Creationism will only destroy science

[mark kennedy]

Mutations do not cause changes. Mutations are changes.

Changes (aka mutations) lead to modified gene products (e.g. proteins). This will often modify the behaviour (functioning) of the protein.

Here we go again back to basic biology:

"In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair."

Mutations

What are the effects of these transcript errors, that's the real question.

 

[mark kennedy]

Mark, the article said that 83% of the genes showed amino acid replacements. Where did it say that the changes were dramatic?

They don't say dramatic, they say 'gross structural changes affecting gene products'. That is 20% showing gross structural changes (actually differences).

You do realize that if a gene has only one amino acid replacement it will be counted among the 83% of the genes which show amino acid replacements?

What do you think these changes add up to when you take into how many nucleotides are actually involved?

“83% of the genes have changed between the human and the chimpanzee—only 17% are identical—so that means that the impression that comes from the 1.2% [sequence] difference is [misleading]. In the case of protein structures, it has a big effect.” A “big effect” indeed! (Yoshijuki Sakaki, head of the International Chimpanzee Chromosome 22 Consortium, 2004)

All that 83% means is that out of 213 genes 192 showed at least one amino acid replacement. It does not mean that every change was dramatic or even that the sum total of the changes was dramatic. They could be, but you can't get that from the 83% figure.

To demonstrate dramatic change you would have to look up exactly what amino acid replacements occurred on each of those 192 genes, and show that the change on all or most of them was dramatic. That information may be contained in the tables attached to the reports. I haven't read the tables, so I am not sure what is in them.

Actually they were not able to identify all of the genes they examined but the 83% tells us that we are only 17% identical to the chimpanzee. When 20% of the protein coding genes have gross structural differences that is a dramatic difference, one no one was expecting to find. That is why the genetic basis for this assumed transition is a complete mystery. That is where the naturalistic assumptions of Darwinians has led us, down a blind hole.

To put this in perspective I found this figure that may help you to see the proportion of differences in the genes.

The figure shows the number of synonymous and nonsynonymous nucleotide differences in 13,731 human–chimpanzee orthologous gene pairs.

Here is the context of the discussion of gene comparisons. I really don't have a lot of time for a more detailed expositive post but I thought it was fairly comprehensive:

"...there are 71,896 nucleotide differences in 13,731 genes."

A Scan for Positively Selected Genes in the Genomes of Humans and Chimpanzees

 

[Crusadar]

Gluadys said: Mutations do not cause changes. Mutations are changes.

A bit of an oversimplification here gluadys, no where in any science text I know state that mutations do not cause change, nor that mutations are changes. It states more along the lines that mutations are the result of copying mistakes and that it might cause change. There is no disagreement that mutations can cause change. What becomes a problem is when the whole process is attributed to blind chance!

The problem with an over simplification of the driving force behind Darwinian evolution is that it tends to be dismissed as posing no difficulty at all in explaining anything and everything with that classic response “evolution did it, we don’t know how but it did it”. My question is where is God in all of this!

But here is the point of it all - in order to miscopy anything there has to be something to copy from. The question is where did the first information come from? This question of course goes back to information theory which due to work (and lack there of) I wasn’t able to respond but shall remedy soon enough.

Changes (aka mutations) lead to modified gene products (e.g. proteins).

That depends on the product you started with and the product you wish to acquire - more importantly if such changes are directed by pure chance as Darwinian evolution requires or by built in mechanisms.

This will often modify the behaviour (functioning) of the protein.

Could this have anything to do with the nylon bug, whose diet simply changed from carbohydrates to nylon (with a mere 2% efficiency). Now how is a change in diet going to add an arm or a leg, I don’t know, but please feel free to object and show that this is a step towards something purposeful as oppose to just a built in adaptation.

 

[gluadys]

This is what I hate about these discussions, it's the evolutionist that need a good basic biology lesson.

"While there are only 4 different nucleotide bases that can occur in a nucleic acid, each nucleic acid contains millions of bases bonded to it. The order in which these nucleotide bases appear in the nucleic acid, codes for the information carried in the molecule. In other words, the nucleotide bases serve as a sort of genetic alphabet on which the structure of each protein in our bodies is encoded."

http://www.visionlearning.com/library/module_viewer.php?mid=63

Now, while it is true that can be bonded into millions bases there are still only four. This means we will be 25% simular to any living thing on the planet.

That’s what I said. Four bases. What you said was four base combinations. Do you not understand the difference?

Jonathan Marks, (department of anthropology, University of California, Berkeley) has pointed out the often-overlooked problem with this “similarity” line of thinking.


"Because DNA is a linear array of those four bases—A,G,C, and T—only four possibilities exist at any specific point in a DNA sequence. The laws of chance tell us that two random sequences from species that have no ancestry in common will match at about one in every four sites. Thus even two unrelated DNA sequences will be 25 percent identical, not 0 percent identical.[/quotes]

And something both you and he are overlooking is that the bases occur in pairs: A + T and G + C. And the pairs do not occur in a 50:50 equilibrium. That is why, in the chromosome comparison study, the researcher measured how much of the chromosome was G + C as opposed to A + T. If you were right about all species having 25% identity, we would not get varying amounts of G + C content from one species to another.

Therefore a human and any earthly DNA-based life form must be at least 25% identical. Would it be correct, then, to state that daffodils are “one-quarter human”?

What you are overlooking again is the process by which DNA affects morphology. There are many steps from a DNA sequence to a character trait.
a) an open reading frame which codes for protein
b) organization of the DNA sequence into triplets for messenger RNA to read
c) a code by which the triplets signify amino acids when passed to transcription DNA
d) the assembly of the amino acids and folding them into a protein
e) the expression of the protein activity as a character of the organism
f) the modification (or annulling) of this expression by regulatory genes, Mendelian relationships and/or environmental conditions.

The notion that a daffodil is 25% “human” just because both species use the same base nucleotides is a reductio ad absurdum

Marks went on to concede:

Moreover, the genetic comparison is misleading because it ignores qualitative differences among genomes.... Thus, even among such close relatives as human and chimpanzee, we find that the chimp’s genome is estimated to be about 10 percent larger than the human’s; that one human chromosome contains a fusion of two small chimpanzee chromosomes; and that the tips of each chimpanzee chromosome contain a DNA sequence that is not present in humans."

http://www.apologeticspress.org/articles/2070

“Concede” ? That’s a loaded word. What is he conceding? He is only stating what is obvious and well-known. Even Mendel knew of the difference between genotype and phenotype. What we know today is that the relation between the two is a good deal more complex than Mendal imagined.

That is what happens when homology is mistaken for science, simularity is mistaken for lineal descent.

Since when? Homology implies relationship, but does not dictate that the relationship is lineal descent.

Those are triplet codons for the RNA sequences and somehow you have missed the whole point, once again.

What point? Your reductio ad absurdum?

 

[rmwilliamsll]

Could this have anything to do with the nylon bug, whose diet simply changed from carbohydrates to nylon (with a mere 2% efficiency). Now how is a change in diet going to add an arm or a leg, I don’t know, but please feel free to object and show that this is a step towards something purposeful as oppose to just a built in adaptation.

you have cause and effect reversed.
nothing caused the mutation that resulted in the nylon bug.*
what happened is that the bacteria where the mutation occurred survived to eat another day in the nylon waste water. those with the wild type genome didnt survive without anything to metabolize.

so the mutation allowed these modified bugs to survive, the cause of the mutation was a cosmic ray or etc not being in the nylon waste soup. nothing purposeful in as far as science can see purpose. it is a statistical error or a stochastic problem not a directed purposed adaptation to the environment as you propose.

What are the effects of these transcript errors, that's the real question.

i believe this has been corrected before, mutations are primarily duplication errors not transcription errors.
duplication is one strand into 2-strand DNA
transcription is 1 strand dna to mRNA to tRNA to protein.
they are very different things.


---
*this is not quite right. there are several different levels of causation. the classic division is due to Aristotle

The traditional picture and terminology (not all Aristotle’s terminology):

1. Material cause: “that out of which a thing comes to be, and which persists,” e.g., bronze, silver, and the genus of these (= metal?).
2. Formal cause: “the statement of essence” “the account of what-it-is- to-be, and the parts of the account.”
3. Efficient cause: “the primary source of change,” e.g., the man who gives advice, the father (of the child).
4. Final cause: “the end (telos), that for the sake of which a thing is done,” e.g., health (is the cause of exercise).

from: http://faculty.washington.edu/smcohen/320/4causes.htm

science never talks about final cause
efficient cause is like cosmic rays knocking an electron out which causes a reaction which transforms C-->G for instance.

your cause is more like either formal or final cause, what is drawing the mutation towards, or why is it happening. these are not scientific causation which is why Darwin is credited with removing teleology from biology. the nylon bug isn't trying to cause mutation to stay alive, those that live are those that experienced the right mutation to live....big difference.

 

[gluadys]

Here we go again back to basic biology:

"In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair."

What are the effects of these transcript errors, that's the real question.

What the effects are is a separate question. The uncorrected chemical change is the mutation.

 

[gluadys]

Gluadys said: Mutations do not cause changes. Mutations are changes.

A bit of an oversimplification here gluadys, no where in any science text I know state that mutations do not cause change, nor that mutations are changes. It states more along the lines that mutations are the result of copying mistakes and that it might cause change. There is no disagreement that mutations can cause change. What becomes a problem is when the whole process is attributed to blind chance!

The background to this statement is Mark’s tendency to ask how mutations could cause indels (insertions or deletions). Mutations don’t cause indels, because indels are mutations.

To be complete, my statement should read, “Mutations do not cause changes in DNA sequences. Mutations are changes in DNA sequences."


Of course, changes in DNA sequences (aka mutations) do cause changes in proteins and body chemistry and morphology and behaviour, etc.

The problem with an over simplification of the driving force behind Darwinian evolution is that it tends to be dismissed as posing no difficulty at all in explaining anything and everything with that classic response “evolution did it, we don’t know how but it did it”. My question is where is God in all of this!

The first problem is that mutations are not the driving force behind Darwinian evolution; natural selection is. If and when you ever read Origin of Species you will see that Darwin says nothing about mutations. His whole focus is on natural selection. Darwin knew nothing at all about mutations.

Where is God in all this? Wherever your faith puts him. Prove to me, for example, that God does not change DNA sequences. Or plan climate change. Or anything else which could affect variation and natural selection. There is plenty of scope in the evolutionary process for God to assure the achievement of his purposes.

But here is the point of it all - in order to miscopy anything there has to be something to copy from. The question is where did the first information come from? This question of course goes back to information theory which due to work (and lack there of) I wasn’t able to respond but shall remedy soon enough.

This is a question abiogeneticists are researching. How did the connection between DNA sequences and amino acids become established? I don’t know how far that research has gone or whether there are even tentative hypotheses yet.

That depends on the product you started with and the product you wish to acquire - more importantly if such changes are directed by pure chance as Darwinian evolution requires or by built in mechanisms.

The natural process of evolution never “wishes” to acquire a new protein. And evolution does not require that the process be directed by “pure chance”; only that the changes be random from a scientific perspective. Philosophically, the active intervention of God in determining which mutations will occur and be preserved cannot be ruled out.

By the way, I am collecting peoples ideas on the meaning of “Darwinism”, “Darwinian” “Darwinist” etc. It is quite amazing how many different ways these terms are used.

When you speak of “Darwinian” evolution, what does “Darwinian” mean to you? How does it differ from non-Darwinian evolution?

Could this have anything to do with the nylon bug, whose diet simply changed from carbohydrates to nylon (with a mere 2% efficiency). Now how is a change in diet going to add an arm or a leg, I don’t know, but please feel free to object and show that this is a step towards something purposeful as oppose to just a built in adaptation.

So a 2% efficiency at digesting nylon makes it more fit in a nylon-rich environment than bacteria with a 0% efficiency at digesting nylon. And when a bacterium comes along whose efficiency at digesting nylon is 2.5%, it will be more fit than the current model and will replace it.

No bacterium is going to add an arm or a leg. Only eukaryotes have done that. And it is more likely that the change in diet came after the morphological change, as the new limb structure would make new food sources more accessible.

There is no such thing as a “built-in” adaptation. It is natural selection which drives a species toward adaptation.

 

[mark kennedy]

That’s what I said. Four bases. What you said was four base combinations. Do you not understand the difference?

The point was that we are 25% simular to any living thing in nature. I think you may have been thinking about the 64, 3-base codon combinations, at any rate I think we have cleared it up now.

Jonathan Marks, (department of anthropology, University of California, Berkeley) has pointed out the often-overlooked problem with this “similarity” line of thinking.


"Because DNA is a linear array of those four bases—A,G,C, and T—only four possibilities exist at any specific point in a DNA sequence. The laws of chance tell us that two random sequences from species that have no ancestry in common will match at about one in every four sites. Thus even two unrelated DNA sequences will be 25 percent identical, not 0 percent identical.[/quotes]

Again, I think what you have missed here is that the level of simularity can misleading. What is being underscored in this section is the random sequences will match in one in every four sites. That any two sequences will be 25% identical so superficial simularity does not constitute lineal descent.

What you are overlooking again is the process by which DNA affects morphology. There are many steps from a DNA sequence to a character trait.
a) an open reading frame which codes for protein
b) organization of the DNA sequence into triplets for messenger RNA to read
c) a code by which the triplets signify amino acids when passed to transcription DNA
d) the assembly of the amino acids and folding them into a protein
e) the expression of the protein activity as a character of the organism
f) the modification (or annulling) of this expression by regulatory genes, Mendelian relationships and/or environmental conditions.

All of which are required qualifications for a morphogenetic change in altering protein coding and regulatory genes. Generally the discussions on the genetic basis for human morphology from apes focus on enzyme modification since they are the chemical reactions that do the work in everything from transcription to protein synthesis.

The notion that a daffodil is 25% “human” just because both species use the same base nucleotides is a reductio ad absurdum

The point being that this level of simularity does not provide supportive evidence for common ancestory.

“Concede” ? That’s a loaded word. What is he conceding? He is only stating what is obvious and well-known. Even Mendel knew of the difference between genotype and phenotype. What we know today is that the relation between the two is a good deal more complex than Mendal imagined.

That is actually an open admission of how the simularities are offset by functional differences. The structural differences are far larger then anyone realized because they have used the 98% simularity of human and chimpanzee DNA as a compelling proof of lineal descent. Now the truth is slowly coming out, its just not that simple.

Since when? Homology implies relationship, but does not dictate that the relationship is lineal descent.

What point? Your reductio ad absurdum?

Homology is part of the darwinian philosophy of science and it's based on the assumption of single common ancestory. If they are more simular they are more closely related, if they are more diverse it is called morphology. Homology does dictate lineal descent with modification based on the apriori assumption of single common ancestory.

 

[mark kennedy]

the nylon bug isn't trying to cause mutation to stay alive, those that live are those that experienced the right mutation to live....big difference.

The nylon bug uses an alternative reading frame:

"The mechanism of gene duplication as the means to acquire new genes with previously nonexistent functions is inherently self limiting in that the function possessed by a new protein, in reality, is but a mere variation of the preexisted theme. As the source of a truly unique protein, I suggest an unused open reading frame of the existing coding sequence."

Birth of a unique enzyme from an alternative reading frame of the preexisted, internally repetitious coding sequence.

This is not an example of a benefical mutation, its a duplication of an allready existing reading frame.

 

[rmwilliamsll]

The nylon bug uses an alternative reading frame:

"The mechanism of gene duplication as the means to acquire new genes with previously nonexistent functions is inherently self limiting in that the function possessed by a new protein, in reality, is but a mere variation of the preexisted theme. As the source of a truly unique protein, I suggest an unused open reading frame of the existing coding sequence."

Birth of a unique enzyme from an alternative reading frame of the preexisted, internally repetitious coding sequence.

This is not an example of a benefical mutation, its a duplication of an allready existing reading frame.

do you have any idea what is meant by "frame reading"?
the nylon bug is an extraordinary example of new information, a new protein-never before seen.

...

 

[mark kennedy]

do you have any idea what is meant by "frame reading"?
the nylon bug is an extraordinary example of new information, a new protein-never before seen.

...

Do you have any idea what a frameshift mutation is? Because this is not the result of a random mutation, its a gene duplication.

"Analysis of the published base sequence residing in the pOAD2 plasmid of Flavobacterium Sp. K172 indicated that the 392-amino acid-residue-long bacterial enzyme 6-aminohexanoic acid linear oligomer hydrolase involved in degradation of nylon oligomers is specified by an alternative open reading frame of the preexisted coding sequence that originally specified a 472-residue-long arginine-rich protein."

Evolutionists want to pass this off as beneficial effect from a frameshift mutation, which is utter nonesense. What this paper is suggesting is that oligometric repeats could constitute a primordial coding sequence. They say:

"A large number of polypeptide chains with divergent functions would have to be created almost simulaneosly."

Oligomeric repeats have virtues that uniquely qualify them as a universal coding system:

1) They are translatable to polypeptide chains of substantial lengths.
2) The periodicity they give to polypeptide chains.
3) Their inherent imperviousness to randomly sustained base substitutions, deletions and insertions.

What is being suggested is that it arose: "de novo independantly from an alternative reading frame of the preeisted, internally repetitous coding sequence...As discussed at the beginning of this paper, the probability of a non repetitous base sequence simulataneously harbroing on 427-codon length and the other 392-codon-length open reading frames is practically nil."

While this did produce a unique enzyme it did not result from a mutation, its an oligomeric repeat. Its from alternative an reading frame that "originally specified a 472-residue-long arginine-rich protein." It's an internally repetative coding system and the paper I cited and linked is explicit on this.

 

[gluadys]

The point was that we are 25% simular to any living thing in nature. I think you may have been thinking about the 64, 3-base codon combinations, at any rate I think we have cleared it up now.

Even at the base nucleotide level we are not necessarily 25% like every other species. That would be true only if all species distributed the base nucleotides evenly through their genomes and they don't.

May I remind you that it was YOU who said "base combinations"? The codons are indeed examples of base combinations. The bases taken individually are not.

Jonathan Marks, (department of anthropology, University of California, Berkeley) has pointed out the often-overlooked problem with this “similarity” line of thinking.


"Because DNA is a linear array of those four bases—A,G,C, and T—only four possibilities exist at any specific point in a DNA sequence. The laws of chance tell us that two random sequences from species that have no ancestry in common will match at about one in every four sites. Thus even two unrelated DNA sequences will be 25 percent identical, not 0 percent identical.[/quotes]

What Jonathan Marks is forgetting is that many DNA sequences in a genome are not the result of chance, but of selection. That throws off the 25% result which only applies when chance is the sole determining element. And even that is a probability which will not apply to every species to species comparison, but only statistically to many species to species comparisons.

Again, I think what you have missed here is that the level of simularity can misleading. What is being underscored in this section is the random sequences will match in one in every four sites. That any two sequences will be 25% identical so superficial simularity does not constitute lineal descent.

see above. You are also avoiding the question: similarity of what?

Where J. Mark's figure will apply is when the DNA sequence is determined wholly by chance. That will apply to much of non-coding DNA where changes in sequence have no impact on the organism. It will not usually apply to coding DNA or regulatory DNA where natural selection will override chance.

Furthermore differences of DNA sequences may or may not lead to differences of proteins which in turn may or may not lead to morphological differences. The latter will be impacted by internal regulation of genes, co-operative action of genes, dominance-recessive relationship of alleles and environmental factors that alter gene expression.

So there are many different factors which can change a straight reading of DNA similarity into a myriad of different phenotypical differences and similarities.

Even if it were true that all species are 25% similar genetically, it would be necessary to determine what that means phenotypically.

All of which are required qualifications for a morphogenetic change in altering protein coding and regulatory genes. Generally the discussions on the genetic basis for human morphology from apes focus on enzyme modification since they are the chemical reactions that do the work in everything from transcription to protein synthesis.

Exactly. And enzymes again are different from DNA sequences. Many different DNA sequences do not alter enzymes to any extent.

The point being that this level of simularity does not provide supportive evidence for common ancestory.

The point being that the 25% figure is wrong in the first place, and even if it were right has no context to give it meaning as a measure of similarity at any higher level.

Homology is part of the darwinian philosophy of science and it's based on the assumption of single common ancestory. If they are more simular they are more closely related, if they are more diverse it is called morphology. Homology does dictate lineal descent with modification based on the apriori assumption of single common ancestory.

No it is not. It is just as much a Linnean concept as a Darwinian one. And it emphatically does not dictate lineal descent. Mammals and birds share homologous skeletal features such as the tetrapod limb structure and no one claims they are related in a lineal fashion.

 

[rmwilliamsll]

Do you have any idea what a frameshift mutation is? Because this is not the result of a random mutation, its a gene duplication.

(the gene duplication has nothing to do with the frame shift, the frame shift is a very particular result of a deletion or insertion that is (X mod 3 = 1,2) X=#of nucleotides in the indel.)

yes, but nothing i've seen here with your cut and pastes demonstrates to me that you do.


abcabcabcabcabcabc has 3 different reading frames
abc abc abc abc abc
bca bca bca bca bca
cab cab cab cab cab

a reading frame mutation is where a protein is produced offset by one or 2 nucleotides at the DNA level. because of the triplet genetic code this is a massive change in the composition of the protein.

essentially what happened with the nylon bug is that twice a gene was mutated by a deletion that caused a reading frame shift, producing a never before seen protein that had a weak enzymatic activity that allowed those bacteria to exist and metabolize nylon waste.

you have shown me that access to, and reading of, scientific papers is not an indicator of understanding them.


post edit addition

by an alternative open reading frame of the preexisted coding sequence

you bolded "preexisted", of course the DNA was there before the mutation. however it had never been used to produce that particular protein, that was the result of a frameshift mutation. all mutation works on preexisting DNA, that is the fundamental reason that life falls into a nested hierarchical structure. you only have what exists to operate on, no deus ex machina for living creatures, at least not visible at the genetic level...


.....

 

[gluadys]

Do you have any idea what a frameshift mutation is? Because this is not the result of a random mutation, its a gene duplication.

A gene duplication is a mutation. When a gene duplication occurs randomly, it is a random mutation. When the consequence benefits the organism it is a beneficial mutation.

Stop ducking plain English, Mark.

 

[gluadys]

They don't say dramatic, they say 'gross structural changes affecting gene products'. That is 20% showing gross structural changes (actually differences).

Did you notice that this was on the chimpanzee chromosome?

47 PTR22q genes show significant structural changes affecting at least one of their transcript isoforms.

Taken together, gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins, as listed in Supplementary Tables 4 and 5).
Table 4. Genes with internal amino acid insertions or deletions in chimpanzee; Table 5. Genes with altered start or stop codons in chimpanzee;​

This was the observation for the human chromosome:

A total of 140 of these 179 genes show amino acid replacements, but no gross structural changes are expected.​

The remaining 39 genes show an identical amino acid sequence between human and chimpanzee, including seven in which the nucleotide sequence of the coding region is also identical

What do you think these changes add up to when you take into how many nucleotides are actually involved?

How many nucleotides do you think were actually involved?

Hint: chimpanzee chromosome consists of 33.3 megabases of which 1.44% show single-base substitutions.

“83% of the genes have changed between the human and the chimpanzee—only 17% are identical—so that means that the impression that comes from the 1.2% [sequence] difference is [misleading]. In the case of protein structures, it has a big effect.” A “big effect” indeed! (Yoshijuki Sakaki, head of the International Chimpanzee Chromosome 22 Consortium, 2004)

What Sakaki is saying is that you get a different picture if you look at the percentage of genes that have changed instead of the percentage of nucleotides that have changed. 1.44% of the nucleotides on this chromosome show substitutions, and these substitutions affect 83% of the genes.

The 83% figure with respect to genes does not invalidate the 1.44% with respect to nucleotides.

Note these figures with respect to the nucleotides:

Estimates of nucleotide substitution rates of aligned sequences range from 1.23% by bacterial artificial chromosome (BAC) end sequencing to about 2% by molecular analysis.

The overall nucleotide substitution level in aligned regions between PTR22q and HSA21q is about 1.44%

For those 179 genes, the average nucleotide and amino acid identity in the coding region is 99.29% and 99.18%, respectively.​

Taking the reciprocal of that last figure (i.e. difference rather than identity) we get a nucleotide difference of only 0.71% in these 179 genes.

These tiny percentages of DNA sequence differences don't change at all the fact that 83% of the 231 genes considered in this comparison showed amino acid differences.

It just means that they are measuring different things.

Actually they were not able to identify all of the genes they examined but the 83% tells us that we are only 17% identical to the chimpanzee.

And that is only in the context of 231 genes on one chromosome.

When 20% of the protein coding genes have gross structural differences that is a dramatic difference, one no one was expecting to find.

For chimpanzees since it was on the chimpanzee chromosome that these genes were found. The verdict for the changes on the human chromosome is that "no gross structural differences are expected".

To put this in perspective I found this figure that may help you to see the proportion of differences in the genes.

The figure shows the number of synonymous and nonsynonymous nucleotide differences in 13,731 human–chimpanzee orthologous gene pairs.

Here is the context of the discussion of gene comparisons. I really don't have a lot of time for a more detailed expositive post but I thought it was fairly comprehensive:

"...there are 71,896 nucleotide differences in 13,731 genes."

A Scan for Positively Selected Genes in the Genomes of Humans and Chimpanzees

I skimmed the paper, but it will take a while to digest it. I do like this sentence from near the beginning (emphasis added):

"..despite the small overall magnitude of DNA sequence divergence, we might expect such evolutionary changes to leave a noticeable signature throughout the genome."

 

[mark kennedy]

A gene duplication is a mutation. When a gene duplication occurs randomly, it is a random mutation. When the consequence benefits the organism it is a beneficial mutation.

Stop ducking plain English, Mark.

No it's not a mutation, stop trying to change the meaning of the word 'mutation' from transcript error to adaptive change.

 

[mark kennedy]

(the gene duplication has nothing to do with the frame shift, the frame shift is a very particular result of a deletion or insertion that is (X mod 3 = 1,2) X=#of nucleotides in the indel.)

yes, but nothing i've seen here with your cut and pastes demonstrates to me that you do.

Then you should realize that this is not a frameshift, it's an alternative reading frame and does not create a novel gene.

a reading frame mutation is where a protein is produced offset by one or 2 nucleotides at the DNA level. because of the triplet genetic code this is a massive change in the composition of the protein.

In frameshift mutation deletion or insertion of 1 or 2 bases causes the proteins to be scrambled and are often lethal. What usually happens is a stop codon is inserted causing a nonesense mutation. The reason it is important to understand exactly what a frameshift mutation is, is because the nylon bug's novel enzyme is not the result of a mutation. You really need to realize the difference between a transcript error and a gene duplication.

essentially what happened with the nylon bug is that twice a gene was mutated by a deletion that caused a reading frame shift, producing a never before seen protein that had a weak enzymatic activity that allowed those bacteria to exist and metabolize nylon waste.

you have shown me that access to, and reading of, scientific papers is not an indicator of understanding them.

At least I read them, had the nylon bug reading frame been mutated it would have been useless or even lethal. I can't believe that evolutionists aren't fascinated at the concept of a univesal coding sequence. The open reading frame was allready functioning before but somehow was transposed into this sequence to produce a key protein for a novel enzyme. This was not a random mutation creating a novel gene, it was a variation of an existing theme.

That is why these discussion leave me cold, evolutionists don't have a clue what these papers are meant to do. If a universal coding sequence and the genome of the mrca of the chimpanzee and human genomes doesn't spark your imagination then your probably not an evolutionist. You may not believe in creationism but you couldn't possibly believe the gibberish your putting out.

post edit addition

you bolded "preexisted", of course the DNA was there before the mutation. however it had never been used to produce that particular protein, that was the result of a frameshift mutation. all mutation works on preexisting DNA, that is the fundamental reason that life falls into a nested hierarchical structure. you only have what exists to operate on, no deus ex machina for living creatures, at least not visible at the genetic level...


.....

First off, there was not mutation, period.
Second, you blew right by the virtues of olimetric repeats as a universal coding seqeunces and the signifigance for the single common ancestor.

Newsflash!​

The single common ancestor would have been a bacteria, this paper suggest a possible genetic basis for the transition from a protoorganism to the various other kingdoms of cells. Instead of really taking a serious look at what the paper was trying to do you keep making these pedantic, condesending remarks and I'm just sick of it.

Thanks for the romp around the mayberry bush and goodbye.

 

[gluadys]

You really need to realize the difference between a transcript error and a gene duplication.

A transcript error is a mutation.
A gene duplication is a mutation.

Just because we distinguish between different types of mutations doesn't mean we are no longer talking about mutations.

A mutation is any change in a DNA (or RNA) sequence. transcript errors, duplications, insertions, deletions, substitutions, etc. are just different ways of changing the sequence.

Everything you claim is not a mutation is a mutation if the effect is to change the DNA sequence.

You agreed to this definition of mutation long ago. Why, then, do you constantly dispute is. Using the name of the specific type of mutation does not change the fact that it is a mutation.

 

[gluadys]

No it's not a mutation, stop trying to change the meaning of the word 'mutation' from transcript error to adaptive change.

The meaning of "mutation" is not limited to transcript error. It includes any and every change in a DNA or RNA sequence. Gene duplications are also mutations. Indels are mutations. Substitutions and transpositions are also mutations.

Mutation is an umbrella term for changes in the DNA sequence.

Adaptive change is not mutation. Adaptive change is a product of natural selection (aka differential reproductive success). Differential reproductive success may occur as a consequence of the phenotypic expression of a mutation. When it does, we refer to the mutation as beneficial or harmful depending on whether the organisms expressing the mutation tend to have a larger or smaller than average number of surviving offspring.

When the mutation is not expressed in the phenotype, or when the expression of the mutation in the phenotype has no effect on reproductive success, it is neutral in terms of adaptation.

 

[rmwilliamsll]

Then you should realize that this is not a frameshift, it's an alternative reading frame and does not create a novel gene.

alternative reading frames exist on all genes. mutations cause reading frame errors which give rise to NOVEL PROTEINS not genes, the mutations caused the new gene.
(as an aside alternative reading frames along with alternative splicing of mRNA strands give rise to the fact that a single gene can produce a variety of proteins, this is NOT what is happening on the nylon bug, not even AiG claims this)

In frameshift mutation deletion or insertion of 1 or 2 bases causes the proteins to be scrambled and are often lethal. What usually happens is a stop codon is inserted causing a nonesense mutation. The reason it is important to understand exactly what a frameshift mutation is, is because the nylon bug's novel enzyme is not the result of a mutation. You really need to realize the difference between a transcript error and a gene duplication.

the stop codon is not inserted into the dna, it is hit by the transcription RNA polymerase and now read as a stop codon because of the frameshift.

gene duplication is a particular kind of mutation.
DNA duplication is creating 2 strands from 1 strand acting as a template, this is done by DNA polymerase
transcription error is DNA-->mRNA strand via RNA polymerase
it creates a faulty protein, maybe a few of them and it is NOT a mutation of the DNA

the nylon bug has 2 deletion mutations that caused frameshifts. yes it is a dna mutation.

you are consistently confusing these terms.

Second, you blew right by the virtues of olimetric repeats as a universal coding seqeunces

this is not the issue with the nylon bug, plus we can't get to this without using the same vocabulary. your insistence that a frameshift is not a mutation, plus the consistent use of transcription as the source of mutation stops the argument from proceeding to any higher more complex levels.

This was not a random mutation creating a novel gene, it was a variation of an existing theme.

the order of what presumably happened in the nylon bug.
existing gene, producting a protein.
gene gets duplicated
duplicate experiences a 300bp deletion that caused a reading frame shift that on transcription produced a new novel protein completely unrelated to the first protein since it is a frameshift that caused it. there is a novel gene, and there is a novel protein. the existing theme is only the DNA sequences the two proteins are the result of. these sequences are much the same, the proteins however are very different. that is why frameshifts are so interesting.

pedantic, condesending remarks

i have tried as best i can to meet you on common ground. i value a scientific discussion and the technical use of terms. that allows real work to be done on the higher levels of the discussion. but that is just me.

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