Is all TRUTH scientifically knowable?

"No. It is purely coincedental. Can I prove that? No... no more than you can prove it is "strong evidence". "

I find it incontrovertible.

You must remember that we are never talking proof in science. We are merely looking for what explanation best fits the data. Young earths often like to throw out some really big numbers and say that those odds mean that evolution could not have happened. Usually such things are short on details of how the odds are calculated or they make faulty assumptions.

But in this case we can derive the odds for coincedence rather easily, at least for part of the procedure.

Now, there are 10^9 locations that a given insertion can take place so an insertion shared between two species at the same location has odds against of 10^9. Now, just this paper discusses twelve specific inserts. So the odds for all twelve being shared between two species is (10^9)^12 or 10^108. I counted ten different species in the list so the odds of the twelve being shared among all ten is (10^108)^(10-1) or 10^972. That is 1 followed by 972 zeros! By comparison there are about 10^85 total protons, neutrons and electrons in the entire visible universe.

Quite long odds for a coincidence!

The odds get longer when you consider that it is only a select group of viruses out of all those that can infect. The odds get longer when you consider the long odds against a given insert becoming fixed in the population. The odds become longer when you consider the likelyhood of the patterns of the mutations in the sequences.

"An alternative is not necessary to prove that the idea given by you fails."

Well, then at least show a place where the ERV data fails!

I contend that you are not out to merely disprove an old earth but to also show a young earth. In that case you DO need to provide an alternative.

"Actually I gave you one."

I must have missed it.

Which mechanism did you propose that accounts for the particular combination of shared viral insertions that we see out of the thousands of different viruses that can infect apes? What data supports your claim?

Which mechanism do you propose that accounts for all the insertions being located at the same locations in the genome? What data supports your claim?

What mechanism do you propose for fixing only these insertions? What data supports your claim?

What mechanism do you propose for all the insertions accumulating mutations in a pattern that matches trees from other methods? What data supports your claim?

"BTW, how many inserts do you assert that man shares with apes? Out of how many total?"

It is a complicated question. There are thousands of such insertions. But most are so old that they are shared not just by all apes, but also by all vertebrates or even all eukaryotes. The total makes up as much as a few percent of the geneome. If you want to talk about apes specifically, I am not sure of the exact number but from what I have read the number is in the dozens for how many inserts the apes share that are not shared by other vertebrates. Finally, I think around one or two inserts have been found in each species that are not shared with other species.

"Frankly... nope."

I disagree. I think the evidence is beyond a reasonable doubt. It is not and never will be beyond an unreasonable doubt. That is to say that you do not find absolute proof in sceince.

"Again, you seem to be contradicting yourself. "

Not when taken in context. Given how rare such events are, having dozens in common for the apes is a fair number. Having thousands in common among the vertebrates is significant.

"However, if indeed there are many of these shared insertions, I would argue that it is evidence of common design, not common ancestory... This presumes something that was not addressed to my knowledge... and that I contended before. The common location could be a function of a genetic blindspot common to several species. Otherwise, we could be talking about a specific capability of the retrovirus itself. "

No, this was addressed. Observation shows that the insertions are truely random.

Varmus, H. E. & Swanstrom, R. (1984) in RNA Tumor Viruses, eds. Weiss, R., Teich, N. M., Varmus, H. E. & Coffin, J. M. (Cold Spring Harbor Lab. Press, Plainview, NY), pp. 369-512.

Brown, P. O. (1997) in Retroviruses, eds. Coffin, J. M., Hughes, S. H. & Varmus, H. E. (Cold Spring Harbor Laboratory Press, Plainview, NY).

"First, I have not argued that viral DNA have not infected species at all. I have argued that since common design attributes were used there would be similar or common reactions to environments."

Not possible for it to be coincidental. See above. It would have to be on purpose.

"Second, we don't actually know enough about the gene to say that anything is necessarily "junk" or "useless"."

But we do. We know they are viral in origin. We know that they are generally not expressed. And we know that they accumulate mutations in a pattern consistent with sequences that have no function.

 

"This counts on the event being a purely random, chance occurrence. I have given at least two possibilities that would undermine that assumption."

There are OBSERVED to be random. These references discuss that observation.

Varmus, H. E. & Swanstrom, R. (1984) in RNA Tumor Viruses, eds. Weiss, R., Teich, N. M., Varmus, H. E. & Coffin, J. M. (Cold Spring Harbor Lab. Press, Plainview, NY), pp. 369-512.

Brown, P. O. (1997) in Retroviruses, eds. Coffin, J. M., Hughes, S. H. & Varmus, H. E. (Cold Spring Harbor Laboratory Press, Plainview, NY).

"BTW, how many are the shared inserts between humans and apes? I have only understood you to claim one."

There are thousands. Most of these, however, are quite ancient and are also shared with the other vertebrates. The number of shared inserts unique to apes are on the order of dozens. I do not know the exact number. It is possible that not all have been found.

The paper that I referenced for you discusses twelve specific inserts.

 

OK. Improbable.

We are looking for the most parsimonious explanation. Something so improbable does not fit that description.

 

"You still have not bridged the gaps between mutation, accummulation of information, and the emergence of new functioning biological. The odds against even a very simple, novel function arising dwarf those given above by you."

I think we have a major difference of opinion on that matter. I assert that observed genetic process involving such things as duplication, point mutations, frame shifts, recombination, exon shuffling and the like are sufficient to generate new information. (I asked on the last page for a definition of information and an example of what you would consider to be new information. Answers might help bridge the gap. It is possible that you are laboring under an uneccesary definition and it is possible that there may be examples of what you would find acceptable so long as you do not try to move the goalposts and ask for direct observation of something that takes place in geologic timescales.) You assert that it is not sufficient though I am unsure what your basis for claiming this is. In my opinion, it sounds like you are asserting that it is not possible without showing why it is not possible.

I have tried to reason through this, but to no avail. So I have a different tact to try. If I the amateur cannot make a good case then I will let the professional. Please read the following two papers. (I am not sure you ever looked at the paper I referenced you on ERVs because you kept asking questions that were spelled out clearly in the text.)

Jianzhi Zhang, "Evolution by gene duplication: an update," TRENDS in Ecology and Evolution Vol.18 No.6 June 2003.

http://www.anthro.utah.edu/~rogers/bio5410/Readings/Zhang-TRE-18-292.pdf

The second may be more applicable but the pdf has disappeared from the web. I can give an abstract and an HTML cache but the figures will be missing and the formatting may be a bit off.

Long, M. 2001. “Evolution of novel genes.” Curr Opin Genet Dev 11(6):673-80.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6VS0-448YP2P-G&_coverDate=12%2F01%2F2001&_alid=243045236&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=6248&_sort=d&view=c&_acct=C 000050221&_version=1&_urlVersion=0&_userid=10&md5=bd5c5b78a754a2e9573cbf7b7bf1cc3e

http://scholar.google.com/scholar?hl=en&lr=&q=cache:aG7lJxTjrXEJ:www.csb.yale.edu/people/gerstein/zl...curr01-evolution-novel-gene.pdf+"Evolution+of +novel+genes%22+long

 

Let's also continue this by giving some more examples of new functions evolving.

Copley, S. D. (2000). “Evolution of a metabolic pathway for degradation of a toxic xenobiotic: the patchwork approach.” Trends Biochem Sci 25(6): 261-265.

Anandarajah K, Kiefer PM Jr, Donohoe BS, Copley SD (2000) "Recruitment of a double bond isomerase to serve as a reductive dehalogenase during biodegradation of pentachlorophenol," Biochemistry. 2000 May 9;39(18):5303-11.

Johnson, G. R., Jain, R. K. and Spain, J. C. (2002). “Origins of the 2,4-dinitrotoluene pathway.” J Bacteriol 184(15): 4219-4232.

Long, M., Betran, E., Thornton, K. and Wang, W. (2003). “The origin of new genes: glimpses from the young and old.” Nat Rev Genet 4(11): 865-875.

from the summary, not the abstract

Nurminsky, D., Aguiar, D. D., Bustamante, C. D. and Hartl, D. L. (2001). “Chromosomal effects of rapid gene evolution in Drosophila melanogaster.” Science 291(5501): 128-130.

So we have a new metabolic pathway (sounds irreducibly complex to me), followed by another new metabolic pathway, followed by another new metabolic pathway, followed by sevel new genes formed by retroposition, followed by another new gene where before and after is compared by looking at populations with and without the new gene.

 

More...

This one may be too speculative for your taste as it involves interpreting data from the past, but I would suggest that we do need to know why a designer would make it look like He invented through tinkering. It is another example of evidence for the mechanisms proposed though I doubt you will accept it.

Patthy, L. (2003). “Modular assembly of genes and the evolution of new functions.” Genetica 118(2-3): 217-231.

Prijambada I. D., Negoro S., Yomo T., Urabe I. (1995). “Emergence of nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through experimental evolution.” Appl Environ Microbiol. 61(5):2020-2.

Ranz, J. M., Ponce, A. R., Hartl, D. L. and Nurminsky, D. (2003). “Origin and evolution of a new gene expressed in the Drosophila sperm axoneme.” Genetica 118(2-3): 233-244.

Seffernick, J. L. and Wackett, L. P. (2001). “Rapid evolution of bacterial catabolic enzymes: a case study with atrazine chlorohydrolase.” Biochemistry 40(43): 12747-12753.

The text of the abstract eludes me. The title should be informative enough. A bacteria evolved to make new enzymes to process a new class of chemicals.

More examples of new genes and new functions arising through the very processes that you assert cannot produce such.

 

"BTW, I ran across an interesting bit of information that you might want to respond to.

Accord to Stephen Meyer, the Cambrian explosion was "top down" in terms of evolution/speciation. He said, "Instead, however, fossils from the Cambrian explosion show a radically different 'top down' pattern. Major differences in form and body plans appear first, with no simpler transitions before them. Later, some minor variations arise within the framework of these separate and disparate body plans."

Now he still apparently believes that this occurred during a "short" 5 million year or less time period about 530 million years ago. Nonetheless, contrary to your contention, evolution is not the system that best explains the fossil record. Gradual evolution would require that ever greater levels of variation occur as time went on."

Could you please flesh out what your objection to evolution based on this are?

For anyone following this thread, Meyer is an ID advocate if that helps to know where he is coming from.

YEers generally make two contradictory criticisms of the Cambrian. One, they will say too many new things appeared too quickly for evolution to have produced it all. Or they will take the opposite approach and say that there was too much variation at the beginning of the Cambrian.

In an interesting anecdote, Well's apparently tries to burn both ends of that candle in his Icons of Evolution. I am not sure how he not his readers manage to miss that he is claiming contradictory things side by side.

"Major differences in form and body plans appear first, with no simpler transitions before them."

Except that there are transitions before then. They are harded to document because the beginning of the Cambrian was also about when the chemistry of the oceans and the increase in predation led to hard body parts that preseved more easily. But there are earlier transitions. The Edicharian fauna and the Burgess shale both show transitional forms beforehand. They also show that there was a very diverse amount of body plan experimentation going on. Many body plans were tried during this period that died out as unsuccessful in the long run. I can hardly see how these experiments going extinct before and during the Cambrian can be considered evidence against it.

"Later, some minor variations arise within the framework of these separate and disparate body plans."

Minor variations? Like all amphibians, reptiles, mammals, birds, and most fish?

He really has to be kidding. I know what he is saying. These are just variations on the bilateral body plan, but he misleads to suggest that all tetrapods are simple variations on this plan and should not be considered macroevolution.

"Now he still apparently believes that this occurred during a "short" 5 million year or less time period about 530 million years ago."

Glad you put the quotes in there because 5 million years is still an enormity. But he also quotes the extreme end of the range of the Cambrian. Most put it at more like 50 million. Ten times as long does change the perception a bit. Consider, for example, all of the mammalian evolution in the last 50 million years. There has been a lot of change in that time.

"Gradual evolution would require that ever greater levels of variation occur as time went on."

For the most part it does increase. Meyer was using a very strained definition to say it did not.

"Here's the basic outline. God created the original types with very rich genomes. The immediate descendents of this group speciated quickly and with great diversity. One of the characteristics of this process was that the great variability was not passed on in equal measure thus hardening-off the species. At the time of the flood, Noah did not take one of every species but rather just a representative of each kind. These animals while far more adaptable than animals today were not as rich as the original copy. Thus, a huge number of species went extinct in the flood. The flood was then followed by a more modest and declining level of speciation. Today, the last vestiges of this ability to "evolve" are adaptations."

Not consistent with observations.

The bottleneck at the flood would be visible in the genomes of todays organisms. Since essentially would have gone through a bottleneck of two individuals, there would be very little diversity within the genomes of todays species. At most there could be four different version of a given gene within populations. Such is not seen.

A rich genome would mean that variation between species would have to occur by the loss of function of certain genes in each species. This is not what we observe. Closely related species are different in the variation of the same genes. This is contradictory to both a rich genome and to having had a recent bottleneck.

If there was a diversification of life before the flood and then another after, then there would be little connection between the fossils of the past and the animals of today. It does not fit observations. (Not to mention that the fossil record itself is inconsistent with having been created largely in a big flood.)

 

To return briefly to the subject of the ERVs.

I have mentioned several times my opinion that common descent is the best explanation for the endogenous retroviral inserts. But there is another contrast to be made here. The power of prediction.

Knowing that certain viruses insert their genes into the host of their genome and knowing from other sources that humans and the other apes share a common ancestor, it is a simple prediction to say that there should be wide agrement between the various ape species on the sequence and location of these inserts. The prediction comes directly out of the premise.

And as geneticists search the genomes, they do indeed find that the species share the location and sequence of such inserts and that the patterns of mutations match that predicted from other means. Whenever they look, the predictions are matched to the observations.

Now, where is this power of prediction from any other explanation? Other ideas offered thus far reach no further than guesses. Perhaps it is coincidental (despite the very low odds). Perhaps there is a preference for a specific location (despite the observations to the contrary. Perhaps they are beneficial (despite them being viral in origin, despite them not coding for proteins and despite them accumulating mutations in the manner that useless DNA does so). No YE theory explains the details of the observation and further no YE theory would predict the observations.

What would we predict for the inserts in a young earth? Well, if we trust observations which say that such insertions that get passed on are rare, then we should expect that there would be few if any insertions at all. In addition, because of the short time period, what insertions there may have been would not have time to have become fixed throughout populations. So, at most, an individual would expect only a couple of insertions and these should not even be shared widely within a species, much less between species. But this is not what we observe. There are thousands of inserts and they are widely shared within and between species.

Well, what if you assume that insertions are accuaaly common and that our observations are wrong? Then you might be surprised by the large number of such inserts but you would expect that individuals would have combinations of inserts that varied widely within a species and even more so between species as far as sequence goes and location would be different as well. This would be because new inserts would be frequent and starting separate lines that did not have chances to merge and fix specific insertions throughout the population. Again, this is not what we observe. The sequence and the location of insertions are highly conserved within and between species.

So, while ERVs are very much what you would expect if common descent were true and common descent can make successful predictions about what else will be found, the same cannot be said of the alternatives. The alternatives make no correct predictions about what else should be found and fail to account for a mechanism to give the current state of observations.

 

UTEOTW, I find this statement quite enlightening. I spend a lot of time analyzing testimony and statements and this one has disturbed me.

You claim to believe in God and God's hand in creation (even if it is through evolution), you claim to believe in the virgin birth, Jesus as diety and His miracles, and miracles of the disciples.

Then you make a blatant open ended statement that says that "Meyer is an ID advocate". Setting the tone that "Meyer" obviously has a problem with his theories because he uses an intelligent design factor in his studies.

Does this mean that you do not take into consideration "intelligent design"?