Antievolution.org - Antievolution.org Discussion Board -Topic::Evolution of the horse; a problem for Darwinism?

Posted: Nov. 04 2007,17:19

Then i'm also curious why you're (directing at Daniel here, ofcourse) so sure of those theory's because apperantly you don't know a lot about them. Is it really just because Shindewolf was mocked at by the scientific community? You do know that that has absolutly nothing to do with the vality of his theory, right?

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Joined: Sep. 2007

Posted: Nov. 04 2007,20:08

Quote (Richard Simons @ Nov. 04 2007,15:30)

Quote

Yes, please provide links to those papers and please elaborate as to how these things "devastated" Schindewolf's theory.

When I asked you about some aspects of Schindewolf's theory your response was

Quote (Daniel Smith @ Oct. 25 2007,13:50)

Quote (Richard Simons @ Oct. 25 2007,00:00)

Back to Schindewolf! I am not sure why a hypothesis that has been essentially dead for 50 years holds so much fascination for you. However, given that it does perhaps you could explain how the information to constrain an organism's evolutionary pathway is held. What conceivable mechanism could stop evolution from taking place, or enable parts to evolve before they became useful?

I am also curious about the saltational events. Do you see these as creating a new genus, order, phylum or what? What actually occurs during a saltational event? How does the DNA get changed and how does it know what to become, as I gather it is preparing for the next few million years of evolution and changing conditions? When did the last saltational event take place? I don't even know if the proposal is that one day a dinosaur chick hatched that had feathers and wings or if the process was spread over many generations, which might make it little different from the rapid evolution phase of punctuated equilibrium.

I'm looking forward to your answers.

I don't know.

How do you expect us to respond when you can't even tell us some of the basics of the theory?

Schindewolf didn't cover many of the questions you asked. His theory was based on the fossil record - not genetics. If you had asked me what evidence exists in the fossil record to support his threefold theory of typogenesis, typostasis and typolysis, I could answer you.

I will say this: Davison's PEH does attempt to answer many of your questions.

Quote

perhaps you could explain how the information to constrain an organism's evolutionary pathway is held.

It is contained in the first individual of a new type, and is maintained by sexual reproduction and/or selection.

Quote

What conceivable mechanism could stop evolution from taking place

Sexual reproduction, selection, extinction...

Quote

or enable parts to evolve before they became useful?

Semi-meiotic reproduction.

Quote

I am also curious about the saltational events. Do you see these as creating a new genus, order, phylum or what?

Schindewolf called them "types". I have no idea what current category that conforms to.

Quote

What actually occurs during a saltational event?

According to Davison's semi-meiotic hypothesis, the structural reordering of genetic information within the chromosomes.

Quote

How does the DNA get changed and how does it know what to become, as I gather it is preparing for the next few million years of evolution and changing conditions?

See above.

Quote

When did the last saltational event take place?

Again, according to Davison - the evolution of humans was the last saltational event.

Now, I have to restate the fact that I don't know the answers to any of your questions, and Schindewolf did not address most of them, so I was not "lying", nor was I unsupportive of Schindewolf's theory.

--------------
"If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." �Orville Wright

"The presence or absence of a creative super-intelligence is unequivocally a scientific question." Richard Dawkins

Jim_Wynne

Posts: 1208
Joined: June 2006

Posted: Nov. 04 2007,20:57

Quote (Daniel Smith @ Nov. 04 2007,20:08)

Quote

I am also curious about the saltational events. Do you see these as creating a new genus, order, phylum or what?

Schindewolf called them "types". I have no idea what current category that conforms to.

I'm guessing "kinds."

--------------
Evolution is not about laws but about randomness on happanchance.--Robert Byers, at PT

Richard Simons

Posts: 425
Joined: Oct. 2006

Posted: Nov. 04 2007,23:19

Quote

perhaps you could explain how the information to constrain an organism's evolutionary pathway is held.

- It is contained in the first individual of a new type, and is maintained by sexual reproduction and/or selection. � � �

The problem is not what stops the organism from changing but rather what determines that it evolves in a particular way. You quoted Schindewolf as saying that changes in horse anatomy anticipated changes in the environment, therefore 'selection' is not an option.
� � �

Quote

What conceivable mechanism could stop evolution from taking place

- Sexual reproduction, selection, extinction...

Selection could only stop evolution if the organism were perfectly adapted to an unchanging environment.
� � �

Quote

�
or enable parts to evolve before they became useful?

- Semi-meiotic reproduction.

Throwing out a phrase does not answer the question. My point was how could the organism know what it is to become? How does this knowledge get incorporated into the genome? �
� � �

Quote

I am also curious about the saltational events. Do you see these as creating a new genus, order, phylum or what? �

- Schindewolf called them "types". �I have no idea what current category that conforms to.

The problem is probably that Schindewolf had no idea either.
� � �

Quote

What actually occurs during a saltational event? �

- According to Davison's semi-meiotic hypothesis, the structural reordering of genetic information within the chromosomes.

�
� � �

Quote

How does the DNA get changed and how does it know what to become, as I gather it is preparing for the next few million years of evolution and changing conditions?

- See above.

I could not see anything in his hypothesis that comes remotely close to explaining how the DNA knows what it should become.
� � �

Quote

When did the last saltational event take place? �

- Again, according to Davison - the evolution of humans was the last saltational event.

Where in this series would the saltational event have happened?

BTW. What is your explanation for Davison's hypothesis having gone nowhere in the last 20 years?

--------------
All sweeping statements are wrong.

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Joined: July 2007

Posted: Nov. 05 2007,00:37

Quote (Daniel Smith @ Nov. 04 2007,13:05)

Let me also add; these scientists have theories that have never been falsified.

Let me add that whether they've been falsified is irrelevant, when they have never been TESTED.

Therefore, you were bearing false witness (check that Ninth Commandment!) when you called them "theories." Theories are hypotheses that have a long track record of withstanding tests designed to falsify them. None of your heroes are willing to do that.

Quote

Their ideas were ridiculed - because they did not fit the current paradigm,

The fact that they are ridiculed doesn't make them right. If they are being ridiculed, they should get to work testing their hypotheses.

Virologists ridiculed Stan Prusiner and his prion hypothesis in the early '80s, too. Did Prusiner blog or write books aimed at lay people? No, he tested his hypothesis inside and out. In 1997, he won the Nobel.

Quote

but I've seen no convincing evidence against them.

We've seen how you can ignore blatant evidence when it's right in front of your face, Daniel. Your credibility is zero.

Quote

...how many have systematically and thoroughly reviewed it and presented convincing evidence against it? �I've not seen any.

It's not our responsibility to "present convincing evidence" against anything, you goof. It's DAVISON'S responsibility to TEST his hypothesis, but he won't. That's the main reason why real scientists ridicule Davison and Behe.

Quote

The same can be said about the theories of Berg and Schindewolf I've presented (albeit limitedly) here. �No one has presented any evidence against them.

Again, you can't be bothered to look at the evidence after you make a prediction. You see just what you want to see, and you tell blatant lies. Make a prediction. Do an experiment. Make an observation. Produce new data.

oldmanintheskydidntdoit

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Posted: Nov. 05 2007,02:48

Quote

...how many have systematically and thoroughly reviewed it and presented convincing evidence against it? I've not seen any.

Nor have I seen systematic evidence against the moon being made of green cheese.

I can propose anything I like, I don't expect the world to jump on it and disprove it. It's up to me to provide positive proof in the first instance.

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I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger�s work, the evo mat narrative cannot stand
Gordon Mullings

VMartin

Posts: 525
Joined: Nov. 2006

Posted: Nov. 05 2007,23:59

JAM

�

Quote

It's not our responsibility to "present convincing evidence" against anything, you goof. It's DAVISON'S responsibility to TEST his hypothesis, but he won't. That's the main reason why real scientists ridicule Davison and Behe.

Unbelievable. John Davison supported his ideas presented in his Manifesto by thoughts of Berg, Broom, Schindewolf, Punnet, Grasse. All of them were real scientists. Grasse was president of French academy of science!
It is utterly ridiculous when you call "real scientists" only your neodarwinian cronies.

Quote

The fact that they are ridiculed doesn't make them right. If they are being ridiculed, they should get to work testing their hypotheses.

Neodarwinists with their babbling about "evolution in action" �and "natural selection" are ridiculous as well. They should better test their hypothesis. Especially considering the fact that evolution is over - how real scientists as Davison, Broom and Grasse claimed.

(that evolution of mammalian orders is finished is admitted fact also by you. You only claim that there are no "empty niches" anymore.)

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I could not answer, but should maintain my ground.-
Charles Darwin

IanBrown_101

Posts: 927
Joined: April 2007

Posted: Nov. 06 2007,02:16

Quote (VMartin @ Nov. 06 2007,05:59)

JAM

Quote

It's not our responsibility to "present convincing evidence" against anything, you goof. It's DAVISON'S responsibility to TEST his hypothesis, but he won't. That's the main reason why real scientists ridicule Davison and Behe.

Unbelievable. John Davison supported his ideas presented in his Manifesto by thoughts of Berg, Broom, Schindewolf, Punnet, Grasse. All of them were real scientists. Grasse was president of French academy of science!
It is utterly ridiculous when you call "real scientists" only your neodarwinian cronies.

Quoting people isn't data (incidentally, how many of these scientists published all/most of their work before 1950?) dumbass.

If it was, I could "prove" there was a god by quoting various religious leaders or, even better, religious scientists.

You're either insane or unbelievably, incurably, ridiculously stupid.

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I'm not the fastest or the baddest or the fatest.

You NEVER seem to address the fact that the grand majority of people supporting Darwinism in these on line forums and blogs are atheists. That doesn't seem to bother you guys in the least. - FtK

Roddenberry is my God.

Assassinator

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Joined: Nov. 2007

Posted: Nov. 06 2007,02:58

Quote

Neodarwinists with their babbling about "evolution in action" and "natural selection" are ridiculous as well. They should better test their hypothesis.

Ya know Martin, it would be nice if you would actually do something more then just rant.

oldmanintheskydidntdoit

Posts: 4999
Joined: July 2006

Posted: Nov. 06 2007,03:06

Quote (VMartin @ Nov. 05 2007,23:59)

Especially considering the fact that evolution is over - how real scientists as Davison, Broom and Grasse claimed.

If it's the case that "real scientists" only mutter to themselves on ISCID then yes, Davidson is a real scientist.

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I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger�s work, the evo mat narrative cannot stand
Gordon Mullings

Posts: 970
Joined: Sep. 2007

Posted: Nov. 06 2007,13:58

Quote (oldmanintheskydidntdoit @ Nov. 05 2007,02:48)

I can propose anything I like, I don't expect the world to jump on it and disprove it. It's up to me to provide positive proof in the first instance.

Davison cites experimental evidence showing that semi-meiotic reproduction is possible even amongst sexually reproductive animals.

But where is the "positive proof" (you say) you require for the assumed mechanisms of gradual evolution?

--------------
"If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." �Orville Wright

"The presence or absence of a creative super-intelligence is unequivocally a scientific question." Richard Dawkins

oldmanintheskydidntdoit

Posts: 4999
Joined: July 2006

Posted: Nov. 06 2007,14:14

Quote (Daniel Smith @ Nov. 06 2007,13:58)

Quote (oldmanintheskydidntdoit @ Nov. 05 2007,02:48)

I can propose anything I like, I don't expect the world to jump on it and disprove it. It's up to me to provide positive proof in the first instance.

Davison cites experimental evidence showing that semi-meiotic reproduction is possible even amongst sexually reproductive animals.

But where is the "positive proof" (you say) you require for the assumed mechanisms of gradual evolution?

Quote

Allen MacNeill
Sources of Heritable Variation (both genotypic and phenotypic) Among Individuals in Populations

Gene Structure (in DNA)
� single point mutations
� deletion and insertion (�frame shift�) mutations
� inversion and translocation mutations
Gene Expression in Prokaryotes
� changes in promoter or terminator sequences (increasing or decreasing binding)
� changes in repressor binding (in prokaryotes); increasing or decreasing binding to operator sites
� changes in repressor binding (in prokaryotes); increasing or decreasing binding to inducers
� changes in repressor binding (in prokaryotes); increasing or decreasing binding to corepressors
Gene Expression in Eukaryotes
� changes in activation factor function in eukaryotes (increasing or decreasing binding to promoters)
� changes in intron length, location, and/or editing by changes in specificity of SNRPs
� changes in interference/antisense RNA regulation (increasing or decreasing binding to sense RNAs)
Gene Interactions
� changes in substrates or products of biochemical pathways
� addition or removal of gene products (especially enzymes) from biochemical pathways
� splitting or combining of biochemical pathways
� addition or alteration of pleiotropic effects, especially in response to changes in other genes/traits
Eukaryotic Chromosome Structure
� gene duplication within chromosomes
� gene duplication in multiple chromosomes
� inversions involving one or more genes in one chromosome
� translocations involving one or more genes between two or more chromosomes
� deletion/insertion of one or more genes via transposons
� fusion of two or more chromosomes or chromosome fragments
� fission of one chromosome into two or more fragments
� changes in chromosome number via nondisjunction (aneuploidy)
� changes in chromosome number via autopolyploidy (especially in plants)
� changes in chromosome number via allopolyploidy (especially in plants)
Eukaryotic Chromosome Function
� changes in regulation of multiple genes in a chromosome as a result of the foregoing structural changes
� changes in gene expression as result of DNA methylation
� changes in gene expression as result of changes in DNA-histone binding
Genetic Recombination
� the exchange of non-identical genetic material between two or more individuals (i.e. sex)
� lateral gene transfer via plasmids and episomes (especially in prokaryotes)
� crossing-over (reciprocal and non-reciprocal) between sister chromatids in meiosis
� crossing-over (non-reciprocal) between sister chromatids in mitosis
� Mendelian independent assortment during meiosis
� hybridization
Genome Structure and Function
� genome reorganization and/or reintegration
� partial or complete genome duplication
� partial or complete genome fusion
Development (among multicellular eukaryotes, especially animals)
� changes in tempo and timing of gene regulation, especially in eukaryotes
� changes in homeotic gene regulation in eukaryotes
� genetic imprinting, especially via hormone-mediated DNA methylation
Symbiosis
� partial or complete endosymbiosis
� partial or complete incorporation of unrelated organisms as part of developmental pathways (especially larval forms)
� changes in presence or absence of mutualists, commensals, and/or parasites
Behavior/Neurobiology
� changes in behavioral anatomy, histology, and/or physiology in response to changes in biotic community
� changes in behavioral anatomy, histology, and/or physiology in response to changes in abiotic environment
� learning (including effects of use and disuse)
Physiological Ecology
� changes in anatomy, histology, and/or physiology in response to changes in biotic community
� changes in anatomy, histology, and/or physiology in response to changes in abiotic environment

Which particular assumed mechanism are you interested in?
creationist and id strawman

--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger�s work, the evo mat narrative cannot stand
Gordon Mullings

Posts: 517
Joined: July 2007

Posted: Nov. 07 2007,09:10

Quote (Daniel Smith @ Nov. 06 2007,13:58)

Quote (oldmanintheskydidntdoit @ Nov. 05 2007,02:48)

I can propose anything I like, I don't expect the world to jump on it and disprove it. It's up to me to provide positive proof in the first instance.

Davison cites experimental evidence showing that semi-meiotic reproduction is possible even amongst sexually reproductive animals.

But where is the "positive proof" (you say) you require for the assumed mechanisms of gradual evolution?

Daniel, I take issue with omitsddi's use of the term "proof," but plenty of positive evidence is available from VISTA. That's why you felt compelled to lie and claim that noncoding regions in genes (introns and 5' and 3' UTRs) were "coding regions."

Again, get this through your thick head. It's not about CITING evidence. It's about PRODUCING NEW EVIDENCE by TESTING YOUR OWN HYPOTHESIS.

Surely you're not so stupid that you can't see the immense difference between those criteria. Are you so dishonest that you cant acknowledge it?

Posts: 970
Joined: Sep. 2007

Posted: Nov. 09 2007,13:51

Quote (JAM @ Nov. 07 2007,09:10)

Quote (Daniel Smith @ Nov. 06 2007,13:58)

Quote (oldmanintheskydidntdoit @ Nov. 05 2007,02:48)

I can propose anything I like, I don't expect the world to jump on it and disprove it. It's up to me to provide positive proof in the first instance.

Davison cites experimental evidence showing that semi-meiotic reproduction is possible even amongst sexually reproductive animals.

But where is the "positive proof" (you say) you require for the assumed mechanisms of gradual evolution?

Daniel, I take issue with omitsddi's use of the term "proof," but plenty of positive evidence is available from VISTA. That's why you felt compelled to lie and claim that noncoding regions in genes (introns and 5' and 3' UTRs) were "coding regions."

Again, get this through your thick head. It's not about CITING evidence. It's about PRODUCING NEW EVIDENCE by TESTING YOUR OWN HYPOTHESIS.

Surely you're not so stupid that you can't see the immense difference between those criteria. Are you so dishonest that you cant acknowledge it?

I'm still waiting for a paper from you.

--------------
"If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." �Orville Wright

"The presence or absence of a creative super-intelligence is unequivocally a scientific question." Richard Dawkins

Posts: 517
Joined: July 2007

Posted: Nov. 09 2007,15:03

Quote (Daniel Smith @ Nov. 09 2007,13:51)

� � �

Quote (JAM @ Nov. 07 2007,09:10)

� � � �

Quote (Daniel Smith @ Nov. 06 2007,13:58)

� � � �

Quote (oldmanintheskydidntdoit @ Nov. 05 2007,02:48)

I can propose anything I like, I don't expect the world to jump on it and disprove it. It's up to me to provide positive proof in the first instance.

Davison cites experimental evidence showing that semi-meiotic reproduction is possible even amongst sexually reproductive animals.

But where is the "positive proof" (you say) you require for the assumed mechanisms of gradual evolution?

Daniel, I take issue with omitsddi's use of the term "proof," but plenty of positive evidence is available from VISTA. That's why you felt compelled to lie and claim that noncoding regions in genes (introns and 5' and 3' UTRs) were "coding regions."

Again, get this through your thick head. It's not about CITING evidence. It's about PRODUCING NEW EVIDENCE by TESTING YOUR OWN HYPOTHESIS.

Surely you're not so stupid that you can't see the immense difference between those criteria. Are you so dishonest that you cant acknowledge it?

I'm still waiting for a paper from you.

I'm still waiting for you to answer some questions, starting with your predictions for the paper:
------------
How do you explain the fact that starting with a random sequence, we can use mutation and selection to evolve a function in real time?

What level reduction do you consider to represent lack of function? For example, if your heart rate was reduced a million-fold, to ~1 beat every 10 days, you'd be dead. Would you agree that your heart failed to function--that it was not meeting design criteria, so to speak?

------------
And some others:
-------
In addition, why aren't these discoveries being made by ID proponents...like, um, at the Discovery Institute?

Why aren't discoveries like these motivating people like you to start careers in science?

What do any of the data have to do with the genetic code, which really isn't very complex?

What's so complex about coding for 20 amino acids, start, and stop in 64 codons?

Or were you just using "genetic code" in a profoundly ignorant way?

...would you mind commenting on the intelligence of having the same codon that starts protein synthesis also encoding the amino acid methionine?

I ask because it seems really, really stupid to me; I can improve the design with my measly human intelligence. Does that therefore make me smarter than God? Why would one want to worship an unintelligent God? Do you see how the ID movement is bad theology slathered onto nonexistent science?

Here's another question: how long does it take to evolve multiple, different, incredibly specific, functional, new protein-protein binding sites, using nothing but genetic variation and selection?

What does "nonrepeat" mean, Daniel? What proportion of "junk" is repeat, and what proportion is nonrepeat (unique)?

How much DNA was reclassified as something other than the provisional classification of "junk" in this case? What proportion of the genome? Be precise and systematic.

What proportion of the genome did they throw out when they only looked at "nonrepeat" sequences? Be precise and systematic.

So how can introns be both coding sequences and junk sequences?

How does studying nonrepeat sequences within and near genes reclassify "junk" DNA?

For example, if God designed your body, He clearly understands the concept of plumbing. Why is there nothing analogous within cells?

Why do cells use a system analogous to throwing lipid water balloons full of food and sewage around (allowing them to fuse and ripping them apart) instead of having simple plumbing?

According to your hypothesis, how many human genes won't have a mouse ortholog and vice versa?

You can start with the bolded ones.

Posts: 970
Joined: Sep. 2007

Posted: Nov. 09 2007,22:05

Quote (oldmanintheskydidntdoit @ Nov. 06 2007,14:14)

Quote (Daniel Smith @ Nov. 06 2007,13:58)

Quote (oldmanintheskydidntdoit @ Nov. 05 2007,02:48)

I can propose anything I like, I don't expect the world to jump on it and disprove it. It's up to me to provide positive proof in the first instance.

Davison cites experimental evidence showing that semi-meiotic reproduction is possible even amongst sexually reproductive animals.

But where is the "positive proof" (you say) you require for the assumed mechanisms of gradual evolution?

Quote

Allen MacNeill
Sources of Heritable Variation (both genotypic and phenotypic) Among Individuals in Populations

Gene Structure (in DNA)
� single point mutations
� deletion and insertion (�frame shift�) mutations
� inversion and translocation mutations
Gene Expression in Prokaryotes
� changes in promoter or terminator sequences (increasing or decreasing binding)
� changes in repressor binding (in prokaryotes); increasing or decreasing binding to operator sites
� changes in repressor binding (in prokaryotes); increasing or decreasing binding to inducers
� changes in repressor binding (in prokaryotes); increasing or decreasing binding to corepressors
Gene Expression in Eukaryotes
� changes in activation factor function in eukaryotes (increasing or decreasing binding to promoters)
� changes in intron length, location, and/or editing by changes in specificity of SNRPs
� changes in interference/antisense RNA regulation (increasing or decreasing binding to sense RNAs)
Gene Interactions
� changes in substrates or products of biochemical pathways
� addition or removal of gene products (especially enzymes) from biochemical pathways
� splitting or combining of biochemical pathways
� addition or alteration of pleiotropic effects, especially in response to changes in other genes/traits
Eukaryotic Chromosome Structure
� gene duplication within chromosomes
� gene duplication in multiple chromosomes
� inversions involving one or more genes in one chromosome
� translocations involving one or more genes between two or more chromosomes
� deletion/insertion of one or more genes via transposons
� fusion of two or more chromosomes or chromosome fragments
� fission of one chromosome into two or more fragments
� changes in chromosome number via nondisjunction (aneuploidy)
� changes in chromosome number via autopolyploidy (especially in plants)
� changes in chromosome number via allopolyploidy (especially in plants)
Eukaryotic Chromosome Function
� changes in regulation of multiple genes in a chromosome as a result of the foregoing structural changes
� changes in gene expression as result of DNA methylation
� changes in gene expression as result of changes in DNA-histone binding
Genetic Recombination
� the exchange of non-identical genetic material between two or more individuals (i.e. sex)
� lateral gene transfer via plasmids and episomes (especially in prokaryotes)
� crossing-over (reciprocal and non-reciprocal) between sister chromatids in meiosis
� crossing-over (non-reciprocal) between sister chromatids in mitosis
� Mendelian independent assortment during meiosis
� hybridization
Genome Structure and Function
� genome reorganization and/or reintegration
� partial or complete genome duplication
� partial or complete genome fusion
Development (among multicellular eukaryotes, especially animals)
� changes in tempo and timing of gene regulation, especially in eukaryotes
� changes in homeotic gene regulation in eukaryotes
� genetic imprinting, especially via hormone-mediated DNA methylation
Symbiosis
� partial or complete endosymbiosis
� partial or complete incorporation of unrelated organisms as part of developmental pathways (especially larval forms)
� changes in presence or absence of mutualists, commensals, and/or parasites
Behavior/Neurobiology
� changes in behavioral anatomy, histology, and/or physiology in response to changes in biotic community
� changes in behavioral anatomy, histology, and/or physiology in response to changes in abiotic environment
� learning (including effects of use and disuse)
Physiological Ecology
� changes in anatomy, histology, and/or physiology in response to changes in biotic community
� changes in anatomy, histology, and/or physiology in response to changes in abiotic environment

Which particular assumed mechanism are you interested in?

I don't care. Pick one and lets look at the experimental evidence showing it's capabilities towards creating complex functional systems.

--------------
"If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." �Orville Wright

"The presence or absence of a creative super-intelligence is unequivocally a scientific question." Richard Dawkins

Jim_Wynne

Posts: 1208
Joined: June 2006

Posted: Nov. 09 2007,22:22

Quote

Pick one and lets look at the experimental evidence showing it's capabilities towards creating complex functional systems.

Define "complex" and tell us how we can identify it, and what the delimiter is between complex and not-complex. While you're at it, you might also want to tell us what you think a "functional system" is.

--------------
Evolution is not about laws but about randomness on happanchance.--Robert Byers, at PT

Posts: 970
Joined: Sep. 2007

Posted: Nov. 09 2007,23:32

OK, only because you're going to keep acting as if I'm the one who's stalling the discussion, I'll attempt to answer your questions.

Quote (JAM @ Nov. 09 2007,15:03)

How do you explain the fact that starting with a random sequence, we can use mutation and selection to evolve a function in real time?

I don't know. I don't know that it is possible. I'd predict that it isn't. But first, don't we have to agree what a "function" is?

Quote

What level reduction do you consider to represent lack of function? For example, if your heart rate was reduced a million-fold, to ~1 beat every 10 days, you'd be dead. Would you agree that your heart failed to function--that it was not meeting design criteria, so to speak?

This is silly. Are you asking for a general level for "lack of function"? Or are you just concerned about the heart? I would agree that a heart that beats once every ten days would be considered "non-functional" for a human - or any other known animal. What does that have to do with the paper you refuse to show me?

Quote

In addition, why aren't these discoveries being made by ID proponents...like, um, at the Discovery Institute?

I don't know.

Quote

Why aren't discoveries like these motivating people like you to start careers in science?

I don't know. I can't speak for "people like me". I can only speak for myself. Science for me, is a hobby. I already have a career.

Quote

What do any of the data have to do with the genetic code, which really isn't very complex?

What's so complex about coding for 20 amino acids, start, and stop in 64 codons?

Or were you just using "genetic code" in a profoundly ignorant way?

Apparently I was. You are right, the code is simple, what it codes for isn't.

Quote

...would you mind commenting on the intelligence of having the same codon that starts protein synthesis also encoding the amino acid methionine?

Is this a problem?

Quote

I ask because it seems really, really stupid to me; I can improve the design with my measly human intelligence.

Then why don't you?

Quote

Does that therefore make me smarter than God?

No.

Quote

Why would one want to worship an unintelligent God?

One wouldn't.

Quote

Do you see how the ID movement is bad theology slathered onto nonexistent science?

No.

Quote

Here's another question: how long does it take to evolve multiple, different, incredibly specific, functional, new protein-protein binding sites, using nothing but genetic variation and selection?

I don't know.

Quote

What does "nonrepeat" mean, Daniel?

I would guess it means "doesn't consist of repeating sequences".

Quote

What proportion of "junk" is repeat, and what proportion is nonrepeat (unique)?

How much DNA was reclassified as something other than the provisional classification of "junk" in this case? What proportion of the genome? Be precise and systematic.

What proportion of the genome did they throw out when they only looked at "nonrepeat" sequences? Be precise and systematic.

So how can introns be both coding sequences and junk sequences?

How does studying nonrepeat sequences within and near genes reclassify "junk" DNA?

Since you've never given me a definition for "junk" DNA, I had to do a google search. I found this here (at the first page I looked at):

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# Less than 2% of the genome codes for proteins.
# Repeated sequences that do not code for proteins ("junk DNA") make up at least 50% of the human genome.

Do you agree with this definition: "Repeated sequences that do not code for proteins = junk DNA"?

If that's the "provisional definition" of junk DNA, then studying non-repeat sequences doesn't have anything to do with junk (as so defined) and I was wrong to argue that it did.

I guess the answer to the other question would be that they "threw out" 50% of the genome when they didn't look at repeat sequences.

I'm curious though, when I asked; "Are you equating repeat sequences with "junk"?", you replied "No, obviously, I'm not.". So, I'm guessing that this isn't exactly your definition of junk. Why don't you just tell me what your definition is?

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For example, if God designed your body, He clearly understands the concept of plumbing. Why is there nothing analogous within cells?

You mean like pumps?

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Why do cells use a system analogous to throwing lipid water balloons full of food and sewage around (allowing them to fuse and ripping them apart) instead of having simple plumbing?

I don't know. It seems to work just fine though.

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According to your hypothesis, how many human genes won't have a mouse ortholog and vice versa?

I don't have a specific number. Did you have one before you found out the actual number?

Now, will you show me the paper?

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"If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." �Orville Wright

"The presence or absence of a creative super-intelligence is unequivocally a scientific question." Richard Dawkins

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Posted: Nov. 09 2007,23:42

Quote (Jim_Wynne @ Nov. 09 2007,22:22)

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Pick one and lets look at the experimental evidence showing it's capabilities towards creating complex functional systems.

Define "complex" and tell us how we can identify it, and what the delimiter is between complex and not-complex. While you're at it, you might also want to tell us what you think a "functional system" is.

Suggested reading.

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"If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." �Orville Wright

"The presence or absence of a creative super-intelligence is unequivocally a scientific question." Richard Dawkins

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Posted: Nov. 10 2007,01:05

Quote (Daniel Smith @ Nov. 09 2007,23:32)

OK, only because you're going to keep acting as if I'm the one who's stalling the discussion, I'll attempt to answer your questions. � � � � � � � � �

Quote (JAM @ Nov. 09 2007,15:03)

How do you explain the fact that starting with a random sequence, we can use mutation and selection to evolve a function in real time?

I don't know. �I don't know that it is possible. �I'd predict that it isn't. �But first, don't we have to agree what a "function" is?

In this case, protein-protein binding.

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What level reduction do you consider to represent lack of function? For example, if your heart rate was reduced a million-fold, to ~1 beat every 10 days, you'd be dead. Would you agree that your heart failed to function--that it was not meeting design criteria, so to speak?

This is silly.

Yes, the standard creationist response to this paper is profoundly silly, which is why I'm asking ahead of time.

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Are you asking for a general level for "lack of function"?

No, I'm just asking if a million-fold reduction crosses the line for you.

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Or are you just concerned about the heart? �I would agree that a heart that beats once every ten days would be considered "non-functional" for a human - or any other known animal.

Good.

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What does that have to do with the paper you refuse to show me?

I'm not refusing to show you; I'm just heading off an evasive, dishonest response.

http://www.springerlink.com/content/hhcx0pur3545x7v3/

Posts: 517
Joined: July 2007

Posted: Nov. 10 2007,01:06

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In addition, why aren't these discoveries being made by ID proponents...like, um, at the Discovery Institute?

I don't know.

My hypothesis is a lack of faith.

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Why aren't discoveries like these motivating people like you to start careers in science?

I don't know. �I can't speak for "people like me". �I can only speak for myself. �Science for me, is a hobby. �I already have a career.

People change careers all the time, and I think that I can confidently say that science is not a hobby for you.

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Apparently I was. �You are right, the code is simple, what it codes for isn't.

Thanks for admitting that. I'm impressed.

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...would you mind commenting on the intelligence of having the same codon that starts protein synthesis also encoding the amino acid methionine?

Is this a problem?

Wouldn't you agree that not combining the stop signal with an amino acid is an intelligent move, given that functional proteins end in all sorts of different aa residues?

Now, since functional proteins BEGIN with many different residues, what does that say about the intelligence of combining start with methionine?

It's really not a difficult question. There's a perfect control to demonstrate the alleged intelligence of the designer!

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I ask because it seems really, really stupid to me; I can improve the design with my measly human intelligence.

Then why don't you?

Huh?

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Does that therefore make me smarter than God?

No. � � � � � � � � � �

Why not?

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Why would one want to worship an unintelligent God?

One wouldn't.

I agree. So why do creationists attribute biological design to God, since so much of it is so obviously unintelligent?

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Do you see how the ID movement is bad theology slathered onto nonexistent science?

No.

Have you considered opening your eyes to the NATURE of biological complexity, and avoiding the dishonest arguments about its presence and extent?

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Posted: Nov. 10 2007,01:07

Quote

� �

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Here's another question: how long does it take to evolve multiple, different, incredibly specific, functional, new protein-protein binding sites, using nothing but genetic variation and selection?

I don't know.

Two weeks.
� �

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Since you've never given me a definition for "junk" DNA, I had to do a google search.

But you're the one that brought it up! Why would I be responsible for defining it?
� �

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� �

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# �Less than 2% of the genome codes for proteins.
# Repeated sequences that do not code for proteins ("junk DNA") make up at least 50% of the human genome.

Do you agree with this definition: "Repeated sequences that do not code for proteins = junk DNA"?

Not at all, primarily because I can point you to repeated sequences that do not code for proteins that have a known function and that no one considers to be junk: ribosomal RNA genes.

Junk is mostly repeated and some nonrepeated DNA that has no known function and is very polymorphic. The classification, being negative, is clearly provisional.
� �

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If that's the "provisional definition" of junk DNA,...

No, the definition isn't provisional, the classification of a certain sequence as junk is. There's a huge difference.
� �

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then studying non-repeat sequences doesn't have anything to do with junk (as so defined) and I was wrong to argue that it did.

Your conclusion is correct, even though the definition wasn't.
� �

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I guess the answer to the other question would be that they "threw out" 50% of the genome when they didn't look at repeat sequences.

More like 90-95%.
� �

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� �

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For example, if God designed your body, He clearly understands the concept of plumbing. Why is there nothing analogous within cells?

You mean like pumps?

Yes, but more like pipes and valves that separate dirty from clean water.

Quote

� �

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Why do cells use a system analogous to throwing lipid water balloons full of food and sewage around (allowing them to fuse and ripping them apart) instead of having simple plumbing?

I don't know. �It seems to work just fine though.

That all depends on your definition of "just fine." It's laughable as an example of intelligent design. Why not just put structures that serve as pipes and valves in there?
� �

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� �

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According to your hypothesis, how many human genes won't have a mouse ortholog and vice versa?

I don't have a specific number. �Did you have one before you found out the actual number?

A range will do: thousands, hundreds, dozens, or <10?

My prediction was too high.

BTW, I did an experiment today that had a really exciting result. My prediction was wrong.
� �

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Now, will you show me the paper?

See the link to the abstract above.

Jim_Wynne

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Posted: Nov. 10 2007,10:04

Quote (Daniel Smith @ Nov. 09 2007,23:42)

Quote (Jim_Wynne @ Nov. 09 2007,22:22)

Quote

Pick one and lets look at the experimental evidence showing it's capabilities towards creating complex functional systems.

Define "complex" and tell us how we can identify it, and what the delimiter is between complex and not-complex. While you're at it, you might also want to tell us what you think a "functional system" is.

Suggested reading.

I've done my reading, and unlike you, I've actually learned from it. Unless you're willing to define your terms in your own words, we have no way of knowing what you're talking about, and you are free to move the goalposts at will. So I'll ask again:
1) What do you mean by "complex," how do you identify it, and what are the empirical delimiters between "complex" and not-complex?
2) How do you define "functional system"?

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Evolution is not about laws but about randomness on happanchance.--Robert Byers, at PT

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http://www.springerlink.com/content/hhcx0pur3545x7v3/

Posted: Nov. 10 2007,10:45

Quote (JAM @ Nov. 10 2007,01:05)

Thank you.

I was not able to read the entire paper, but only the abstract:

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Abstract

To explore the possibility that an arbitrary sequence can evolve towards acquiring functional role when fused with other pre-existing protein modules, we replaced the D2 domain of the fd-tet phage genome with the soluble random polypeptide RP3-42. The replacement yielded an fd-RP defective phage that is six-order magnitude lower infectivity than the wild-type fd-tet phage. The evolvability of RP3-42 was investigated through iterative mutation and selection. Each generation consists of a maximum of ten arbitrarily chosen clones, whereby the clone with highest infectivity was selected to be the parent clone of the generation that followed. The experimental evolution attested that, from an initial single random sequence, there will be selectable variation in a property of interest and that the property in question was able to improve over several generations. fd-7, the clone with highest infectivity at the end of the experimental evolution, showed a 240-fold increase in infectivity as compared to its origin, fd-RP. Analysis by phage ELISA using anti-M13 antibody and anti-T7 antibody revealed that about 37-fold increase in the infectivity of fd-7 was attributed to the changes in the molecular property of the single polypeptide that replaced the D2 domain of the g3p protein. This study therefore exemplifies the process of a random polypeptide generating a functional role in rejuvenating the infectivity of a defective bacteriophage when fused to some preexisting protein modules, indicating that an arbitrary sequence can evolve toward acquiring a functional role. Overall, this study could herald the conception of new perspective regarding primordial polypeptides in the field of molecular evolution.

This is an interesting experiment. I have a couple questions:
1. Why did they use artificial selection as opposed to natural selection?
2. My math isn't the greatest so when they say that the replacement phage had "six-order magnitude lower infectivity" than the original phage, and the newly evolved phage "showed a 240-fold increase in infectivity as compared to its origin, fd-RP", they're talking about 0.00024 less infectivity than the original wild phage - correct?

--------------
"If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." �Orville Wright

"The presence or absence of a creative super-intelligence is unequivocally a scientific question." Richard Dawkins

Posts: 970
Joined: Sep. 2007

Posted: Nov. 10 2007,11:05

Quote (JAM @ Nov. 10 2007,01:07)

Quote

Here's another question: how long does it take to evolve multiple, different, incredibly specific, functional, new protein-protein binding sites, using nothing but genetic variation and selection?

I don't know.

Two weeks.

Is this information in the paper you linked to?

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Since you've never given me a definition for "junk" DNA, I had to do a google search.

But you're the one that brought it up! Why would I be responsible for defining it?

Quote

# Less than 2% of the genome codes for proteins.
# Repeated sequences that do not code for proteins ("junk DNA") make up at least 50% of the human genome.

Do you agree with this definition: "Repeated sequences that do not code for proteins = junk DNA"?

Not at all, primarily because I can point you to repeated sequences that do not code for proteins that have a known function and that no one considers to be junk: ribosomal RNA genes.

Junk is mostly repeated and some nonrepeated DNA that has no known function and is very polymorphic. The classification, being negative, is clearly provisional.

My expectation then is that the provisional definition of "junk DNA" will continually evolve until it no longer includes any portion of the genome.

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If that's the "provisional definition" of junk DNA,...

No, the definition isn't provisional, the classification of a certain sequence as junk is. There's a huge difference.

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then studying non-repeat sequences doesn't have anything to do with junk (as so defined) and I was wrong to argue that it did.

Your conclusion is correct, even though the definition wasn't.

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I guess the answer to the other question would be that they "threw out" 50% of the genome when they didn't look at repeat sequences.

More like 90-95%.

Are you saying that 90-95% of the human genome is repeats?

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For example, if God designed your body, He clearly understands the concept of plumbing. Why is there nothing analogous within cells?

You mean like pumps?

Yes, but more like pipes and valves that separate dirty from clean water.

Quote

Why do cells use a system analogous to throwing lipid water balloons full of food and sewage around (allowing them to fuse and ripping them apart) instead of having simple plumbing?

I don't know. It seems to work just fine though.

That all depends on your definition of "just fine." It's laughable as an example of intelligent design. Why not just put structures that serve as pipes and valves in there?

I don't know why most designers do what they do - that is not an argument against design. It might be an effective argument against the competency of the designer, provided you can come up with a better workable system.

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According to your hypothesis, how many human genes won't have a mouse ortholog and vice versa?

I don't have a specific number. Did you have one before you found out the actual number?

A range will do: thousands, hundreds, dozens, or <10?

My prediction was too high.

I have no idea. My hypothesis doesn't really work that way. What I mean is; since I view each of the multitude of evolutionary events between mouse and man as saltational, there's no way to predict the number of orthologs.

My main contention is that the genomic sequences of organisms will be found to be fully functional and evolutionarily constrained within species - leaving the only possible mechanisms for the true evolution of new species saltational ones.

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BTW, I did an experiment today that had a really exciting result. My prediction was wrong.

So a wrong prediction is not "lying" then I take it? ;)

--------------
"If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." �Orville Wright

"The presence or absence of a creative super-intelligence is unequivocally a scientific question." Richard Dawkins

Posts: 970
Joined: Sep. 2007

Posted: Nov. 10 2007,11:26

Quote (JAM @ Nov. 10 2007,01:06)

Quote

...would you mind commenting on the intelligence of having the same codon that starts protein synthesis also encoding the amino acid methionine?

Is this a problem?

Wouldn't you agree that not combining the stop signal with an amino acid is an intelligent move, given that functional proteins end in all sorts of different aa residues?

Now, since functional proteins BEGIN with many different residues, what does that say about the intelligence of combining start with methionine?

It's really not a difficult question. There's a perfect control to demonstrate the alleged intelligence of the designer!

Not necessarily. Many genomic sequences are multi-functional - containing overlapping coding and non-coding functional sequences. Perhaps we just don't know the functional advantage for combining the codon that starts protein synthesis and methionine.

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I ask because it seems really, really stupid to me; I can improve the design with my measly human intelligence.

Then why don't you?

Huh?

Why don't you engineer a better design and show it to the world?

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Does that therefore make me smarter than God?

No.

Why not?

It just means you think you're smarter than God. You have to make a workable system to actually show yourself smarter than God.

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Why would one want to worship an unintelligent God?

One wouldn't.

I agree. So why do creationists attribute biological design to God, since so much of it is so obviously unintelligent?

So now that you have mastered all the various elements of biological design, you are prepared to say that anyone who was able to design it all would have to be unintelligent and that you could have come up with a better design? That's a mighty big boast. Good luck in your new venture (creating an alternate (and improved) form of life)!

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Do you see how the ID movement is bad theology slathered onto nonexistent science?

No.

Have you considered opening your eyes to the NATURE of biological complexity, and avoiding the dishonest arguments about its presence and extent?

I am attempting to "open my eyes" to anything and everything. Please explain (or link to) anything that will help me better understand "the NATURE of biological complexity".

--------------
"If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." �Orville Wright

"The presence or absence of a creative super-intelligence is unequivocally a scientific question." Richard Dawkins

Posts: 970
Joined: Sep. 2007

Posted: Nov. 10 2007,11:29

I have a question for anyone who wants to take a shot at it:

In the human genome, what percentage of genomic sequence would you say is likely to be transcribed as nuclear primary transcripts?

--------------
"If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." �Orville Wright

"The presence or absence of a creative super-intelligence is unequivocally a scientific question." Richard Dawkins

Posts: 970
Joined: Sep. 2007

Posted: Nov. 10 2007,11:40

Quote (Jim_Wynne @ Nov. 10 2007,10:04)

Unless you're willing to define your terms in your own words, we have no way of knowing what you're talking about, and you are free to move the goalposts at will. So I'll ask again:
1) What do you mean by "complex," how do you identify it, and what are the empirical delimiters between "complex" and not-complex?
2) How do you define "functional system"?

Fair enough.

"Complex" means "composed of many interconnected parts".
As a general rule: more parts = more complex.

"Functional system" means "an assemblage of parts which work together towards the same purpose or function"

--------------
"If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance." �Orville Wright

"The presence or absence of a creative super-intelligence is unequivocally a scientific question." Richard Dawkins

VMartin

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