Annoying creationists

[I less than three logic]

Actually, no I didn't.

Sorry your ability to comprehend failed you. Happen often?

What distinguishes your useless psycobabble from his?

 

[joobz]

There also wasn’t a lack of evidence for the flat earth theory; however that evidence was overwhelmed by further discoveries.

Actually, there wasn't a ton of evidence for flat earth. I do agree with the further discoveries point though. As we discover and know more we fit the data to the most logical models. But I'm still waiting for the evidence to be "stacked against" evolutionary theory. It needs work hammering out the details. (I think Paul's presentation of the cooperative effect represents this).

But saying, point mutation and natural selection isn't enough doesn't equate into evoution it wrong.

The field of immunology advances despite the theory of evolution, not because of the theory of evolution.

Please explain this statement? Do you have some interesting examples where this is the case?

It’s the mathematics joobz, the theory does not add up.

You keep saying this, but the evidence has argued against it. All simulations that have been presented agree with Paul's analysis of the data. If you feel that the Rcapacity limitation in the model has a meaningful real world significance and is not a simulation oddity, that would be one thing. But as it stands, you are more interested in pretending to have found the proof against evolution than remaining within the bounds of reality. I would place more weight on your ideas/theories if you stopped contridicting hard data and stopped engaging in personal attacks.

 

[joobz]

Nah, I read it as useless psycobabble posted by a useless nobody.

Not that you would care, but this post disappoints me a bit. I have enjoyed greatly your participation on the threads I've read. Admittedly, Foster Zygote had directly attacked the presentation style to your posts, but presented reasons for that attack. You countered with a single line personal value judgement that provided no reason for that statement.

Now, I don't expect every post to possess lengthy explanations, but something with this much ire should contain some justification. Otherwise it seems to come from pure emotion and devalues many of the interesting comments you've made up til now.

 

[hammegk]

What distinguishes your useless psycobabble from his?

In your case, perhaps it's an in-ability to separate his meaningless psychobabble from my meaningful commentary.

 

[hammegk]

Not that you would care, but this post disappoints me a bit.

Actually, I would care.

I have enjoyed greatly your participation on the threads I've read.

Thank you.

Admittedly, Foster Zygote had directly attacked the presentation style to your posts, but presented reasons for that attack. You countered with a single line personal value judgement that provided no reason for that statement.

Yeah, I find little value in glib personal analysis, nor is he alone in piling on this instance. I take plenty of nastiness from one of our resident jerkettes, articulett, and from time-to-time return the favor. Butt-in-skies who choose to stick their oar in those previously roiled waters may not appreciate the result.

Now, I don't expect every post to possess lengthy explanations, but something with this much ire should contain some justification. Otherwise it seems to come from pure emotion and devalues many of the interesting comments you've made up til now.

Thanks for sharing.

 

[kleinman]

Annoying Creationists

Don’t confuse that I am not making any scientific claims about the origin of life with a claim that it occurs by magic.

Why not? You refuse to state your hypothesis. If not by magic and not by evolution, then by what? Either life is a process of matter which occurs under suitable conditions or it's the product of some supernatural force.

And, if you have developed some third alternative, then tell us all what it is.Otherwise, I will assume that you are just dodging the issue, so you don't have to reveal that you do indeed believe in magic. Which is juvenile.

Now what are you whining about? I happen to have some interest in Dr Schneider’s ev program and what it shows when you put realistic parameters in the model. Just because his model shows that evolution by random point mutations and natural selection is mathematically impossible, somehow you figure it is my responsibility to give you a scientific explanation of how life appeared. I happen to believe that we were created, if you want to believe that life arose in a crock pot, that’s fine with me, just don’t try to pass off your beliefs as science.

Neither have I decried any scientific investigations we have been discussing. On numerous occasions I have applauded Dr Schneider’s work in developing ev. I am only critical of the superficial analysis he did with his model but I believe he did a good job applying the fundamental theories involved.

You have yet to answer his three responses posted on his blog. You won't model anything further to see if it affects the outcome of EV. You're content to merely pound on your one point as if it is self evident that no selection mechanism, other than the artificial mechanism found in EV, has any effect on information gain.

Schneider doesn't think it's self evident. So if you actually respect him, then prove he's wrong. Until you do, you're just demanding that the evolutionary proponents exclude all possible alternatives to God, before you will concede that God is not the cause. Also juvenile.

You lazy Dilbert, you didn’t read the Evolutionisdead thread on this topic. If you had, you would have seen my responses to what Dr Schneider had posted on his blog. Since you are too lazy to read the thread, I’ll repost my responses to Dr Schneider’s points that he raised on his blog. These issues were raised on http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/blog-ev.html

2006 Jun 27. Alan Kleinman started a discussion at Evolution Is Dead!. He ran the Evj program with exponentially increasing genome size and proportionally increasing number of binding sites. He found that the time to evolution increases exponentially. From this he claims that although Ev is a good model for small genetic elements, it cannot be extended to large genomes. In particular, he is responding to this statement in the Ev paper

This is not an accurate representation of what I am contending about ev. At the time he posted this message, I had not varied the number of binding sites on any of the cases that I ran with ev. My initial cases presented in my initial post on this site simply consisted of doubling the genome length while keeping all other parameters fixed. In those cases, the generations for convergence quadrupled when the genome length was doubled. I believe ev is a plausible model for both small and large genomes.

Likewise, at this rate, roughly an entire human genome of ~4x109 bits (assuming an average of 1 bit/base, which is clearly an over­estimate) could evolve in a billion years, even without the advantages of large environmentally diverse world-wide populations, sexual recombination and interspecies genetic transfer.

The reason Dr Schneider’s case accumulated 1 bit/base with the 256 base genome used in his ev paper is that a mutation rate of 1 mutation per generation for a genome this size is 10,000 times larger than would be seen in a real organism. Extending the genome length while keeping the mutation rate at 1 mutation per genome per generation starts to reflect the more realistic rate at which information would be accumulated.

There are a number of errors in Dr. Kleinman's argument:

1. The mutation rate was kept constant per genome. This is not what occurs in nature, where DNA polymerases make errors at a certain rate per base. I used a fixed mutation rate in Ev because that made the program simple and it was not the focus of the initial model. Paul Anagnostopoulos has modified Evj so that it can now have a constant error per base.

The error rate for DNA polymerases in E coli has been measured at 1 in 10^6 to 10^7 nucleotides. That is one wrong nucleotide per organism per generation. I have no problem with Dr Schneider using a constant error rate per base but in order to represent reality, that number should be between 10^-6 and 10^-7, not 1 per 512 bases as Paul Anagnostopoulos was using in the cases he was presenting. A mutation rate that high could not be sustained by any living thing.

2. Large genomes are known to appear by many duplication mechanisms that are not in the Ev model. There are polymerase slippage, illegitimate recombination, transposons, insertion sequences, tetraploidization, and Robertsonain translations. These can all increase genome size rapidly. The mechanisms are currently not part of the Ev/Evj model.

Ultimately, all these mechanisms of duplication and recombination errors must yield functional genes in order for evolution to proceed. Unless these genes are immediately functional, then more errors or mutations must occur to morph these pieces of genetic material into functional genes. You are now back to the ev model to accomplish this morphing process which as ev shows is profoundly slow for realistic sized genomes. Transposons and insertion sequences are seen in manufacture of antibodies. Dr Schneider, do you believe this same mechanism is involved in evolution? If so, how does this differ from crossing over recombination that is seen in meiosis? Dr Schneider works at the National Cancer Institute. He must be aware what genetic errors lead to.

3. Genes diverge after duplication. Once a genome has increased in size or a gene has duplicated, we know that genes diverge and take up similar but not identical function. An example is the vast family of ABC transporter genes. Kleinman objected to the idea of duplication because he could not see that there can be advantages eventually as the genes diverge. That is, he neglected the third point.

Dr Schneider’s example of the ABC transporter genes is a good example of what happens when someone is heavily indoctrinated into the evolutionary way of thinking. If you look at the link to the ABC transporter genes, you will see a list of these genes and where they diverge and the diseases associated with each of these divergences. The following quote is taken from that web site:

A more detailed account of each of the human ABC genes is given below. For each gene, a concise description is given on the known function and disease involvement,

Natural selection prevents divergence from taking the structure of each of these genes too far from their baseline structure. Too much divergence in a ABC gene causes disease.

I never objected to the idea of gene duplication. When Dr Schneider originally proposed this idea to me in our email communications, my argument to him was duplicating a gene introduces no new information. The gene still produces the same enzyme or protein. The duplicated gene must still be mutated to a new gene for new enzyme to be produced. If you are depending on point mutations and natural selection to convert the duplicated gene to a new gene, you are going to have a long, long, long wait according to ev.

When Paul Anagnostopoulos ran a model with 96 creatures, 16 sites, and 1 mutation per 256 bases, varying the genome size from 256 to 16,384 he got (generations to Rs >= Rf) = 3.37 (genome size)0.97 with r=.99. This is less than exponential.

It surprises me that a PhD Molecular Biologist would use such a large mutation rate. Introductory Biochemistry texts give mutation rates for DNA polymerases at much smaller values. The mutation rate used in the above cases was more than 10,000 times greater than seen in reality. His selection process only kills off half the creatures per generation. A mutation rate this high would surely kill off every creature. The mutation is the questioning process and the weight matrix is the natural selection answering process. This is how information in the genome is accumulated. Unfortunately for evolutionists, mutation rates as high as Dr Schneider would like to use can not and do not exist in reality. When a realistic mutation rate is used, the exponential nature of the genome length/generations for convergence presents itself.

2006 Jun 27. Alan Kleinman stated:

Some people may start questioning the validity of ev based on the marked variations of the generations for Rs->Rf simply by changing the random seed to start the calculation. Given that Evj is a stochastic process, we expect variation in the generation time. To investigate this, I ran Ev (the original Pascal program) 1000 times and got this distribution. Clearly it is not a Gaussian but it is a defined distribution. (The full analysis is available.)

I found it peculiar that a random seed would have such a large effect on the generations for convergence for ev. Perhaps this variance would not be as noticeable for large genomes. If Dr Schneider is convinced of the validity of his model, that is fine with me.

These responses were posted months ago on the Evolutionisdead forum and have been discussed on both the EID forum and this forum in more detail.

I haven’t lived in Clovis for years but now you can easily verify my medical credentials. With that piece of information and the title and publisher of my PhD thesis you can verify my engineering credentials. You are really trying to find the exit to your cubicle.

I just needed to identify your county of residence. Thanks for making it so easy, by taking the bait and admitting you're licensed to practice in California. Doubtless your PO Box is located in the same county.

As for the exit to my cubical, I know where that is, too

This is all public information. You need the help; otherwise its going to take as long for you to present your marketing plan as it takes ev to converge with a realistic genome length and mutation rate.

How did you find the exit to your cubicle? Did you use the process of elimination?

Hammegk wasn’t the only one to interject God into a scientific discussion. You did this yourself...

Your statement demonstrates your disingenuousness. You're smart enough to know that I only raised the God issue to question why someone else would raise it. So, what you're really doing is nothing more than juvenile baiting. Try to stick to what you know, and leave sarcasm to the professional comedians.

Stop bellyaching and prepare your marketing plan.

There also wasn’t a lack of evidence for the flat earth theory; however that evidence was overwhelmed by further discoveries.

Actually, there wasn't a ton of evidence for flat earth. I do agree with the further discoveries point though. As we discover and know more we fit the data to the most logical models. But I'm still waiting for the evidence to be "stacked against" evolutionary theory. It needs work hammering out the details. (I think Paul's presentation of the cooperative effect represents this).

But saying, point mutation and natural selection isn't enough doesn't equate into evoution it wrong.

Random mutations and natural selection has always been the slogan for the theory of evolution. Random point mutations and natural selection has been the cornerstone for the theory. Ev demonstrates how profoundly slow this process is even with a very stringent selection process. I can not think of and have not heard a plausible explanation from evolutionists how other forms of mutations such as gene duplications, frame shifts, etc. would overcome this mathematical deficiency that ev demonstrates in the theory of evolution.

The field of immunology advances despite the theory of evolution, not because of the theory of evolution.

Please explain this statement? Do you have some interesting examples where this is the case?

Consider the very example you raised of Flu vaccinations. The concept of immunization appeared before Darwin was born. Attempts at immunization for smallpox were done before 1800. The concept of immunization was not drawn from the theory of evolution.

It’s the mathematics joobz, the theory does not add up.

You keep saying this, but the evidence has argued against it. All simulations that have been presented agree with Paul's analysis of the data. If you feel that the Rcapacity limitation in the model has a meaningful real world significance and is not a simulation oddity, that would be one thing. But as it stands, you are more interested in pretending to have found the proof against evolution than remaining within the bounds of reality. I would place more weight on your ideas/theories if you stopped contridicting hard data and stopped engaging in personal attacks.

What analysis of the data are you talking about? Why is Paul running a series with a wider binding site? The only thing Paul has been doing is retracting statements which support my contentions. I’m wondering when Paul is going to throw the entire ev model out.

I am considering co-opting Paul’s concept of Rcapacity. What is preventing me at this time is that I can’t tell whether this is a peculiar characteristic of Dr Schneider’s model or whether it represents something which would occur with a real genome. I suspect that in reality, natural selection doesn’t have the precision that Dr Schneider has given his model with his weight matrix and that Rcapacity is a reflection of this effect. What you have to consider is that Dr Schneider has designed a selection process that converges very quickly for short genomes but slows down very rapidly as you use larger genomes and slower mutation rates in the model. I don’t believe there is any selection process that would speed up convergence for longer genomes or correct the Rcapacity issue. This is the underlying mathematical conundrum that must be overcome for the theory of evolution to have real hard scientific validity. I don’t believe there is any known mechanism that overcomes this mathematical hurdle.

 

[kjkent1]

Now what are you whining about? I happen to have some interest in Dr Schneider’s ev program and what it shows when you put realistic parameters in the model. Just because his model shows that evolution by random point mutations and natural selection is mathematically impossible, somehow you figure it is my responsibility to give you a scientific explanation of how life appeared. I happen to believe that we were created, if you want to believe that life arose in a crock pot, that’s fine with me, just don’t try to pass off your beliefs as science.

So, like I said, you believe in magic. The gods of Mt. Olympus are no less believable than the god of Moses. The stories are equally fanciful, and equally for children. If that's how you balance the left and right sides of your brain -- I'm fine with it. But, don't try to pan it off as anything other than exactly what it appears to be: nonsense.

You lazy Dilbert, you didn’t read the Evolutionisdead thread on this topic. If you had, you would have seen my responses to what Dr Schneider had posted on his blog. Since you are too lazy to read the thread, I’ll repost my responses to Dr Schneider’s points that he raised on his blog. These issues were raised on [URL]http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/blog-ev.html [/URL]

See, it took a while for me to keep on poking you in the ribs, but you finally put up your argument in one place where everyone can see it. Congratulations on having your balls descend.

I'll leave it to the more scientifically knowledgeable here to argue your specific points. I'm just glad to be of service to the community.

This is all public information. You need the help; otherwise its going to take as long for you to present your marketing plan as it takes ev to converge with a realistic genome length and mutation rate.

You are still blissfully ignorant of why I might want to know your county of residence. That's okay. As long as you remain civil with me, it will never be an issue.

How did you find the exit to your cubicle? Did you use the process of elimination?

No, I use the toilet for elimination purposes. But, if you prefer to mark your territory the "old fashioned way," I can see why you'd live way out there by Yosemite.

Stop bellyaching and prepare your marketing plan.

There's a world of difference between a marketing plan and a scientific research proposal. I'll handle the marketing plan, after you produce the research proposal.

 

[Paul C. Anagnostopoulos]

I am considering co-opting Paul’s concept of Rcapacity. What is preventing me at this time is that I can’t tell whether this is a peculiar characteristic of Dr Schneider’s model or whether it represents something which would occur with a real genome. I suspect that in reality, natural selection doesn’t have the precision that Dr Schneider has given his model with his weight matrix and that Rcapacity is a reflection of this effect.

I think you are correct. The binding site width isn't constrained in nature like it is in Ev. All I'm saying about Rcapacity is that you have to make sure it is large enough to accommodate the genomes sizes you're experimenting with, so you don't mistake an Rcapacity issue for some unknown dampening effect.

However, consider an existing binding site when a genome is enlarged by some sort of duplication or acquisition event. Then suddenly perhaps Rcapacity < Rfrequency. So it's not entirely irrelevant.

What analysis of the data are you talking about? Why is Paul running a series with a wider binding site?

See above.

~~ Paul

 

[Paul C. Anagnostopoulos]

Folks, it's getting a tad bickericious in here. Take it easy.

~~ Paul

 

[kleinman]

Annoying Creationists

This is all public information. You need the help; otherwise its going to take as long for you to present your marketing plan as it takes ev to converge with a realistic genome length and mutation rate.

You are still blissfully ignorant of why I might want to know your county of residence. That's okay. As long as you remain civil with me, it will never be an issue.

Let’s do a remake of the Scopes-monkey trial, you can play the monkey.

 

[joobz]

Random mutations and natural selection has always been the slogan for the theory of evolution. Random point mutations and natural selection has been the cornerstone for the theory.

This may at one time had been the case, but I don't know a single biologist who would hold to this.

Ev demonstrates how profoundly slow this process is even with a very stringent selection process. I can not think of and have not heard a plausible explanation from evolutionists how other forms of mutations such as gene duplications, frame shifts, etc. would overcome this mathematical deficiency that ev demonstrates in the theory of evolution.

Here is where we disagree. This model shows that point mutations alone within a ceratin functional window can form new binding sites. Any argument from a time line is erroneous. There exists too many different types of stimulii that can speed up the process.

Consider the very example you raised of Flu vaccinations. The concept of immunization appeared before Darwin was born. Attempts at immunization for smallpox were done before 1800. The concept of immunization was not drawn from the theory of evolution.

look into the idea of original sin and immunizations. Flu shots can (and have been shown) known to enhance a person's likelyhood of contracting the disease. Genetic drift in the antigen sites reduce the effectiveness of the antibodies generated from a vaccine. If the drift is huge and the antibody raised is completely ineffective, the body can use a rapid antibody generation method to fend off the infection. If they drifted only slightly, the body trys to rework the existing antibodies to target the virus. this is a slower process and typically results in a enhanced likelyhood of catching the disease.

The game is, we can never really know which virus strain will propogate and how much genetic drift it will exhibit. Some change more than others. Our ability at understanding this viral evolution allows us to better select a range of viruses to immunize against. Also, it has suggested that a 4 strain (instead of the 3 used)selection spaced ideally across the epitope space would greatly minimize the likelyhood of "original sin" from occuring. This is directly a feature of evolution that has been modeled and effectively used in handling medical care.

What analysis of the data are you talking about? Why is Paul running a series with a wider binding site? The only thing Paul has been doing is retracting statements which support my contentions. I’m wondering when Paul is going to throw the entire ev model out.

I guess we've been reading different threads. I've seen ev work quite well within the Rcapacity bounds.

I am considering co-opting Paul’s concept of Rcapacity. What is preventing me at this time is that I can’t tell whether this is a peculiar characteristic of Dr Schneider’s model or whether it represents something which would occur with a real genome. I suspect that in reality, natural selection doesn’t have the precision that Dr Schneider has given his model with his weight matrix and that Rcapacity is a reflection of this effect.

I have a feeling you are right. But it also provides another look at an interesting fact. Binding sites don't evolve in a meaningless genome. In the model, every site can mutate and has no seperate positive negative effect. Such a system would be unlikely to evolve. However, the genomes didn't evolve that way. They seemed to have grown with time. At least current theory doesn't suggest it and this model agrees with that. We don't start with a informationless background genome.

 

[kleinman]

Annoying Creationists

I am considering co-opting Paul’s concept of Rcapacity. What is preventing me at this time is that I can’t tell whether this is a peculiar characteristic of Dr Schneider’s model or whether it represents something which would occur with a real genome. I suspect that in reality, natural selection doesn’t have the precision that Dr Schneider has given his model with his weight matrix and that Rcapacity is a reflection of this effect.

I think you are correct. The binding site width isn't constrained in nature like it is in Ev. All I'm saying about Rcapacity is that you have to make sure it is large enough to accommodate the genomes sizes you're experimenting with, so you don't mistake an Rcapacity issue for some unknown dampening effect.

However, consider an existing binding site when a genome is enlarged by some sort of duplication or acquisition event. Then suddenly perhaps Rcapacity < Rfrequency. So it's not entirely irrelevant.

I understand your hypothesis about Rcapacity. I view this as a side issue.

What analysis of the data are you talking about? Why is Paul running a series with a wider binding site?

See above.

These questions were address to joobz. I know you understand why you are doing a series with a wider site width. I’ll stick my neck out here and guess that the wider site width will not give a significant reduction in the number of generations for convergence. The series you are doing now will show that your extrapolation of 200,000,000 generations for the 100k genome with a 10^-6 mutation rate and a population of 1meg was reasonably accurate.

I believe there is only one possible use for ev in support of the theory of evolution and that is for huge populations to accelerate evolution sufficiently. I can’t do any larger population series with my computer and you can only do one more data point than my machine. In order to do a population of 10^9 you would need a machine with 1000 gigabytes of memory and that would be for a genome length of 1k.

Folks, it's getting a tad bickericious in here. Take it easy.

Did I miss something?

 

[kjkent1]

Let’s do a remake of the Scopes-monkey trial, you can play the monkey.

That's fine. You can be...the defendant.

 

[John Hewitt]

If you want to engage in a scientific discussion on this topic, you have to come up with a workable definition that people can agree on. I think I see the distinction you are making between the words “data” and “information”. For example data could be the measured state of a system while the degree of order of the data would represent the information content.

Unfortunately, one would wait a long time for people to agree on definitions. The distinction I make between data and information is standard in school level IT but it tends to be ignored by experts in the same field. In the context of standard biochemistry, the genetic data would be the sequence of bases in a gene, while the biochemical activity of the gene's product (most often the enzymatic activity of a protein) would be information, the interpretation of that data.

If selection is as powerful as to be able to organize atoms and molecules to create the genetic molecules and proteins necessary for life and then evolve these complex molecules to the life forms we observe today you should be able to mathematically model such a profound force. Dr Schneider’s use of a binding protein (weight matrix) which imposes a very stringent selection process yet is still profoundly slow in evolving binding sites.

Selection is quite logical but I do not think one can necessarily model it mathematically, one may be able to do so. Computer simulations are generally more powerful than mathematical modelling. My work is a metabolism first theory and my concern is with the selection of sun induced chemical oscillations to produce metabolic pathways. It may be techically possible to model that process but I think such simulations are beyond my capacities. I therefore confine myself to the general chemical picture.

 

[Paul C. Anagnostopoulos]

These questions were address to joobz. I know you understand why you are doing a series with a wider site width. I’ll stick my neck out here and guess that the wider site width will not give a significant reduction in the number of generations for convergence. The series you are doing now will show that your extrapolation of 200,000,000 generations for the 100k genome with a 10^-6 mutation rate and a population of 1meg was reasonably accurate.

Here is my data so far:

population 32
binding sites 8
weight width 9
site width 10
1 mutation / 512 bases

genome size, generations

1024, 8000
2048, 20000
4096, 34000
8192, 37000
16384, 76000
32768, 272000
65536, 392000
128000, 1000000 (est.)

(fits -15837 + 7.61G) So at 1 mutation per million bases, that's about 2 billion generations. If it varies as population^-.25, as our population experiments show, then at a tiny population of 1 million it would take about 63 million generations.

I'll post the final numbers when the 128K experiment finishes. This experiment will take about 150 hours of processor time, so I doubt I'll be running anything larger. Maybe while I'm on vacation in February.

~~ Paul

 

[RecoveringYuppy]

The distinction I make between data and information is standard in school level IT but it tends to be ignored by experts in the same field. In the context of standard biochemistry, the genetic data would be the sequence of bases in a gene, while the biochemical activity of the gene's product (most often the enzymatic activity of a protein) would be information, the interpretation of that data.

Since evolutionary theory is based on both genes their expression, what exactly did you mean earlier when you said that evolutionary theory should be based on information and not data?

And why not use the words "genes" and "expressions" rather than two terms that you got from some other field where you acknowledge that aren't even consistently used in your manner?? And not even to mean the same thing you are using them for here?

 

[Paul C. Anagnostopoulos]

In the context of standard biochemistry, the genetic data would be the sequence of bases in a gene, while the biochemical activity of the gene's product (most often the enzymatic activity of a protein) would be information, the interpretation of that data.

So there's no information in DNA? If not, then how does the information leak into the proteins?

Hey Kleinman, we can stop having this conversation. There's no information in DNA.

~~ Paul

 

[John Hewitt]

Since evolutionary theory is based on both genes their expression, what exactly did you mean earlier when you said that evolutionary theory should be based on information and not data?

And why not use the words "genes" and "expressions" rather than two terms that you got from some other field where you acknowledge that aren't even consistently used in your manner?? And not even to mean the same thing you are using them for here?

I believe I said that evolution should be based on data not genes.

I develop evolutionary theory that way because organisms seem to derive from, do contain and are involved in other manifestations of evolution besides biological evolution and genes. I have attempted to construct a generalised form of evolutionary theory capable of describing all manifestations of evolution in all milieu. "Genes" and "expressions" do not generalise in this way.

Certain concepts are necessarily present in all forms of evolution - data, interpretation, information, selection and knowledge - here defined as selected information. It is true that both data and information are necessarily common to all forms of evolution but the definition "information is interpreted data" clearly makes data the core concept and information into a derived concept.

I have no idea why luminaries of the IT field tend to ignore the distinction between data and information but experts in all fields seem to do similar things and ignore changes in nomenclature. Senior chemists, for example, sometimes still talk about "acetic acid." (IUPAC now ask us to call it ethanoic acid.)

 

[John Hewitt]

So there's no information in DNA? If not, then how does the information leak into the proteins?

Hey Kleinman, we can stop having this conversation. There's no information in DNA.

~~ Paul

This comment appears to be facetious.

I assure you that the distinction between data and information was not invented by me, it is taught in schools. It is given in Wikipedia and in the BBC's GCSE bitesize for school IT.

You might find the distinction between information and data easier if you think about a word processor file. You may write the same English text into a "word" document or into a wordperfect document. The data in the two files would be quite different but would be interpreted by English speaking readers in the same way. However, a non-English speaking readers might place a different interpretation. Information comes from data and from interpretation.

There is, in fact, very little information in DNA. The external shape and chemistry of the double helix is very uniform, regardless of its base sequence. Variability, and hence potential for biochemical interpretation, arise mainly after translation of base sequence data into protein.

 

[RecoveringYuppy]

I believe I said that evolution should be based on data not genes.

OK. But no matter what combination you use of the four words you are equivocating over you can find plenty of people studying evolution form that POV. So what exactly are you proposing?