What exactly is ID?

Great. So tell us what testable predictions ID makes. Boy, talk about not reading the very message you're replying to. It wouldn't surprise me if somewhere in this message chain I mention the geological distribution of life, but here again is my question from your Message 1031 where you actually quote it word for word: See the question in the passage from me that you quoted? Let me repeat it again: Since this thread is about developing a clear picture of what ID is, why don't you tell us how ID explains the recorded history of change over time that you allude to here.Now examine your response to this inquiry: "ID is a science of design detection. Nothing more. Nothing less."You go on to say even more which I quoted in my previous message, but let me quote it again, more selectively this time: So now I've quoted a couple of times where in response to my inquiry about what ID says about the history of life you carefully explain that ID and evolution are "two totally different fields of inquiry".But now in your latest message you're changing your story and saying something completely different: So now you're saying that ID *does* have something to say about evolution. Specifically, you're now saying that ID has something very precise to say about the history of life on Earth, claiming that ID says common descent is impossible.So here's the question once again, and please don't yank me through another series of three or four evasive and misleading posts: What is the ID explanation for the history of life on Earth, and more specifically, what is the ID explanation for why common descent is impossible?--PercyEdited by Percy, : Grammar.

Then ID fails to explain biodiversity."We see in these facts some deep organic bond, prevailing throughout space and time, over the same areas of land and water, and independent of their physical conditions. The naturalist must feel little curiosity, who is not led to inquire what this bond is."--Charles Darwin, "Origin of Species", Chapter 11Aren't IDer's curious as to biogeography? Is biogeography not something that ID must explain in order to explain modern biodiversity? As we have already demonstrated, due to the dogmatic nature of ID there is nothing we could ever show which would falsify ID. Rather, the theory of evolution demonstrates that these observable and natural processes are sufficient to explain modern biodiversity in the same way that the Germ Theory of Disease is sufficient to explain infectious diseases but incapable of completely ruling out disease causing demons.

In order to claim that mutation only results in a loss of function then you must know all functions that the protein has. Given the wide range of possible function it is extremely difficult to do this for every protein. This is why the "mutation only results in loss of information" is such bunk.For example:

quote:

---

J Mol Biol. 2010 Jan 8;395(1):79-88. Epub 2009 Sep 18.

​

Changing the DNA recognition specificity of the EcoDam DNA-(adenine-N6)-methyltransferase by directed evolution.
Chahar S, Elsawy H, Ragozin S, Jeltsch A.

​

School of Engineering and Science, Jacobs University Bremen, Campus Ring 1, 28725 Bremen, Germany.

​

EcoDam is an adenine-N6 DNA methyltransferase that methylates the GATC sites in the Escherichia coli genome. We have changed the target specificity of EcoDam from GATC to GATT by directed evolution, combining different random mutagenesis methods with restriction protection at GATT sites for selection and screening. By co-evolution of an enzyme library and a substrate library, we identified GATT as the best non-GATC site and discover a double mutation, R124S/P134S, as the first step to increase enzyme activity at GATT sites. After four generations of mutagenesis and selection, we obtained enzyme variants with new specificity for GATT. While the wild-type EcoDam shows no detectable activity at GATT sites in E. coli cells, some variants prefer methylation at GATT over GATC sites by about 10-fold in cells. In vitro DNA methylation kinetics carried out under single-turnover conditions using a hemimethylated GATC and a GATT oligonucleotide substrate confirmed that the evolved proteins prefer methylation of GATT sites to a similar degree. They show up to 1600-fold change in specificity in vitro and methylate the new GATT target site with 20% of the rate of GATC methylation by the wild-type enzyme, indicating good activity. We conclude that the new methyltransferases are fully functional in vivo and in vitro but show a new target-site specificity.

​

PMID: 19766657 [PubMed - indexed for MEDLINE]

---

Unless you designed your experiments correctly you would just notice the lack of methylation at the GATC sites. You would call this a loss of function. However, these mutations lead to a new function, methylation at GATT sites. Mutations can and do lead to specifity for new substrates, and given the vast number of possible substrates it is nearly impossible to claim that a protein of no known function lacks function in all situations. Do you have any evidence for this, other than your bald assertions? I think you are making the same mistake you made earlier. The paper you referred to earlier suggested that the SMALL POPULATION size of LARGE ANIMALS could lead to genetic entropy. They used the size of the animals as a proxy for their population size since larger animals need more territory, hence smaller populations.

quote:

---

So some are left? Which are those?

---

If you think that the fact that you said all function is lost is sufficient to prove that some function remains you have great faith in your ability to get things wrong.

quote:

---

The point, is that this one was lost. Regardless of what else happened, this one was lost. The point of the article was to show how much you can mutate a particular function before it is lost. That is all.

---

We're not discussing that at all, because that was accepted long ago. Instead we go round and round in circles with you switching between asserting that all function was lost and then trying to act as if you never said it.

quote:

---

It doesn't matter. I'm talking about those same proteins. Just more of them.

---

It certainly does matter. Since the only "50 proteins" figure we have is the number of different proteins in the E coli flagellum - which is made up of a good many more than 50 protein molecules using that figure implied distinct proteins. But OK, why would 1,000,000 units of 50 distinct proteins be significantly more improbable than 1 of each ?

quote:

---

First of all, it's not "complexity" it's complexity. And it's obvious that there would be vast differences in complexity. More dies more complexity. More proteins more complexity.

---

Given that the "complexity" we are talking about is a measure of improbability and not closely related to the normal usage then the scare quote are entirely justified.

quote:

---

Evolution is the chance hypothesis in this case. You don't use it. You calculate the probability based on it.

---

Then it's a pity that Dembski did no such thing.

quote:

---

No, he does it because that's how statistical calculations are done. If you have no prior knowledge of the sequence space you are searching, you assume uniform probability. Everyondoy does that every single time they do a statistical calculation.

---

No, they don't. At least not if they want the result that they get to be anything more than a rough estimate. For things like dice and coins we use a uniform distribution - but that's because of knowledge, not ignorance. (And even there we acknowledge that there might be subtle biases in the real objects).

quote:

---

Umm no. Generalization means that this works for all cases.

---

In this case it means an idea that is often close to being right (but can be drastically wrong).

quote:

---

Poit out where.

---

Message 1056.

quote:

---

They are the noise. I never said they are not. But the point I'm trying to make is that genetic entropy itself means deterioration of genetic information due to accumulation of mutations.

---

In fact you did say that and attempted to misuse Sanford's definition to back up your claim.

quote:

---

They were modeling real populations. Not aliens or mythical beings.

---

Please show that the figures used in the runs which lead to mutational meltdowns in large populations used figures derived from a real population.

quote:

---

The point is that the doomed cheetah lost vital functions. You can keep loosing genetic information and not die out for a very long time.

---

WHich of course means that the issue is not the loss of all genetic information, but just sufficient to disrupt one or more vital functions. Therefore the absolute measure of genetic information is not relevant (the more so because many of the "vital functions" will be "vital" because other aspects of the animal require them - the simpler the life form, the less it has to go wrong). [quote] In reality it does just that. Like I said. The probability is to small. Simple RNA chains won't find any new functions. And even if they did, they wouldn't be beneficial enough to actually outperform other and take over the population.

quote:

---

So you refuse? Fine.

---

You are also refusing to do the very same thing. But I am happy to let my argument stand unrefuted.

quote:

---

Just remember that I didn't make this up. This is from Sanford himself. He know what he's talking about.

---

If Sanford really claimed that population genetics really required all those assumptions to work at all then Sanford doesn't know what he is talking about.

quote:

---

1.) Genes are inherited in blocks. These things do not go under genetic recombination. So if one of the genes in such blocks has a beneficial and the other a deleterious mutation, they both get passed on.

​

2.) Nucleotides do interact. The ENCODE project has shown that genes are polyfunctional and poly constrained. Which means you can start translation of one gene, hop on on to another and finish the translation. You can also read them in the opposite direction. Nucleotides do interact in just such a way. That means, that the gene can not, in any ossible way be the unit of selection.

---

1) is not strictly true since the chromosomes are broken up by recombination. Genes that are very close will tend to stick together but that is all. And even if this were not the case, then the most you could do is to take a chromosome as the unit of selection, not the genome.2) is just illogical. The fact that genes interact doesn't mean that they can't be the unit of selection.

quote:

---

The genome is. The genome gets passed on in full. Natural selection does not pick out the best genes and drops the rest. To claim the opposite is to be in argument with reality itself.

---

In sexually reproducing species the genome does NOT get passed on in full. And in the long term natural selection will tend to favour the better alleles. "Hitchhiking" relies on the linkage remaining intact, which is not guaranteed even for adjacent genes - and you've got nothing else.

quote:

---

Something is or is not CSI, that's true. But something can contain more or less CSI. That's also obvious. And since information is measured in bits. CSI is also.

---

How many bits of having more bits than the bound can a thing have ?

quote:

---

Such as?

---

Requiring exactly 50 proteins - that isn't in the specification. using the same proteins as in the E coli flagellum or variants of them - that isn't in the specification either.

quote:

---

The idea that genes are not rearranged by genetic recombination is simply wrong. What do you even think genetic recombination means if not that the genes are recombined? The closer genes are to each other the less likely they are to be seperated by crossing over, but that is just a question of probability, it doesn't mean that they can't be seperated, even different regions of the same gene can be recombined. And that is without even beginning to look at other mechanisms which can lead to changes between complementary gene regions.

---

Where did I say that? Please point ot where I sad that genes are not rearranged by genetic recombination? I never said that. So why would you claim I did? Is it because you misunderstood me? Probably. What I said is that linkeg genes in genetic blocks do not undergo recombination. Do blocks themselevs do, but not the genes inside the blocks.

quote:

---

All this shows is that you A) don't understand what ENCODE was looking at, and B) dont understand genetics at all.

---

Or, that a) You're full of yourself, or B) You're full of it.

quote:

---

The main problem is that 'unit of selection' is not a very useful term. A single nucleotide change can certainly produce the neccessary phenotypic difference to form a basis for selection to act on.

---

And you miss the point completely. I never said that a single mutation won't have such a strong effect that it won't cause the individual to be selected. Maybe it will. I never said it can't be done.But what I said, is that, even thoug that might happen, let's even say that it happens most of the time, natural selection is going to evaluate the whole organism, and than it's either going to select it or not. What this means is that however great the effect that single mutation had, let's say it was beneficial, all the other deleterious mutations the individual had within it's genome, are going for a ride! They all get passed on together. This is what it means that the genome is the unit of selection. Not the gene, or the nucleotide. Because natural selection is going to evaluate how the whole organism (genome) is compared to the other organisms and select it. It's not evaluating specific genes, or nucleotides against genes or nucleotides of other individuals.Either all genes and nuclotides are selected and passed on, or they are not. This means that the genome is the unit of selection.

quote:

---

The whole point is that the mixing of different complements of genes within a population's gene pool does allow a degree of seperation between genes allowing us to look at the increase in specific alleles rather than looking at whole genomes. It is impossible to make any sort of case in sexual organisms that whole genomes are inherited.

---

So let me get this straight. When meiosis occures, the mechanisms inside the cell, PICK OUT THE BEST GENES, and pass them on to the next generation? OBVIOUSLY NOT!

quote:

---

In terms of the ENCODE data what you are talking about is presumably the identified ransripts, the thing is that the ENCODE data showed that the majotrity of the genome is transcribed, but only 5% of it seems to have any sort of selective constraint suggestive of function. This makes it a pretty substantial leap to go from the existence of transcripts to their having a functional role which would be destroyed by any single nucleotide changes.

---

I never said anything like that. Why do you keep misrepresenting me?

quote:

---

As genes, mRNAs, and eventually complete genomes were sequenced,
the simple operon model turned out to be applicable
only to genes of prokaryotes and their phages. Eukaryotes were
different in many respects, including genetic organization and
information flow. The model of genes as hereditary units that are
nonoverlapping and continuous was shown to be incorrect by
the precise mapping of the coding sequences of genes. In fact,
some genes have been found to overlap one another, sharing the
same DNA sequence in a different reading frame or on the opposite
strand. The discontinuous structure of genes potentially
allows one gene to be completely contained inside another one’s
intron, or one gene to overlap with another on the same strand
without sharing any exons or regulatory elements.

---

What is a gene, post-ENCODE? History and updated definition What I was talking about is this. Genes are not descrete units of code. There is no such a thing as one gene one trait. Biological functions are coded for by lot's of genes that are either a.) placed on different sites on the chromosome, or b.) overlap each other. Meaning that 2 different functions can share a single gene. Not only that, but some genes are also coded for by the intron regions which were thought not to contain any code at all.So any talk about a gene being the unit of selection is painfully wrong by today's standards.As for the 5% number of functions you cite, I have no idea how you interpreted that, or where you got that, but it seems to me, that you are talking about this quote right here.

quote:

---

Moreover, comparison of the human, dog, mouse, and other vertebrate genomes showed that a large fraction of these was conserved, with ∼5% under negative selection since the divergence of these species

---

What this shows is that they are simply assuming that there is 5% of code that is conserved since humans, dogs and mice diverged. This is obviously an assumption. Since they don't actually know this to be the case.

quote:

---

It is important to understand that when the ENCODE project talks about functional areas of the genome they are talking about biochemical function in the context of transcription or identifiable binding sites, this doesn't mean that these regions actually perform any functional purpose in the life of the organism. Indeed one of their conclusions is that there is a large amount of functionally active but selectionally neutral genetic material.

---

I don't care. Those are still functional regions we are talking about. I don't care if they are selectable or not. I was the one who was claiming that selection is almost non-existnt from the start. What we have is almost constant geentic drift or near neutral selection.

quote:

---

ENCODE certainly showed that the transcriptome is much more complex than we would have expeected, but it doesn't show in any way that single nucleotides cannot form a suitable substarte for selection, or that genetic recombination cannot resegrate nearby beneficial and deleterious mutations.

---

1.) Common sense is actually what I was appealing to to show you that. A unit of selection is what gets evaluated and passed on. Specific genes do not get evaluated and passed on, neitehr do nucleotides. The overall fitness of the organism is what gets evaluated together with beneficial and deleterious mutations.2.) If we are talking about physically linked genes that there is no way they are going to get recombined. Unless there is some new mechanism for that. Which I'll be glad to accept once it has been found.

quote:

---

Clearly there are deleterious mutations which hitchhike to fixation, but it would be very hard to make a coherent case for any way in which this could happen unless the beneficial mutation they are accompanying outwieghs them.

---

This pretty much happens all teh time. You do know that deleteriious mutations are way, way more overrepresented than the deleterious ones? And you do know that there are about 175 new mutations added to the lineage of human species with every brirth? And now you are going to tell me that deleterious mutations are not going for a ride together with beneficial ones? Are you seriously going to suggest that!?Edited by Smooth Operator, : No reason given.

quote:

---

Great. So tell us what testable predictions ID makes.

---

This is such an old topic? Must we really go over it?(1) High information content machine-like irreducibly complex structures will be found.
(2) Forms will be found in the fossil record that appear suddenly and without any precursors.
(3) Genes and functional parts will be re-used in different unrelated organisms.
(4) The genetic code will NOT contain much discarded genetic baggage code or functionless "junk DNA".FAQ: Does intelligent design make predictions? Is it testable?

quote:

---

So now you're saying that ID *does* have something to say about evolution. Specifically, you're now saying that ID has something very precise to say about the history of life on Earth, claiming that ID says common descent is impossible.

​

So here's the question once again, and please don't yank me through another series of three or four evasive and misleading posts: What is the ID explanation for the history of life on Earth, and more specifically, what is the ID explanation for why common descent is impossible?

---

Wow, just wow.I mean... wow...Really? I said that ID says that CD is impossible? Where, oh where did I say that? Except never. Actually, what I did say is THE COMPLETE OPPOSITE! Yet you somehow missed that. Let my quote myself now...

quote:

---

No, it's fine by me. I like the discussion to be as broad as possible. However, ID is clearly compatible with CD. Michael Behe accepts both ID and CD. So no, there is no problem in accepting both.

---

EvC Forum: Message PeekHow exactly did you miss this one where I said the exact opposite of what you claimed that I said?Once again, just wow...Okay, before this turns into an unnecessarily long discussion, which it basicly already is, let me explain myself thoroughly. I never claimed ID was no compatible with CD. It is compatible. It's also compatible with random mutations that would be acted upon by natural selection to increase the information in the genome. So, a sort of a darwinian evolution is also fine. The only thing that ID is not compatible with is that this kind of darwinian evolution did not have an intelligent cause. There must have been an intelligence at the start. That is what ID claims.And now, if you are goig to invoke a full darwinian evolution to falsify ID, and claim that there can be such a thing as a design without a designer, it's clear that to falsify your argument I have to attack it! Since a full darwinian explanation consists of 3 parts, which are 1.) Common descent, 2.) Random mutations, 3.) Natural selection, me falsifying any of those 3 will make your argument against ID fail.So, yeah if you are going to invoke a darwinian evolution to show that there is sucha thing as a design without a designer, than I have to discuss all 3 aspects of your argument, falsify at least one of them, and show that there is only design with a designer and that ID is correct.

quote:

---

Then ID fails to explain biodiversity.

---

Maybe because it's not trying to do such a thing? Evolution also fails to explain the origin of life? But is that any sort of an argument, since evolution isn't even trying to explain the origin of life. So why would you make such an argument against ID? ID explains the cause behind the design of patterns we observe in the universe. Some of them are found in living organisms. So ID also explains the cause of design in life, it doesn't try to do anything else.

quote:

---

"We see in these facts some deep organic bond, prevailing throughout space and time, over the same areas of land and water, and independent of their physical conditions. The naturalist must feel little curiosity, who is not led to inquire what this bond is."--Charles Darwin, "Origin of Species", Chapter 11

---

Ah yes, Saint Darwin and his Holy Book. Great read...

quote:

---

Aren't IDer's curious as to biogeography? Is biogeography not something that ID must explain in order to explain modern biodiversity?

---

Aren't evolutionists curious as to origin of life? Is origin of life not something that evolution must explain in order to explain modern biodiversity?

quote:

---

As we have already demonstrated, due to the dogmatic nature of ID there is nothing we could ever show which would falsify ID.

---

Either, a.) Show that an event is probable enough to be produced by chance, or b.) show that an event is due to high probability of natural laws. This is how you falsify the design hypothesis.

quote:

---

Rather, the theory of evolution demonstrates that these observable and natural processes are sufficient to explain modern biodiversity in the same way that the Germ Theory of Disease is sufficient to explain infectious diseases but incapable of completely ruling out disease causing demons.

---

Oh, really? Please than do explain the modern biodiversity. I'm waiting.

quote:

---

In order to claim that mutation only results in a loss of function then you must know all functions that the protein has. Given the wide range of possible function it is extremely difficult to do this for every protein. This is why the "mutation only results in loss of information" is such bunk.

---

My main argument isn't even about loss of all information. I simply said that all known functions were lost.

quote:

---

Unless you designed your experiments correctly you would just notice the lack of methylation at the GATC sites. You would call this a loss of function. However, these mutations lead to a new function, methylation at GATT sites. Mutations can and do lead to specifity for new substrates, and given the vast number of possible substrates it is nearly impossible to claim that a protein of no known function lacks function in all situations.

---

Did I ever claim that mutatoins can't leed to new function? I don't remember saying that. Maybe I did, but I really don't remember that.But what I do remember saying is that chance alone can not generate new CSI. Did your experiment claim that that happened? No, it didn't. What did it claim happened? That new functions evolved. Fine? But what kind of evolution was it? A full darwinian evolution, or a directed one? Let me remind you with a quote from your own article.

quote:

---

We have changed the target specificity of EcoDam from GATC to GATT by directed evolution, combining different random mutagenesis methods with restriction protection at GATT sites for selection and screening.

---

A directed one. And it was directed by what? What was the source of direction? What was the information origin for the direction of where evolution is going to go? An intelligence. So the conclusion is, that this is a clear case of intelligent design. Intelligent agents are the ones that produced new functions. Not an undirected process like a darwinian evolution.So you were saying?

quote:

---

Do you have any evidence for this, other than your bald assertions?

---

If you actually payed any attention to the thread you would have noticed the facts I presented a long time ago.Spiegelman's Monster - Wikipedia

quote:

---

I think you are making the same mistake you made earlier. The paper you referred to earlier suggested that the SMALL POPULATION size of LARGE ANIMALS could lead to genetic entropy. They used the size of the animals as a proxy for their population size since larger animals need more territory, hence smaller populations.

---

And after that I showed a paper that is a mathematical model of large sexual populations, which claims that such populations are in the same danger as small populations.Edited by Smooth Operator, : No reason given.Edited by Smooth Operator, : No reason given.

quote:

---

If you think that the fact that you said all function is lost is sufficient to prove that some function remains you have great faith in your ability to get things wrong.

---

I'm simply asking you to name teh functions that are left? Keep in mind that we are totally of the subject now. I neevr claimed that loss of all functions is my main argument. It's you who simply doesn't want to drop this. Why? I don't know. But please do continue, tell me which functions have remained.

quote:

---

We're not discussing that at all, because that was accepted long ago. Instead we go round and round in circles with you switching between asserting that all function was lost and then trying to act as if you never said it.

---

But I did say it. And I told you why I said it. So why again are we talking about it?

quote:

---

It certainly does matter. Since the only "50 proteins" figure we have is the number of different proteins in the E coli flagellum - which is made up of a good many more than 50 protein molecules using that figure implied distinct proteins. But OK, why would 1,000,000 units of 50 distinct proteins be significantly more improbable than 1 of each ?

---

What a question... For the same raeason that getting 6 of 5 dice is less probable than getting one 6 on one die.

quote:

---

Given that the "complexity" we are talking about is a measure of improbability and not closely related to the normal usage then the scare quote are entirely justified.

---

Excuse me, but it's your, not my problem that those two words, complexity and improbability are inversly proportional. When one increases, the otehr decreases. This is a well known fact of statistics. Increase the number of dice, the complexity increases, yet the probbili probability of getting a specific outcome decreases.

quote:

---

Then it's a pity that Dembski did no such thing.

---

Explain why. Point out where you did so, if you already did it.

quote:

---

No, they don't.

---

Where! Show me where is non-uniform pobability used without prior knowledge!

quote:

---

At least not if they want the result that they get to be anything more than a rough estimate.

---

Well, duh! That's what statistics are all about. It's about probability! It's not exact like standard algebra where 1+1=2. It's about approximation.

quote:

---

For things like dice and coins we use a uniform distribution - but that's because of knowledge, not ignorance. (And even there we acknowledge that there might be subtle biases in the real objects).

---

Of course there could be. Nobody is claimng that there couldn't be! I'm not claiming it. Dembski isn't claiming it! Nobody is!But we certainly are ignorat about teh principle of unifom probability of because of ignorance. That is a fact.

quote:

---

As with coins, it is assumed that the initial conditions of throwing the dice are not known with enough precision to predict the outcome according to the laws of mechanics. Dice are typically thrown so as to bounce on a table or other surface. This interaction makes prediction of the outcome much more difficult.

---

Principle of indifference - WikipediaAs you can clearly see, the principle of insufficient reason, or as it is also called the principle of indifference, is uset precisely because we do not know the laws of nature 100%. If we did, we would be doing a statistical analysis in the first place! We would just know what would happen when we threw the die!Anyway, the point I'm trying to make is that we use this principle because it's the best approximation. If you have a better one, please do share it with us. If you don't than we are sticking with this one. If you claim that this method is false because it's not perfect and it's not giving us exact results, than your criticism fails. Because approximations are not supposed to be exact. Approximations are by definitions not exact. And that is what the field of statistics is.So basicly you have no real argument anymore.

quote:

---

In this case it means an idea that is often close to being right (but can be drastically wrong).

---

But it's the best we have. Care to give us a better method? No? Didn't think so...

quote:

---

Re: CSI & Genetic Entropy discussions (Message 1056).

---

Please quote the relevant part.

quote:

---

In fact you did say that and attempted to misuse Sanford's definition to back up your claim.

---

LOL, accusing me of lying again. Goog, good for you...

quote:

---

Please show that the figures used in the runs which lead to mutational meltdowns in large populations used figures derived from a real population.

---

Umm... that's what the scientists were supposed to show not me.

quote:

---

WHich of course means that the issue is not the loss of all genetic information, but just sufficient to disrupt one or more vital functions. Therefore the absolute measure of genetic information is not relevant (the more so because many of the "vital functions" will be "vital" because other aspects of the animal require them - the simpler the life form, the less it has to go wrong).

---

We are still talking about the absolute measure of information. A specific vital fuction is coded for by an absolute, not relative amount of information. And no, it's the individuals with more genetic information that can survive longer while loosing genetic information. Because they can be loosing those functions that are not vital. Unlike simple RNA chains that can loose som much and practically be done with.

quote:

---

You are also refusing to do the very same thing. But I am happy to let my argument stand unrefuted.

---

What the hell did I refuse to do?

quote:

---

If Sanford really claimed that population genetics really required all those assumptions to work at all then Sanford doesn't know what he is talking about.

---

Of course, and that is because you are smarter than he is. You know better than he does. You invented the Gene gun, not him.

quote:

---

1) is not strictly true since the chromosomes are broken up by recombination. Genes that are very close will tend to stick together but that is all. And even if this were not the case, then the most you could do is to take a chromosome as the unit of selection, not the genome.

​

2) is just illogical. The fact that genes interact doesn't mean that they can't be the unit of selection.

---

1.) It doesn't matter if the chromosomes are broken up or not. The blocks of genes stick together. And there is no way that the chromosome is the unit of selection. Does natural selection remove the bad chromosomes and sticks with the rest?2.) Uhh, yes it does. Because a gene is not a specific region. It's multiple regions which overlap. If one region mutates two traits can be affected. So there is not such a thing as one gene one trait.

quote:

---

In sexually reproducing species the genome does NOT get passed on in full.

---

By full I mean the half that gets passed on. That half is not examined by some mechanims inside the cell and all the deleterious mutations are not picked out. And again, by full, I mean that natural selection evaluates the full genome. It evaluates how the whole organism functions, and than it either selects it, or it does not. Only than does that organism pass on that half you were talking about. But first, thw whole genome is evaluated overall.

quote:

---

And in the long term natural selection will tend to favour the better alleles.

---

No it won't. Noise is too large for this to happen. Remember those 6 sources of noise I was talking about? Like epigenetics? It interferes with the selection.

quote:

---

"Hitchhiking" relies on the linkage remaining intact, which is not guaranteed even for adjacent genes - and you've got nothing else.

---

Umm... hitchhiking is what's happening all day everyday. It's caused by the 6 sources of noise I was talking about before. Nto jsut one you just mentioned.

quote:

---

How many bits of having more bits than the bound can a thing have ?

---

What?

quote:

---

Requiring exactly 50 proteins - that isn't in the specification. using the same proteins as in the E coli flagellum or variants of them - that isn't in the specification either.

---

And Dembski never said that 50 proteins is the specification. It's the complexity of the event D*.

quote:

---

I'm simply asking you to name teh functions that are left? Keep in mind that we are totally of the subject now. I neevr claimed that loss of all functions is my main argument. It's you who simply doesn't want to drop this. Why? I don't know. But please do continue, tell me which functions have remained.

---

I am quite happy to leave it at the known function was lost, but we don't know if there were any other functions which remained or other functions gained. You, on the other hand will only leave it there if we hide the fact that you originally argued that ALL functions were lost.

quote:

---

But I did say it. And I told you why I said it. So why again are we talking about it?

---

Because your reason was incorrect, but the closest you will get to admitting it is trying to conceal the fact that you said it.

quote:

---

What a question... For the same raeason that getting 6 of 5 dice is less probable than getting one 6 on one die.

---

THe reason why it is more likely for dice is that the result of the throw is random. The production of proteins is not random - the structure is controlled by the gene. So getting multiple copies of the same protein is not at all like throwing dice.

quote:

---

Excuse me, but it's your, not my problem that those two words, complexity and improbability are inversly proportional. When one increases, the otehr decreases. This is a well known fact of statistics. Increase the number of dice, the complexity increases, yet the probbili probability of getting a specific outcome decreases.

---

Of course what you say is quite silly. If we simply consider Dembski's idiosyncratic usage of complexity getting 500 heads in a row is a "complex" sequence. But in normal usage it would be seen as simple.

quote:

---

Explain why. Point out where you did so, if you already did it.

---

I wouldn't like to speculate on Dembski's motives here.

quote:

---

Where! Show me where is non-uniform pobability used without prior knowledge!

---

I didn't say that it was.

quote:

---

Well, duh! That's what statistics are all about. It's about probability! It's not exact like standard algebra where 1+1=2. It's about approximation.

---

That's also wrong. Statistics are useful in dealing with approximations (e.g. calculation of error bars) but approximations are no better in statistics than in any other branch of maths.

quote:

---

As you can clearly see, the principle of insufficient reason, or as it is also called the principle of indifference, is uset precisely because we do not know the laws of nature 100%. If we did, we would be doing a statistical analysis in the first place! We would just know what would happen when we threw the die!

---

And you will notice that your wikipedia quote says nothing about uniform probability or the reasons for assuming it... In fact all it does is give the reasons for treating dice in terms of probabilities instead of exact predictions. Maybe you should have quoted the previous paragraph, but then that contains a reason FOR assuming that each number is equally likely.

quote:

---

Anyway, the point I'm trying to make is that we use this principle because it's the best approximation. If you have a better one, please do share it with us. If you don't than we are sticking with this one. If you claim that this method is false because it's not perfect and it's not giving us exact results, than your criticism fails. Because approximations are not supposed to be exact. Approximations are by definitions not exact.

---

Dembski claims that his method produces a mathematical proof of design - so no, approximations aren't good enough,

quote:

---

Umm... that's what the scientists were supposed to show not me.

---

I don;t see why they should be expected to come here to back up your claims. And if they were supposed to show it in the paper all you have to do is to find the section where they did it.

quote:

---

We are still talking about the absolute measure of information. A specific vital fuction is coded for by an absolute, not relative amount of information. And no, it's the individuals with more genetic information that can survive longer while loosing genetic information. Because they can be loosing those functions that are not vital. Unlike simple RNA chains that can loose som much and practically be done with.

---

Well that's a confused mess. Nevertheless it seems clear that even an inviable cheetah embryo will have more genetic information than a perfectly viable RNA self-reproducing RNA strand - so obviously the absolute measure is not what we need.

quote:

---

What the hell did I refuse to do?

---

The same thing that you asked me to do. That is what "you are refusing to do the same thing" means.

quote:

---

Of course, and that is because you are smarter than he is. You know better than he does. You invented the Gene gun, not him.

---

Just two problems with that. On is that inventing the gene gun doesn't require a knowledge of population genetics. The second is that it is quite possible that Sanford doesn;t agree with you.

quote:

---

By full I mean the half that gets passed on. That half is not examined by some mechanims inside the cell and all the deleterious mutations are not picked out. And again, by full, I mean that natural selection evaluates the full genome. It evaluates how the whole organism functions, and than it either selects it, or it does not. Only than does that organism pass on that half you were talking about. But first, thw whole genome is evaluated overall.

---

In other words "reality itself" does not say that the full genome is passed on by sexually reproducing species. Only half the genes are, and those are mixed by recombination. This is why we can't use the genome as the unit of selection - it doesn't persist long enough for the statistical effects to build up and dominate over noise. We need something that lasts, something that can spread through a population - and the full genome obviously isn't it.

quote:

---

No it won't. Noise is too large for this to happen. Remember those 6 sources of noise I was talking about? Like epigenetics? It interferes with the selection.

---

And that is simply an assumption. Oddly enough the "noise" didn't stop the alleles producing the melanic form of the peppered moth from spreading, once pollution turned the trees black.
Natural selection can overcome noise.

quote:

---

Umm... hitchhiking is what's happening all day everyday. It's caused by the 6 sources of noise I was talking about before. Nto jsut one you just mentioned.

---

And it also fails to happen every day. Recombination mixes things up.

quote:

---

What?

---

It's a simple question. Being CSI is having more bits of information than the bound. How is that measured in bits ? Why would you ever need more than one ?

quote:

---

And Dembski never said that 50 proteins is the specification. It's the complexity of the event D*.

---

If it's not in the specification his calculation of the probability can't use it. And do you really think that log2-P(D*) is 50 proteins ?

And that is what is wrong. There is no such thing as a genetic block which is immune from recombination. It sounds like you don't know what genetic linkage really is, it is no universal law producing indivisible genetic blocks, it is a statistical reflection of the distance between discrete genetic loci.These discrete loci could even occur within one gene. To state baldly that genes cannot undergo recombination Intragenically is simply to ignore the molecular biology in favour of your own fantasy.The fact that you wilfully ignore the reality of crossing-over naturally lead you to continue being wrong when you talk about natural selection. Yes, of course it is organisms that survive and pass on their genetic material, but they don't pass it all on and the allelic complements get rearranged by meiosis. It is this rearrangement which allows the breaking of linkage between alleles not genes and can allow us to consider the gene an appropriate level of selection. Obviously the genome isn't since the whole genome is never passed on, your contention that a beneficial mutation must carry with it every deleterious mutation in its originating genome just flies in the face of so many basic principles of genetics it is hard to know where to begin. Um, for someone who likes to whine about being misrepresentied you seem to be doing a bang up job here yourself. The point is that selection is a statistical phenomenon, by breaking linkages between discrete allele loci mechanisms such as recombination allow for the alleles to be selected more independently.No one other than you is positing any mechanism in the cell picking out the best genes. What I am describing is that within a population the various rounds of recombination will lead to a dissociation of particular genetic allelic combinations, which will be proportional to their linkage but still provides the possibility of even the most closely linked loci being seperated. Over time this means that selection will tend to lead a favourable allele to increase in proportion.No one is denying the existence of deleterious hitchiking residues, there is plenty of genetic evidence for them although since you don't seem to accept gentic evidence, questioning as you do the idea of sequence conservation between mammalian genomes, I guess you must just be assuming this based on common sense since you deny the actual scientific basis which has allowed those determinations to be made.Sorry about the mixup on the 5% thing, I was talking about the ENCODE data, which is what you claimed you were talking about. It turns out that in fact you were talking about a part of the review you cite which in fact had nothing to do with ENCODE. I think this rather supports my contention that you don't know what ENCODE did. What you are ascribing to ENCODE is research that has been ongoing for decades, the review itself discusses how Jaques Monod in the 60's was disrupting the naive 'one gene == one trait' conception. That doesn't make the idea of a gene being the unit of selection erroneous, although myself I think the nucleotide might be a better choice since it is a truly discrete genetic unit, it just shows that the historical conception of what constitutes a gene was erroneous.You say you don't care about the distinction the ENCODE project highlight between biochemical function, a region of DNA being transcribed, and biological function/effect. But by this standard it is trivially easy to show the generation of novel biochemical function in the genome, many trx factor binding sites and transcription start sites are comparatively simple to create by chance and certainly may be moved around very easily.All you are doing by talking about pervasive neutral evolution is agreeing that in fact most of the genome serves no biological function even if it is biochemically functional. I though the more common ID position was the exact opposite of that, that the majority of the genome does perform a neccessary function but that we just don't understand it yet.You complain about being misunderstood, but as far as I can see that is because you are talking about things you yourslef don't understand which makes your argument very unclear.Recombination within genes happens, recombination between closely linked loci happens. The fact that you think a new mechanism is needed to explain this just shows how unfamiliar you are with the already well characterised mechanisms. Here you have confused weight for number, if I have 1 block of granite wieghing a tonne and you have 800 feathers weighing only a few kilogrammes then clearly my block outweighs your feathers for all that they outnumber it. It isn't the number but the effect that is important. Of course deleterious mutations are hitchhiking, and some are just being fixed by drift, it is the size of the effect of these mutations that is important.TTFN,WK

I think your problem is that you say whatever is expedient at the time. Here's you saying that common descent is impossible in Message 1092: So, reinterpreting the above in light of your reemphasis that you have no problem with common descent, this is apparently saying that ID states that evolution's removal of the designer from the process is impossible.I would say it a bit differently, that evolution is a theory that explains the evidence through a process of descent with modification and natural selection, while ID is a theory that explains the evidence through the intervention of a designer. You're in effect claiming that a theory that doesn't include a designer is impossible, so if ID has evidence of the designer then this is the time to introduce it, but what we usually hear from IDists is that we cannot know the identity of the designer or how he designed. Yes, we know. And what happens if you project this requirement back in time? Let's say that life on Earth was created by an intelligence. Where did that intelligence come from? Maybe, following Shermer's example from the November debate, that intelligence came from Antares (a nearby star). Maybe intelligent aliens from Antares came to Earth a few billion years ago and placed the first life on this planet.But since there must have been an intelligence at the start, Antarean life must also have come from an intelligence, so where did the Antarean life come from? A planet orbitting a star in the Andromeda galaxy maybe? And where did that life come from? And the life before that and before that?After a while we're back to the plasma of the Big Bang before there were atoms, and there was no life anywhere to create the next life. So where did that first life in the universe come from?At this point most IDists concede that they believe the designer is God, and at that point they've definitely left the realm of anything supported by scientific evidence, although they'd already done that when they posited a designer for life on Earth in the first place. All four are predictions made after the fact and aren't predictions at all, plus all four are consistent with evolution. Does ID make any predictions that are different from evolution?AbE: To be more clear concerning point 1, evolution is consistent with specification and complexity, since evolutionary solutions must by necessity be very specific to the requirements of the environment and since competition generates increasing complexity in a way analogous to escalating arms races, but evolution is not consistent with the irreducible complexity of Behe for which there is no evidence.--PercyEdited by Percy, : Add AbE comment.Edited by Percy, : Fix message link.

I'd quibble with this, specifically based on SO's point 3, 'Genes and functional parts will be re-used in different unrelated organisms', after all in a framework incorporating common descent, even just for the animalia, there are no 'unrelated' organism examples for this to apply to.I'd also point out that it is far from established that most of the genome serves any function other than just being there. So far the proportion with any actual identified biological functionality is still in single figure percents, although if we allow the ENCODE project's very loose concept of biochemical function then I agree that this increases the proportion massively, but it doesn't actaully have any clear relevance to the actual biological functioning of the organism. There clearly is a large amount of genetic baggage in terms of repetitive elements and processed pseudogenes. That isn't to say that some such elements are not functional, but to leap from that to saying that almost all of them are is to go way beyond anything the evidence actually supports.TTFN,WK

I didn't want to put too fine a point on it, but agreed. SO called his list predictions of ID, but I didn't say they were predictions of evolution, just that they were consistent with evolution.About point 3, I interpreted it as a claim that ID predicted things like viruses inserting genes, though of course ID interprets it as the designer inserting genes.About point 4, there's a wide range of the proportion of functional DNA that would be consistent with evolution. My guess is that evolution would predict that the amount of functional DNA in any species would be a function of the specific changes that DNA had experienced over time, and that therefore we should find wide variation in nature. For example, there's the amoeba that has a huge amount more DNA than humans. If amoeba and human have roughly the same proportion of functional DNA then that would mean the amoeba has far more functional DNA than humans. This doesn't seem likely, so I think the prediction make sense, what do you think?But the main point I was making was that SO's supposed predictions were after the fact. ID and creationism never make a prediction first then go looking for it and find it.--Percy

You mean evidence like orthologous ERV's, shared pseudogenes, etc.? We have that evidence in spades. The genetic evidence is conclusive. Ignoring the evidence is not helping you. We do observe a nested hierarchy. Yes, there is a little noise as would be expected from homoplasies and reverse mutations, but the overwhelming signal is a nested hierarchy. A bush is a nested hierarchy. From that same article:"A phylogenetic analysis unambiguously confirms the conclusion that chimpanzees were our closest relatives to the exclusion of other primates and the relative divergence of the Homo—Pan and that of (Homo—Pan)— Gorilla are 4.93 million years and 7.26 million years, respectively."They agree with me. The nested hierarchy is unambiguous. Why aren't airbags found in a single lineage of cars? Why don't cars fall into a nested hierarhcy? Feathers are found in a single lineage of vertebrates. Three middle ear bones is found in a single lineage of vertebrates. So why aren't airbags found in a single lineage of cars, both morphologically and chronologically? Why are there cars with jet engines? If cars can have jet engines why can't bats have feathers? Why do human constructs consistently fail to produce a single nested hierarchy? You tell me. Why can't a designer change the architecture at will? Why a nested hierarchy? Do you have any siblings? If so, the features you share are due to common descent. It really isn't that hard to figure out.At the same time, can you show how mutations that occur in one species can spread to another species? It doesn't happen in metazoans. This produces a nested hierarchy. You seem to be really mixed up here. A nested hierarchy can not be built for a bat with feathers. Can't be done. A nested hierarchy is clearly falsifiable. A flagellum is just one possible solution for motility, and those odds are only for a flagellum like the one that appeared. I'm sorry, but your probabilities are built on baseless assertions. I already spelled it out for you with the hemoglobin S example. It is plain as day. You say it is stupid, and yet that is exactly what the data indicates. The single nucleotide change in hemoglobin S has been selected through positive malarial resistance selection (positive) and sickle cell anemia selection (negative selection).

So ID is not trying to determine why bacteria have flagella? Really? So I guess we can say that ID explains nothing about biology? Evolution deals with CHANGE in life, not the origin thereof. Abiogenesis deals with the origin of life. My example demonstrated that the specificity of an enzyme changed due to random mutations. The authors simply created an environment where such mutants would be detectable using their methodologies. That's it. This is no different than penicillin intelligently selecting for resistance mutations in bacteria. Is penicillin an intelligent agent? If you could be so kind, could you give the link for that paper again.