributed was featured here. As to the discussion on the direction and magnitude of selection on the retrotransposon population of the genome goes, it sounds like some of the discussions/arguments that happen around the lunch table in the lab here periodically.

My opinion as a researcher in the field of mobile elements for the last six years (I got my PhD studying these elements and am about to finish my finish my first year as a postdoc continuing to study them) is that the vast majority of mobile element insertions in the genome are neutral. A portion are deleterious when they hit exons, regulatory regions, or splice sites. And, there are a number of examples in the literature that make a case for a small portion of insertions being beneficial, too (e.g. band-aids, exon shuffling, etc.).

But any discussion of the selection on these elements shouldn't stop only at insertions, because the high degree of homology between copies of elements of the same type allow for a tremendous amount of interaction (e.g. recombination-mediated deletions, recombination-mediated inversions) that appear to significantly contribute to genomic fluidity and dynamism. These interactions can be between elements separated by quite large stretches of other intervening sequence, and can therefore affect phenotypes should those stretches be coding or regulator in nature. As with the insertions, though, most INDELs and rearrangements of this type likely happen only within gene deserts, and are therefore mostly neutral. But, they can be both deleterious and beneficial in genic regions. Plus, it remains to be quantified whether the sequence variation produced through these interactions provides raw material on which selection may operate.

It's a complex question without a single, clear answer. It's one of my favorites. My current opinion is that they're mostly neutral inhabitants, but there are instances and mechanisms that may give benefits in some cases, potentially offsetting to some small degree those instances in which they are deleterious.

FRIDAY, SEPTEMBER 23, 2011 12:18:00 PM

Don't forget to read Larry Moran's post as well.
It seems pretty straightforward: Transposons behave like other mutations. They are mostly neutral, probably deleterious in coding regions, and once in a rare while they may be beneficial. Sorry Charlie, I don't see any evidence of guidance here either.

CharlieM wrote:

sciencedaily wrote:The Yale team studying the evolutionary history of pregnancy looked at cells found in the uterus associated with placental development. They compared the genetic make-up of these cells in opossums -- marsupials that give birth two weeks after conception -- to armadillos and humans, distantly related mammals with highly developed placentas that nurture developing fetuses for nine months.
They found more than 1500 genes that were expressed in the uterus solely in the placental mammals. Intriguingly, note the researchers, the expression of these genes in the uterus is coordinated by transposons -- essentially selfish pieces of genetic material that replicate within the host genome and used to be called junk DNA.
"Transposons grow like parasites that have invaded the body, multiplying and taking up space in the genome," said Vincent J. Lynch, research scientist in EEB and lead author of the paper.
But they also activate or repress genes related to pregnancy, he said.

1500 difference between placentals and other mammals in the uterine system, that's a fair bit of mutation going on.

There's something you need to know about placental syncitiotrophoblasts, CharlieM, before you claim they must have been the work of God:
Actually, they are referring to a HERV W gene (Human Endogenous RetroVirus, class W). It did not occur by multiple mutation, it was a viral insertion - one which happened to contain a gene that the virus used to dissolve cell membranes in early mammals, from its mechanism for invading cells. It was useful, because it provided a ready-made mechanism for implantation of a placenta in the uterine wall.
http://www.pnas.org/content/105/45/17532.full

Syncytin-2 is an envelope gene from the human endogenous retrovirus FRD (HERV-FRD) co-opted by an ancestral primate host, conserved in evolution over >40 Myr, specifically expressed in the placenta, and with a cell–cell fusogenic activity likely contributing to placenta morphogenesis.

The relevant HERV-W gene is expresssed by syncitiotrophoblasts, which are multi-nuclear cells that form a vital part of the placenta.

One thing that puzzles me and you may be able to help me out with this. Viral like insertions in an organism's DNA are said to be put there by viruses some time in the organisms past. How do we know that these stretches of DNA are not a normal part of the genome and viruses have come about due to portions of DNA escaping and manifesting themselves as viruses? In other words what is the evidence for it being one way and not the other? I think I'm right in assuming that no one knows the origin of viruses, or have I got this wrong?

CharlieM wrote:One thing that puzzles me and you may be able to help me out with this. Viral like insertions in an organism's DNA are said to be put there by viruses some time in the organisms past. How do we know that these stretches of DNA are not a normal part of the genome and viruses have come about due to portions of DNA escaping and manifesting themselves as viruses?

Because, if that was the case, the sequence would pre-exist in the ancestors of the species concerned. The point about all ERVs is that they represent DNA sequences that are new to the species concerned, and the match between HERV-W gene concerned and known viral genes for dissolving cell membranes is too good to be a coincidence.

CharlieM wrote:One thing that puzzles me and you may be able to help me out with this. Viral like insertions in an organism's DNA are said to be put there by viruses some time in the organisms past. How do we know that these stretches of DNA are not a normal part of the genome and viruses have come about due to portions of DNA escaping and manifesting themselves as viruses? In other words what is the evidence for it being one way and not the other? I think I'm right in assuming that no one knows the origin of viruses, or have I got this wrong?

You've got it wrong:

http://genomebiology.com/2006/7/11/241