dkogan ([info]dkogan) wrote in [info]convert_me,

benefit of (the) evolution (model)

A while back, I posted a query regarding the usefulness of the evolution model. While much of the discussion was off topic, I did get some leads out of it which I subsequently investigated, so here is a followup. The post is long, so if all you care about is the arguments, skip down to them.

What I care about: This is an argument on why the evolutionary model of life is practically useful as compared to an ID model. In other words, how the following model of the tree of life:
EV:      A
        / \
       B   C
      / \   \
     /  D    \
    E         F
   / \       /
  G   H     I 

has been useful in ways that the following model is incapable of:
ID:  A     B      C
     |     |     / \
    / \    |    /\  \
   |   |   |   /  \  \
   A' A''  B  C' C'' C''' 

Please avoid arguing about the scientific merits of these models - I am interested in the practical merit. I am also not interested in arguing against other variations of ID such as guided evolution or artificial abiogenesis or creation of the universe. Those are largely irrelevant to the public controversy for the time being.




The arguments here are intended for the layman, because to those outside scientific professions, much of the public controversy is opaque in the scientific sense. People don't care about models, or what is science, etc. However, people do care about what works, and here, I try to go into that direction of argument in the hope that this could prove useful to others when speaking to ID proponents.

Inadmissible arguments: There are various applications I discarded. Almost everything to do with single-celled organisms was unacceptable because proponents of ID generally agree that microevolution happens (the distinction between micro and macro evolution is not something most scientists agree with, but this is not meant to be targeted at scientists). Second, areas for which evolution was a motivator, but not necessary (such as understanding the genetic code), did not fit my criteria, because that research could have been motivated by ID theory.

In essence, I was looking for research which depends on the model of common descent (beyond that within a species) and for which there have been real world applications. I was also particularly interested in applications which were not already commonly discussed.



Arguments:

So, here are real world applications of the theory of common descent.

1) Treating long-term genetic defects:

Given the EV model above, a genetic defect can be introduced at some point and propagate to its children. Then, if we notice a defect among several modern animals (e.g. G and H), it is possible to do a search across species to localize when this problem was introduced (if it occurs in G, H and D, it could have originated at B), identify where in the genetic code it is (by comparative genetic analysis), and how to circumvent it.

This was used in the investigation of an absence of an enzyme that produces ascorbic acid. This lack is the underlying cause of scurvy. The (previously thought to be human-only) disease was found in a guinea pig around 1907, which caused a search which found the defect to also occur in some monkeys, but not other mammals. Further searches narrowed down the boundary, which led to an estimate of where and when the defect originated in evolutionary history. This helped explain why the disease exists. Examining the lifestyle of the species affected by it changed the accepted ideal doses of vitamin C. Further: knowing which species are similar but do not have the defect can allow it to be removed from human genetic code in the future. (Just think - our progeny may no longer need to eat those healthy fruits and vegetables.)

This area of research is nonsensical if you do not believe in common descent. A design would either have the defect or not - so either all the animals would be affected or they would not be. A subsequent mutation could cause some of the animals to have the defect, but it would not be grouped within evolutionary history by a common ancestor. Therefore, the line of inquiry would not have been pursued, and the medically helpful information would not have been discovered.


2) Understanding and modeling protein folds:

Currently, one of the most difficult problems in biology is mapping genetic function, typically by finding out how a gene maps to a protein. Understanding this is key to figuring out solutions to genetic problems. This has been extremely challenging because of the complexity of the models involved, and there has been no way to simulate protein structure based solely on the genetic string.

Recently, however, there has been some success in identifying key genetic elements by comparative genetic analysis. The genetic strings that represent similarly functioning proteins within various animals are compared. Based on the evolutionary distance between the animals, it is possible to analyze which parts of the genes change quickly, and which change more slowly. (If you compare G, H, and D above, then there is more 'distance' between G and D than between G and H, and knowing the common ancestor allows the estimation of rate of change.) The genes that change more slowly are the ones that are more key to the way the corresponding protein folds and functions. Using this method, it has been possible to isolate gene sequences commonly responsible for folding, which resulted in some success in predicting via simulation what a protein looks like based on the gene sequence. (Jonathan A. Eisen and Martin Wu, 2002. "Phylogenetic Analysis and Gene Functional Predictions: Phylogenomics in Action", Theoretical Population Biology 61)

Again, this is an area of research that is nonsensical with the ID model. There, the genetic distance between species is absolute - based on the original design plus mutation since then, so there is no way to get a sequence of gradually diverging gene sequences and no reason to pursue this line of inquiry.

3) Finding functional genes / Filtering out 'noise'

An extension of the above is that beyond just understanding protein folds, it is possible to gain a lot of understanding of the functionality of genetic segments by seeing how much and how quickly they tend to change. DNA segments which change rapidly and randomly tend to be non-coding or noncritical. Segments which change very slowly typically represent important functionality. Moreover, genes which are selected for more rapidly than chance would suggest (the mutation rate does not change, but the gene's shift in a population can and does) may be ones which represent functionality that is being selected for. An example of this is the FOXP2 gene, which was discovered to have changed very rapidly in humans in recent (in terms of evolution) history. The gene turns out to be critical to the development of part of the brain, and it is believed that its rapid change is what helped humans develop language. (Anyone have examples of noise being filtered out / or genes thought to be noise found out to be functional after such comparison?)

4) Assessing vestigial structures:

If the common descent model is accepted, organs whose function is unknown can be assessed through comparative anatomy, and we can decide whether or not it is harmful to mess with certain parts of our bodies. In humans, the appendix, wisdom teeth and coccyx are fairly commonly removed when they cause problems. It is understood that it is safe to do so because we understand the origins of the organs, and thus their lack of functionality. If the common descent model is not accepted, we do not have that rationale for removing these organs, so would not so lightly be able to proceed with such surgeries. In that way, the evolution model is medically useful. (The converse is true: we can understand functional organs through comparative anatomy, but this meshes with template reuse in ID theory, so is not a good argument.)




Discarded arguments: These are some examples I discarded as not being sufficiently strong. If there is a way to strengthen any of them, that would be great, but for now, I think they will be easily taken apart by a someone prepped for them or someone of reasonable intelligence.
  • Genetic algorithms: The idea of evolution has been used extensively in programming. This shows that evolution is a powerful and effective model, and demonstrates its plausibility, but just because something can work does not mean it happened, so it is not a good argument for biological evolution.
  • Evolutionary psychology: Evolutionary psychology has been a highly hyped notion, and may go a long way to explain certain aspects of human behavior, but I have not found any studies that show it being immediately useful, other than possibly subjectively to individual patients (which is a weak argument).
  • Genetics: Modern genetics was largely prompted by evolution. Trying to understand how traits are passed on and change is what prompted Gregor Mendel's research, but this work would still have been done at some point even with the ID model, since traits still get passed down. On the other hand, there would have been no case for the assumption that all organisms share the same or similar genetic structure, so the work may have been adversely affected/delayed.
  • Ecology: You can use the idea of evolution to understand and aid response to things like invasive species. However, this can generally be done via observation/common sense, so the degree to which the idea of evolution is helpful is unclear.
  • Interpolation: Given some set of organisms with desired traits, we can estimate where in the evolutionary tree the trait originated, and then be able to identify other organisms which would likely share the same trait. I have not found any actual uses for this, however.
  • Diseases/Pathology: Practically every aspect of modern disease research, including things like forensics using genetic comparison, requires an understanding of evolution. However, as stated above, ID proponents reject this being evolution... annoying, but true.




Discuss:

For those who actually made it through all that, a few questions. Do you think these arguments are/would be effective, particularly when talking to a layman? Could they be made better, and how do they compare to the typical arguments from the nature of science? Given the examples, can you think of other ways the model has been used?

For those who favor ID theory, do you have counter arguments to these points? Are there weaknesses here that were not listed?

Thanks to those who made suggestions in the aforementioned thread, and below, particularly [info]lowk for a sequence of references, [info]tom_kbel for various suggestions below, and [info]scorpy1 for the ascorbic acid article.

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  • 91 comments

[info]kai

October 28 2005, 21:11:27 UTC 6 years ago

"Hmm. No scathing replies yet. Too long?"

Yeah, little bit.

[info]dkogan

October 28 2005, 21:22:25 UTC 6 years ago

:(

[info]tom_kbel

October 28 2005, 22:15:42 UTC 6 years ago

You need to add to your list: finding the specific functionality of particular genes; finding functional gene sequences, particularly non-coding gene sequences which can be found by their stability in cross generic comparisons, but not by fishing for transfer RNAs; and cross generic sequence comparisons can also indicate sequences that have been under recent strong selection.

As to whether discussing these cases will have any particular tendency to convert a sceptical public - I think not. The application is too theoretically abstract for it to immediately impact on Joe public, and Joe public is not sceptical about evolution for reasons of applicability, but because of theological/philosophical reasons and because they are continuously lied to by creationists so that they are radically confused about the state of the evidence.

[info]dkogan

October 28 2005, 22:55:47 UTC 6 years ago

finding the specific functionality of particular genes

Isn't that what's listed under (2)?

finding functional gene sequences, particularly non-coding gene sequences which can be found by their stability in cross generic comparisons, but not by fishing for transfer RNAs

Good point. Got any references for when that has actually been done? (other than as a theoretical possibility)?

and cross generic sequence comparisons can also indicate sequences that have been under recent strong selection.

When would this be useful?

As to the second paragraph, it's certainly true that the problem arises from a perceived conflict with religion. However, when people are confronted with practical applications for something, religion is often overruled. Thus, for example, there were religious objections to anesthesia, but they were overruled by the usefulness of the procedure.

On the other hand, I agree all the applications are pretty advanced for someone with no scientific background, which is somewhat unfortunate.

[info]tom_kbel

October 29 2005, 00:00:13 UTC 6 years ago

Finding specific functionality of genes is more general than 2, in that 2 refers specifically to protein folds. Fully elucidated, you are probably on the same track.

I cannot point you to finding particular functional but non-coding sequences. I have come across examples in the past, often when following up on another creationist "evolutionists called this junk DNA but it really isn't" argument. But I cannot give you links or articles for particular research at the moment.

Highly conserved sequences (ie, sequences under strong negative selection) are likely to be functionally important; but sequences that have altered at a significantly greater rate than would be accounted for by genetic drift (ie, sequences under strong positive selection) are also likely to be functionally important. Further, they are also likely to be functionally important in ways that differentiate closely related species. An example of research partly directed by this line of reasoning is that into the FOXP2 gene.

http://www.corante.com/loom/archives/000811.html

[info]dkogan

6 years ago

[info]dkogan

6 years ago

[info]theswede

October 28 2005, 22:29:25 UTC 6 years ago

Scientific merit is practical merit; you are asking very strange questions, which seem to be by definition pointless.

[info]dkogan

October 28 2005, 22:45:52 UTC 6 years ago

While science as a whole is undoubtedly helpful, some specific research within it may be largely pointless. It is mostly when there are practical applications to research that laymen care.

[info]theswede

October 28 2005, 22:53:26 UTC 6 years ago

You miss my point; the ONLY thing which is helpful is science, in the sense of that which is learned through scientific methodology.

All else is bollocks.

[info]dkogan

6 years ago

[info]theswede

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[info]dkogan

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[info]theswede

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[info]dkogan

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[info]theswede

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[info]dkogan

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[info]theswede

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[info]dkogan

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[info]theswede

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[info]dkogan

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[info]theswede

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[info]dkogan

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[info]tom_kbel

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[info]theswede

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[info]tom_kbel

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[info]dkogan

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[info]theswede

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[info]tom_kbel

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[info]theswede

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[info]tom_kbel

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[info]theswede

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[info]dkogan

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[info]dkogan

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[info]theswede

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[info]dkogan

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[info]theswede

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[info]tom_kbel

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[info]theswede

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[info]tom_kbel

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[info]theswede

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[info]tom_kbel

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[info]theswede

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[info]lowk

October 29 2005, 08:29:47 UTC 6 years ago

Nice :-) And also nice that you read Carl Zimmer, the man is a veritable Don.

A few minor issues. First up, not all scientists dislike the Micro/Macro evolution distinction. Some feel that there are differing methods, and that there are some forms of 'macroevolution' that are set in motion by different phenomenon to normal gene-allele selection (there is almost certainly some truth to that, c.f. rapid polyploidy speciation or chromosome fusion events).

Anyway, the point is that the reason we dislike the idea that the huge genetic change we see in prokaryotes (bacteria etc) and protistic eukaryotes is not that there is no distinction between Micro and Macro. It is that it is in no way micro evolution. The changes we see are immense, profound, powerful and highly important, we see genetic, biochemical and micro-physiological changes that dwarf anything we have ever seen in animals. The genetic reworkings that they go through in a few years is comparable to the difference between us and chimps. The only differences is that you can't see these changes with the naked eye, and therefore we deem them 'not important', 'just little changes in little organisms'. This is, of course, a result of our own stupidly athrocentric view of the world, whereby 'real' evolution is any change that we can see and recognised using our naked eyes.

And a minor technical objection: the statement "genes which change more rapidly than chance" is a bit iffy. Since the mutation rate (which is random) is the source of genetic variation, that is the limit to how fast selective genetic pressure can change an organism at.

The rapid change of the FOXP2 gene was found via comparative genetics, so in comparison to chimps and other primates, to find that it was important. You actually CAN find genes with high selection pressure in an individual species by examining the allele ratios in a population, as was done recently with the genes Microcephalin and ASPM (which code for proteins involved in brain function). They were found to exist in certain allele ratios that were inconsistent with a layout due to random chance, and therefore is an indication of selection.

[info]tom_kbel

October 29 2005, 11:35:42 UTC 6 years ago

And a minor technical objection: the statement "genes which change more rapidly than chance" is a bit iffy. Since the mutation rate (which is random) is the source of genetic variation, that is the limit to how fast selective genetic pressure can change an organism at.

Although the statement is vague, it is essentially correct. A central prediction of the neutral theory of evolution is that, for a stable population, the rate at which new neutral mutations get fixed is equal to the mutation rate. That is, if a particular nucleotide will mutate once in every 100 million copies, then if the mutations are neutral, a new allele at that site will become fixed once every 100 million generations. This is way below the rate at which that new allele will appear in the population. In fact, on average, the new allele will have appeared as a mutant 100 million times for every single occasion on which it becomes fixed, but on the vast majority of occasions it will have been eliminated from the population be chance within a few generations of its occuring.

If all variant alleles at a site are harmfull, then none of them will suplant the existing allele, which consequently will be replaced at a much lower rate than the base mutation rate. If half are harmful, it will be replaced at half the rate. But this is only detectible by multiple cross species comparisons, and only if it is correct that at some time in the past, there was a common ancestor of all the compared species.

If a variant allele is favourable, then though a majority of its occurences will still be eliminated by chance, around 1/(the fitness) of the new alleles will survive to become fixed. As the rate of occurences of the mutation is the base mutation rate times the population size, times 2 (for a diploid population), this means favourable mutations will become fixed at a rate equal to 2 x fitness x population size x base mutation rate, which is typically several thousand times faster than the rate of fixation by drift (ie, by chance alone).

Laying this out, if we have a gene that is a thousand base pairs long, and if it seperated from a comparison species five million years ago, and has a base mutation rate of 1/100 million per year, we would expect , we would expect 100 of the base pairs to differ between the genes in the two species by chance. If instead we found that only 20 differed, we would expect the gene was very highly conserved, with 80% of possible mutations being unfavourable. Alternatively, if we found 200 differences, we would expect that some transitions in one or both species were strongly driven by positive selection.

You actually CAN find genes with high selection pressure in an individual species by examining the allele ratios in a population, as was done recently with the genes Microcephalin and ASPM (which code for proteins involved in brain function).

I assume you are refering to heterozygote advantage. If not, how else did they determine the allele ratios were inconsistent with chance?

[info]lowk

6 years ago

[info]dkogan

6 years ago

[info]tom_kbel

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[info]lowk

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[info]dkogan

6 years ago

[info]dkogan

October 29 2005, 19:40:50 UTC 6 years ago

Who's Carl Zimmer?

First up, not all scientists dislike the Micro/Macro evolution distinction.

Yeah, I see what you're saying. In this case, I mean what ID proponents mean by micro v. macro, which is to say 'omg, it has a new set of limbs' kind of thing. I think those scientists who accept there is some distinction between the two have an entirely different view of what the difference is than what ID proponents think... which tends to be whatever is convenient.

And a minor technical objection: the statement "genes which change more rapidly than chance" is a bit iffy.

Well, as below in the discussion, it refers to the shift of a gene in a population rather than the mutation rate that causes it. I'll try and be more clear.

[info]root_fu

October 29 2005, 10:46:27 UTC 6 years ago

You can find more "arguments" here:

http://www.livejournal.com/community/id_theory/7450.html

[info]lowk

October 29 2005, 12:18:50 UTC 6 years ago

Did you even read the above post? It's not 'arguments', it is full of places in Science and Medicide where the theory of evolution is used explicitly to produce useful things that help people. If evolution wasn't a fact, then these things just plain wouldn't work. But they do. How on earth do you explain that?

[info]root_fu

6 years ago

[info]lowk

6 years ago

[info]root_fu

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[info]dkogan

6 years ago

[info]theswede

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[info]root_fu

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[info]theswede

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[info]tom_kbel

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[info]lowk

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[info]dkogan

October 29 2005, 19:34:55 UTC 6 years ago

... That post in no way goes along with (or contradicts, or has anything to do with) mine. I think you missed the point entirely.

[info]fauxreal

October 29 2005, 21:05:51 UTC 6 years ago

In humans, the appendix, wisdom teeth and coccyx are fairly commonly removed when they cause problems. It is understood that it is safe to do so because we understand the origins of the organs, and thus their lack of functionality. If the common descent model is not accepted, we do not have that rationale for removing these organs, so would not so lightly be able to proceed with such surgeries.

I suppose that's why such things were never removed before the advent of Darwinist theory.

[info]dkogan

October 29 2005, 22:37:06 UTC 6 years ago

we do not have that rationale for removing these organs, so would not so lightly be able to proceed with such surgeries.

'so lightly'

Certainly, some of those (appendix) were removed before. But knowing the reason behind their uselessness makes the procedures more acceptable, so they can be rationally done for reasons short of emergency.

[info]fauxreal

6 years ago

[info]dkogan

6 years ago

[info]root_fu

October 29 2005, 22:58:18 UTC 6 years ago

replying to your earlier post

Since it seems no one's taken you up on your offer.

The first thing an ID proponent of the "no common descent" group would probably do is to ask how problems such as genetic defects due to occurrences such as inbreeding could be overcome. Coming from a single organism, what mechanisms would prevent said organism from in-breeding itself into extinction.

Based on that, they might propose that it would have been easier for life to have come from several different ancestors, than a single common one.

Common gene-types like the one for scurvy you pointed out. They don't necessitate a common ancestor. It could simply be that in adapting, life utilized the same adaptations. The argument that similar attributes equates to shared history. Is like suggesting that the invention of the wheel was one that could only have spread by shared experience. When in reality, it may simply be the most expedient solution. As well as one that people everywhere may have eventually thought up on their own.

Perhaps, some genes were simply the most expedient solution, as well. And were utilized for sake of necessity alone. Rather than a branch point from which different organisms, sprung.

Like say, it might be difficult to imagine a beetle having a common ancestor with a human being. I s'pose someone could point out the fact that they both have legs & suggest they have a common ancestor, when in reality, legs may simply be the adaptation best suited for mobility & thus it is utilized. Rather than a trait inherited at a common branch point by both insects & people.

There's probably more that could be brought up concerning your post. Good post, I must say. If only we had more of these..

[info]dkogan

October 29 2005, 23:24:48 UTC 6 years ago

Re: replying to your earlier post

I think you're getting it more, but you're still missing the crux of the post. Sure, you can come up with justifications for the observed patterns from an ID perspective (it would be hard, but I'm sure you could). That's not the point.

The point is that this research was motivated by the common descent model.

How could the benefits of this research have been arrived at using the ID model?

[info]root_fu

October 31 2005, 00:05:53 UTC 6 years ago

Re: replying to your earlier post

How could the benefits of this research have been arrived at using the ID model?

Very easily.

[info]dkogan

6 years ago

[info]root_fu

6 years ago

[info]dkogan

6 years ago

[info]root_fu

6 years ago

[info]tom_kbel

October 30 2005, 00:17:37 UTC 6 years ago

Re: replying to your earlier post

The first thing an ID proponent of the "no common descent" group would probably do is to ask how problems such as genetic defects due to occurrences such as inbreeding could be overcome. Coming from a single organism, what mechanisms would prevent said organism from in-breeding itself into extinction.

By resorting to this argument they would only show that they do not understand the theory they purport to criticise. Darwinism is gradualist. It asserts that only very rarely do speciations occur in a single generation, or even in a few hundreds of generations.

Common gene-types like the one for scurvy you pointed out. They don't necessitate a common ancestor. It could simply be that in adapting, life utilized the same adaptations. The argument that similar attributes equates to shared history.

Likewise this argument shows a rhetorically convenient ignorance of detail. The gene for the manufacture of vitamin c could have been disabled in a variety of different ways, most easily by simply not existing. But the disabled gene found in gorillas, chimps and humans are all disabled in the same way. The fact that it is disabled in the same way is predicted by common descent, but inexplicable by special creation.

Like say, it might be difficult to imagine a beetle having a common ancestor with a human being. I s'pose someone could point out the fact that they both have legs & suggest they have a common ancestor, when in reality, legs may simply be the adaptation best suited for mobility & thus it is utilized. Rather than a trait inherited at a common branch point by both insects & people.

And again, this argument depends on misrepresenting Darwinism. A Darwinist would hardly point to a shared feature of legs as being evidence of common ancestory between beetles , as the common ancestor had no legs (and was a very small worm). They do point to the difference in lengths of particular bones, and suspension points of membranes as being evidence of independant evolution of flight in birds, bats and pteradactyls; but they also point to the common bone structure shared by birds, bats and pteradactyls; not to mention moles, dinosaurs, and frogs (and so on) as evidence of common ancestry because that particular arrangement of bones is not mandated by functional necessity.

[info]root_fu

October 31 2005, 00:05:06 UTC 6 years ago

Re: replying to your earlier post

By resorting to this argument they would only show that they do not understand the theory they purport to criticise. Darwinism is gradualist. It asserts that only very rarely do speciations occur in a single generation, or even in a few hundreds of generations.

If anything that wouldn't that work against the notion that all human beings descended from a woman in Africa? If not, why?

Likewise this argument shows a rhetorically convenient ignorance of detail. The gene for the manufacture of vitamin c could have been disabled in a variety of different ways, most easily by simply not existing. But the disabled gene found in gorillas, chimps and humans are all disabled in the same way. The fact that it is disabled in the same way is predicted by common descent, but inexplicable by special creation.

Let me analogize for a second. Speaking theoretically, let us say that there was another planet where intelligent life developed. Now, let's say for sake of discussion that upon this planet there were life forms who evolved a sequence of genes that gave them a similar if not identical bone structure as many organisms on this planet. And therefore some of the very same genes. Without common descent.

My point here is that *predicting something* does not constitute irrefutable proof of shared lineage. As evolution progresses its not entirely unreasonable to suspect that the very same genes that might prove a good adaptation for one organism may also prove a good adaptation/mutation for another.

And again, this argument depends on misrepresenting Darwinism. A Darwinist would hardly point to a shared feature of legs as being evidence of common ancestory between beetles , as the common ancestor had no legs (and was a very small worm). They do point to the difference in lengths of particular bones...

There's a fine line between accepting common ancestry and being closed to the possibility of traits that resemble common ancestry, developing for other reasons, I think.

[info]tom_kbel

6 years ago

[info]root_fu

6 years ago

[info]root_fu

6 years ago

[info]tom_kbel

6 years ago

[info]tom_kbel

6 years ago

[info]pangolin

October 30 2005, 00:49:32 UTC 6 years ago

Re: replying to your earlier post

Sexual reproduction, and the associated problem of inbreeding, is not necessary for life to occur.

The first organisms were probably exceedingly simple single celled organisms that reproduced asexually at a vast rate, eventually filling up the "primordial soup". At some point, differentiation due to mutation occurs, and eventually sexual reproduction develops, probably still at the microscopic unicellular level, after there are billions of life forms in existence.

The common ancestor of humans and beetles probably occured around this level too, or at least at a fairly simple multicellular level. Macroscopic animals generally have some form of locomotor apparatus. That's part of what makes them animals and not plants.

[info]tom_kbel

October 30 2005, 00:54:30 UTC 6 years ago

Re: replying to your earlier post

The last common ancestor of humans and beetles occured after the evolution of a triploblastic animal, with a through flowing gut, and some locomotive and sensory apparatus. Specifically it occured after the last common ancestor of humans and sponges (which are multicellular) and after the last common ancestor of humans and jelly fish, which are not triploblastic.

[info]pangolin

6 years ago

[info]tom_kbel

6 years ago

[info]root_fu

6 years ago

[info]pangolin

6 years ago

[info]tom_kbel

November 3 2005, 02:36:39 UTC 6 years ago

Here is another example you may be interested in:

http://pharyngula.org/index/weblog/comments/evolution_of_the_mammalian_vagina

Note the use made of the different proportions of synonymous and non-synonymous mutations. Synonymous mutations give a direct (but approximate) measure of the rate of fixation of neutral mutations. Non-synonymous mutations give an direct but approximate measure of the rate of fixation of all mutations. High fixation rate of all mutations compared to neutral mutations implies strong positive selection is fixing non-synonymous mutations; low fixation rate fo all mutations compared to synonymous mutations implies strong negative selection. The baseline rate depends on the ratio of neutral non-synonomous mutations to synonymous mutations.

This is a special case of the techniques used in 2 and 3, but it does not require an independant estimation of the time of divergence of two lineages, nor of the overall mutation rate.

[info]dkogan

November 3 2005, 17:55:05 UTC 6 years ago

Hmmm. Interesting stuff.

Pity they don't show how the knowledge could be useful...

[info]tom_kbel

6 years ago

[info]dkogan

6 years ago

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