Genetics and Genesis

[mark kennedy]

Don't put paraphrases into block quotation format, since it misleads the reader. And you should avoid paraphrasing, since you conisistently misunderstand scientific papers, including this one.

Right, I'm always wrong, I got that part.

Correct.

Ok

That's the incorrect part. DNA is not replicated (copied into DNA) during transcirption. During transcription it is copied into RNA. Replication is a different process.

That is not what I originally said, I said I don't know how much transcript errors, point mutations...etc had to do with adaptations. That's when I was informed that transcript errors have nothing to do with mutations which is not true. Any error in the DNA strand that isn't corrected is a mutation.

I went on to say that the central dogma of Biology was DNA-transcription-RNA-translation. That's all there is to that and you guys are making a fuss about how transcription and translation and replication are different things. The fact is I have been trying to discuss molecular mechanisms that produce adaptive traits. I still don't know how much transcription errors, point mutations...etc can help organisms adapt over time.

I don't care about the distinction between replication and transcription. What I am interested in is mutations and adaptive evolution, specifically the molecular mechanisms involved.

No, Mark, I wanted to explain some basic biology to you. Your response was rudeness and an accusation that I was lying. You obviously still don't understand what I (and many other people) told you. (Note: I never said that "bp" does not mean base pair -- that's a little fantasy you cooked up yourself.)

Really? This is the statement that was made:

"The 2x10^-8/bp/generation is the number of mutation events, not the number of base pairs."​

I asked you if the bp stood for base pair, you said no it stood for mutation event.

I didn't make this up, that is what you said:

http://www.evcforum.net/cgi-bin/dm.cgi?action=msg&f=9&t=97&m=76

Right. And what does this have to do with transcription, which takes place throughout the cell cycle, and which does not result in replication of DNA?

I was not interested in transcription as opposed to replication in the slightest. I'm not the one who made this into an issue, all I said was I don't know how much transcription errors, point mutations...etc can help organisms adapt. You guys have talked about nothing else since.

The first two are facts. The last three are all errors you've made from misreading the Zhang paper. The paper describes a model. In that model, indels come in all sizes. They assume that those indels that happen to be multiples of three bases will not disrupt the ORF; the others will. They also assume that point mutations (which are not indels) occur at a rate of 1x10-9/site/year. Some of those point mutations, the ones that produce a premature stop codon, will also disrupt the ORF.

A point mutation rate of 1 x 10-9/site/year,

I used an indel mutation rate of 1.1 x 10-10/site/year
​

You told me once that in each generation you had ~50 single nucleotide substitutions fixing and 7 indels fixing overall. At what rate are the mutations being fixed in the ASPM gene and how long did it take?

Don't ask me because I'm always wrong, just answer the question Steve and maybe we can talk about molecular mechanisms that create adaptations.

That's what the paper actually says. The point of the model is to demonstrate that ASPM has not experienced a loss of selective constraint, and is in fact under strong purifying selection. Since this is a point you accept, I have no clue why you have gone off on this tangent.

I'm just waiting for someone to take an interest in the ASPM gene and I have been bored stiff with the last two or three pages.

Mark, you're making a fool out of yourself. (If you want to interpret that statement as evidence that you have superior insight into biology to all the actual biologists, and that I'm only resorting to ad hominem comments because of your insight, you can do so. If you do, you'll simply be making a bigger fool out of yourself. Your call.)

Biology has nothing to do with this, it never has. This is about evolution as natural history as opposed to the Bible as redemptive history. You cannot believe both. Now as far as evolution as the change of the frequency of alleles in populations over time, that creates not problems. It's the assumption of common descent that is the 'fundamental' issue here and I refuse to accept it as an a priori self evident fact.

This has nothing to do with Biology or that is what we would be talking about.

You know many things that just aren't so.

Don't we all.

No. "In the above genomic data analyzed, 19% of the total 1019 indels are of sizes that are multiples of three nucleotides." That's from the same paragraph in the Zhang paper that you already quoted.

Ok great, all the rest are neutral or nearly neutral I guess. Maybe you can help me out with something I really don't understand. How many amino acids are different and how much time are they allowing for their accumulation?

Quite. It is certainly possible that transcription causes mutations to occur, just as recombination probably causes mutations to occur. In both cases the DNA is exposed and subject to damage during the process. The mutations are not transcription errors, however; transcription errors are mistakes in the transcript (the RNA copy), while the mutations are changes to the original DNA. And note that this is a different mutation process than the one you were talking about earlier, which occurs during DNA replication in S phase.

I never argued that they were, I just said I didn't know how much mutations had to do with adaptation. I'm not the one who made such a big deal about it, I was using 'transcription' in a very general sense not making detailed descriptions about how transcription errors create mutations.

Yes, and what you originally said was wrong. Transcript errors (that is, errors in transcripts) are not a source of mutation here.

It's not a source of mutation where? I don't know of another way of saying this Steve, I don't care!

Look, if you want to talk about how mutations of various kinds are generated that suits me just fine. I said I didn't know how much transcript errors, point mutations...etc help organisms to adapt.

That's all I said and I was not talking about transcription as opposed to replication I was just talking about mutations in general. Since then you guys have been hurling insults one right after the other.

Transcription exposes ssDNA. The most common base substitution events in the spectra of background mutations in E. coli and mammalian cells are G • C-to-A • T transitions. Fix and Glickman (28) observe that 77% of these mutations originate on the nontranscribed strand in E. coli mutants unable to repair deaminated cytosines. This suggests that the unprotected single strand in the transcription "bubble" is significantly more vulnerable to mutations than the transcribed strand, which is protected as a DNA-RNA hybrid (Fig. 1A). (A Biochemical Mechanism for Nonrandom Mutations and Evolution, TWO MECHANISMS BY WHICH TRANSCRIPTION CAN INCREASE MUTATION RATES. Journal of Bacteriology, June 2000)​

I simply refuted the statement that Transcription errors have nothing to do with mutations. It's not that big of a deal and I never made any reference to transcription as opposed to replication much less argued it.

Ok, transcription and replication are two different things. So what?

 

[Deamiter]

Mark. How can you blithly keep repeating your mantra that you ONLY said you weren't sure when you said this:

"I'm not totally wrong? He can't recognize that a mutation most often is a transcript error and flagrantly denies that it is..."

Nobody cared one bit about these transcription errors until you flat out claimed that "mutations are most often transcript errors." Maybe you just misspoke, but when you said most mutations are transcript errors, that you earlier had said you didn't have a clue doesn't erase the mistake! We're totally willing to move on, but don't try to cover up your mistakes by quoting earlier posts!

And to reiterate a question that you've managed to avoid in your focus on our reaction to this wildly inaccurate statement, what would this "molecular mechanism" you're looking for look like? In the papers you've cited, the unknown mechanism is always in reference to the fact that the exact mutations that affect brain size are unknown. You seem to be looking for a different mechanism for mutation itself.

 

[sfs]

Right, I'm always wrong, I got that part.

You're not always wrong, but you're wrong often enough and in serious enough ways that you are not a reliable interpreter of scientific papers in genetics. There are lots of things that I can't reliably interpret either; I shouldn't paraphrase papers about string theory, or organic chemistry, because I don't know enough.

That is not what I originally said,

What you originally said (about transcript errors being a major source of mutation) was wrong. What you said here (about transcription occurring during S phase) was also wrong. I don't know whether those represent two different errors, or just one, but what you're saying is still wrong. You're ignoring the first rule of damage control: when you're in a hole, stop digging.

I said I don't know how much transcript errors, point mutations...etc had to do with adaptations. That's when I was informed that transcript errors have nothing to do with mutations which is not true. Any error in the DNA strand that isn't corrected is a mutation.

Sorry, but it is true that trancript errors have nothing to do with mutation. A transcript error is an error in the transcript, which is RNA. An error that occurs in the DNA strand is not a transcript error, even if it occurs during transcription. That error is a mutation.

The fact is I have been trying to discuss molecular mechanisms that produce adaptive traits. I still don't know how much transcription errors, point mutations...etc can help organisms adapt over time.

Mutations, whether point mutations or larger changes, can change the traits of an organism. Some of those traits are adaptive. For example, Europeans have developed lactose tolerance and lighter skin color, both adaptive traits in their environment, because of point mutations.

Look, do you agree that the differences between humans are chimpanzees are the result of genetic differences? Do you understand that those genetic differences could all occur as the result of individual mutations? What part of the this process is it that you have problems with?

Really? This is the statement that was made:

"The 2x10^-8/bp/generation is the number of mutation events, not the number of base pairs."​

Right. My statement was correct. The mutation rate tells you the number of mutations that will occur for a given number of bases present and for a given period of time. Similarly, the speed (measured as miles/hr) tells you how many miles will be covered for a given number of hours travelled. The distance is not measured in hours, and the number of mutations is not measured in base pairs.

I asked you if the bp stood for base pair, you said no it stood for mutation event.

No, that's you paraphrasing badly again.

I didn't make this up, that is what you said:

http://www.evcforum.net/cgi-bin/dm.cgi?action=msg&f=9&t=97&m=76

Your link points to one of your own posts.

You told me once that in each generation you had ~50 single nucleotide substitutions fixing and 7 indels fixing overall. At what rate are the mutations being fixed in the ASPM gene and how long did it take?

Point mutations in ASPM have been fixed in the human lineage at a rate of one per 14,000 generations (approximately).

Biology has nothing to do with this, it never has. This is about evolution as natural history as opposed to the Bible as redemptive history. You cannot believe both.

Since I do believe both you would seem to be wrong here. Why not confine yourself to the statement that you can't believe both, rather than telling me what I can believe?

Now as far as evolution as the change of the frequency of alleles in populations over time, that creates not problems. It's the assumption of common descent that is the 'fundamental' issue here and I refuse to accept it as an a priori self evident fact.

Good -- no one should accept common descent as an a priori fact. I accept it as a fact based on the overwhelming weight of evidence, and on the inability of anyone to offer an alternative explanation for that evidence.

Maybe you can help me out with something I really don't understand. How many amino acids are different and how much time are they allowing for their accumulation?

The Zhang paper attributes 16 amino acid changes in ASPM to mutations in the human line. They would have accumulated over 5 to 7 million years.

It's not a source of mutation where?

Transcript errors are not a source of mutation in ASPM.

I don't know of another way of saying this Steve, I don't care!

Then stop talking about it.

I simply refuted the statement that Transcription errors have nothing to do with mutations. It's not that big of a deal and I never made any reference to transcription as opposed to replication much less argued it.

It's not that big a deal, but you still don't get it. Mutations that occur during transcription are not transcription errors. Transcription errors are errors in the process of transcription, and are not mutations.

Ok, transcription and replication are two different things. So what?

So they're different things: talking about them as if they were the same is wrong. If you make false statements about genetics to a geneticist, he's apt to correct you.

 

[mark kennedy]

Mark. How can you blithly keep repeating your mantra that you ONLY said you weren't sure when you said this:

Look, this is not a mantra it's an actual fact, transcription errors are mutations if they are [not corrected:

Transcription exposes ssDNA. The most common base substitution events in the spectra of background mutations in E. coli and mammalian cells are G • C-to-A • T transitions. Fix and Glickman (28) observe that 77% of these mutations originate on the nontranscribed strand in E. coli mutants unable to repair deaminated cytosines. This suggests that the unprotected single strand in the transcription "bubble" is significantly more vulnerable to mutations than the transcribed strand, which is protected as a DNA-RNA hybrid (Fig. 1A).​

"I'm not totally wrong? He can't recognize that a mutation most often is a transcript error and flagrantly denies that it is..."

What I said was that I don't know how much transcription errors have to do with adaptations. I'm not making this up, that is actually what I said and he went spastic and you guys have talked about nothing else since. You guys are making a major issue of something that really doesn't matter and I certainly never cared about.

Every single post has been the same mindless chant. Once and for all, this is what I said:

I don't know how much a transcript error, deletion, insertion, point mutation or rearrangement can help adapt organisms over time. It's difficult for me to track down but I get the impression that I have stumbled into a very complicated world of exploration.

All I said was I didn't know how much it had to do with adaptation. You guys have went on for half the thread on the same stupid point. This is how he responded and you guys just chimed right in:

Firstly, "transcript errors" have nothing to do with mutations. It's high time you get your terminology and conceptual understanding correct. Secondly, are you simply trying to say there are no such things as beneficial mutations?

First of all I list 'transcript errors' as one of a number of causes of mutations. Then he asks if I meant that there are no such thing as beneficial mutations which again had nothing to do with what I said in content or in the immediate context.

You guys have talked about nothing else, now look at this quote:

Transcription exposes ssDNA. The most common base substitution events in the spectra of background mutations in E. coli and mammalian cells are G • C-to-A • T transitions. Fix and Glickman (28) observe that 77% of these mutations originate on the nontranscribed strand in E. coli mutants unable to repair deaminated cytosines. This suggests that the unprotected single strand in the transcription "bubble" is significantly more vulnerable to mutations than the transcribed strand, which is protected as a DNA-RNA hybrid (Fig. 1A). (A Biochemical Mechanism for Nonrandom Mutations and Evolution Barbara E. Wright)​

Did you read it? Do you understand it? What exactly is your problem with transcription errors being the most common source of mutations?

Answer the question!

Nobody cared one bit about these transcription errors until you flat out claimed that "mutations are most often transcript errors." Maybe you just misspoke, but when you said most mutations are transcript errors, that you earlier had said you didn't have a clue doesn't erase the mistake! We're totally willing to move on, but don't try to cover up your mistakes by quoting earlier posts!

Ok, what is the most common source of mutations?

And to reiterate a question that you've managed to avoid in your focus on our reaction to this wildly inaccurate statement, what would this "molecular mechanism" you're looking for look like? In the papers you've cited, the unknown mechanism is always in reference to the fact that the exact mutations that affect brain size are unknown. You seem to be looking for a different mechanism for mutation itself.

You guys have unanimously agreed to support a conflated misrepresentation of basic biology. The unprotected single strand in the transcription bubble is significantly more vulnerable to mutations than the transcribed strand.

I have no idea why anyone would want to make such a major effort to defend an obvious error. The only mistake that I am aware of is responding to what he said in the first place.

As for the rest of you, you don't even want to know what I think of ad hominem attacks. It is especially telling that it is blatantly wrong in substance and ridicules in it's unwaivering support.

Transcription factors have been something I have been interested for some time and I have just about lost my patience discussing these things with died in the wool secularists.

 

[mark kennedy]

You're not always wrong, but you're wrong often enough and in serious enough ways that you are not a reliable interpreter of scientific papers in genetics. There are lots of things that I can't reliably interpret either; I shouldn't paraphrase papers about string theory, or organic chemistry, because I don't know enough.

I'm not trying to tell anyone how to read one of these papers. To tell you the truth I don't have a clue why so many scientists are so interested in creationism. It seems like they would just ignore it if it's just pseudo science like UFOs and Zero Gravity machines.

What you originally said (about transcript errors being a major source of mutation) was wrong. What you said here (about transcription occurring during S phase) was also wrong. I don't know whether those represent two different errors, or just one, but what you're saying is still wrong. You're ignoring the first rule of damage control: when you're in a hole, stop digging.

I don't know why you have such a problem with it, I really don't. As far as transcription during the S phase to tell you the truth I was thinking about cell cycle check points and not really following this tangent you guys are so obsessed with. I still don't care, it still doesn't matter and bp still means base pair.

Sorry, but it is true that trancript errors have nothing to do with mutation. A transcript error is an error in the transcript, which is RNA. An error that occurs in the DNA strand is not a transcript error, even if it occurs during transcription. That error is a mutation.

A transcript error is an error in the transcript (aka RNA). An error in the DNA error is not a transcript error even if it occurs during transcription and has nothing to do with mutations but the error is a mutation. Got it, why didn't I see it before?

Mutations, whether point mutations or larger changes, can change the traits of an organism. Some of those traits are adaptive. For example, Europeans have developed lactose tolerance and lighter skin color, both adaptive traits in their environment, because of point mutations.

It's just that I wonder if there is a molecular mechanism that can alter the nucleotide sequence in, shall we say, a nonrandom way.

Look, do you agree that the differences between humans are chimpanzees are the result of genetic differences? Do you understand that those genetic differences could all occur as the result of individual mutations? What part of the this process is it that you have problems with?

What part of what process? The process by which a primate brain experiences exponential growth? Did you ever notice that there are no chimpanzee fossils about 2-6 million years ago? You know why, because they are all marked Homo XXX when they should be Pan XXX, that's why. The biggest problem with evolutionists is that they try to prove too much and in so doing beg the question of proof on their hands and knees.

Right. My statement was correct. The mutation rate tells you the number of mutations that will occur for a given number of bases present and for a given period of time. Similarly, the speed (measured as miles/hr) tells you how many miles will be covered for a given number of hours travelled. The distance is not measured in hours, and the number of mutations is not measured in base pairs.

Point mutations are but to tell you the truth I never really had an issue with what you were saying. You guys had a problem with just about everything I posted in their and I have had exchanges with WK since. He didn't seem to have any idea about what molecular mechanisms were responsible for the expansion of the human brain either.

No, that's you paraphrasing badly again.

What do you expect when I work on detailed expositions that are ignored?

Your link points to one of your own posts.

Yea so?

Point mutations in ASPM have been fixed in the human lineage at a rate of one per 14,000 generations (approximately).

The expansion of the human ancestors would have started at 400cc to 500cc 2 mya to almost twice that proceeded by, and followed by, long periods of stasis.

Since I do believe both you would seem to be wrong here. Why not confine yourself to the statement that you can't believe both, rather than telling me what I can believe?

Sure, no problem.

Good -- no one should accept common descent as an a priori fact. I accept it as a fact based on the overwhelming weight of evidence, and on the inability of anyone to offer an alternative explanation for that evidence.

It's an a priori assumption with no directly observed or demonstrated mechanism, it's a myth.

The Zhang paper attributes 16 amino acid changes in ASPM to mutations in the human line. They would have accumulated over 5 to 7 million years.

Has there ever been a beneficial effect found resulting from a mutation in a protein coding gene involved in human neural functions?

I only ask because mental retardation, brain tumors and various forms of dementia result from them.

Transcript errors are not a source of mutation in ASPM.

Never said they were, I said that transcription errors are a major source of mutations. I don't know why you care or why we can't get off the topic.

Then stop talking about it.

When you guys quit making to the central focus of every post in the thread I will be glad to.

It's not that big a deal, but you still don't get it. Mutations that occur during transcription are not transcription errors. Transcription errors are errors in the process of transcription, and are not mutations.

Mutations that occur during transcription are not transcription errors and they are not mutations.

If I agree and repent with sackcloth and ashes will you kindly please find something else to waste our time on. The fastest growing field of natural science in the world and we are playing these semantical shell games. I just don't get it.

So they're different things: talking about them as if they were the same is wrong. If you make false statements about genetics to a geneticist, he's apt to correct you.

Yes he will, if you are a creationist. If you are an evolutionists on the other hand errors are ok with him.

 

[shernren]

Did you ever notice that there are no chimpanzee fossils about 2-6 million years ago? You know why, because they are all marked Homo XXX, that's why.

The last time we talked about this (a month ago) you were not able to prove that any Homo XXX fossils actually were chimpanzee fossils. Talk is cheap. Where's the evidence?

 

[mark kennedy]

The last time we talked about this (a month ago) you were not able to prove that any Homo XXX fossils actually were chimpanzee fossils. Talk is cheap. Where's the evidence?

Links are easy, take it to the formal debate forum. I'm tired of the head trips, it's time to put up or shut up.

 

[Deamiter]

Did you read it? Do you understand it? What exactly is your problem with transcription errors being the most common source of mutations?

Answer the question!

Um... the quote says that mutations are most common DURING transcription. This is true, mutations ARE most common during transcription. These mutations are NOT called transcription errors. But it seems you've figured that out now as you changed your tune and acknowledged that transcription errors are NOT a source of mutations in the very next post:

A transcript error is an error in the transcript (aka RNA). An error in the DNA error is not a transcript error even if it occurs during transcription and has nothing to do with mutations but the error is a mutation. Got it, why didn't I see it before?

Since you posted these back-to-back, I suspect the second is sarcasm, so since the first is blatantly wrong isn't it worth correcting since you've been claiming that transcription errors cause mutations for pages now? Have you really acknowledged that mutations during transcription are not the same as transcription errors? Seems like such a basic understanding would be good to get straight before we move on to exactly how mutations could cause changes in alleles.

 

[Deamiter]

I'm not trying to tell anyone how to read one of these papers. To tell you the truth I don't have a clue why so many scientists are so interested in creationism. It seems like they would just ignore it if it's just pseudo science like UFOs and Zero Gravity machines.

Scientists really didn't give creationism a second thought until creationists started insisting that it be taught to our children in science classes. Further, most people posting here are interested in the topic for theological as well as purely scientific reasons. We are all Christians here after all.

 

[mark kennedy]

Um... the quote says that mutations are most common DURING transcription. This is true, mutations ARE most common during transcription. These mutations are NOT called transcription errors. But it seems you've figured that out now as you changed your tune and acknowledged that transcription errors are NOT a source of mutations in the very next post:



Since you posted these back-to-back, I suspect the second is sarcasm, so since the first is blatantly wrong isn't it worth correcting since you've been claiming that transcription errors cause mutations for pages now? Have you really acknowledged that mutations during transcription are not the same as transcription errors? Seems like such a basic understanding would be good to get straight before we move on to exactly how mutations could cause changes in alleles.

Since I nothing about transcription or transcription errors had anything to do with what I have been saying I really don't care. If a mutation during transcription is not a transcription error I don't know what to tell you.

I browse scientific papers most of the time I spend on the web, mostly looking for direct comparisons of chimpanzee and human genes. I just happened upon this a while ago just to give you an idea of what I am running into:

Three genes of unknown function, abnormal spindle-like primary microcephaly (ASPM), KIAA0036, and KIAA1023, were expressed strongly in nearly all transformed human cell lines and in a panel of 16 adult human tissues by reverse transcription polymerase chain reaction. However, ASPM gene expression was not detected in adult brain or skeletal muscle. To better understand function, the domain structure of ASPM was examined. Abnormal spindle-like primary (ASP) protein (abnormal spindle) of Drosophila spp, an orthologue of ASPM, is involved in mitosis, and mutations lead to abnormal spindles and inhibition of cytokinesis.

Expression of IQ-motif genes in human cells and ASPM domain structure.)Ethn Dis 2005)


I have ran into this constantly, highly conserved genes involved in neural genes have to accumulate mutations. The problem is that every time an effect is expressed it damages the early development of the brain. Blood cells evolve, hair color changes, metabolic functions adapt but genes involved in the early development of the brain do not respond well to mutations...ever.

I'm talking about molecular mechanisms that change genes, I know that they exist. I have plenty of examples of them and I want to know how they work.

That is all there is to this and when I am being told that a transcript error is not a mutation. I don't know why you guys insist on pushing this point since it is wrong:

ranscription /trans·crip·tion/ (-krip´shun) the synthesis of RNA using a DNA template catalyzed by RNA polymerase; the base sequences of the RNA and DNA are complementary.

Here is a typical example of what I am talking about and it's not hard to find examples:

The affected members of IFCAS-28 (fig. 2A) are heterozygous for a C→G substitution (fig. 2B) in exon 8 at nucleotide position 601 of the coding sequence. Similar to IFCAS-41, the migration pattern of the cDNA (fig. 2C) of IFCAS-28 shows that affected individuals have two different-sized alleles, whereas the unaffected individual is homozygous for the larger allele. This result suggests that the substitution may truncate the transcript. Sequencing of the different cDNA alleles shows that alternative splicing is occurring in the mutated allele (fig. 2D). The C→G shift creates an alternative splice site that, when used, results in premature splicing of exon 8 and in splicing of exon 9 at the correct position but in an incorrect reading frame. This results in a frameshift, which is predicted to lead to a truncated protein of 201 amino acids that has a novel amino acid and contains only the NPXY motif.​

Krit1 Missense Mutations Lead to Splicing Errors in Cerebral Cavernous Malformation

This is a truncated transcript that results in a frameshift and finally a truncated protein.

With fragile X you get the opposite effect since it is an enlarged gene:

Fragile X Syndrome

Several disorders in humans are caused by the inheritance of genes that have undergone insertions of a string of 3 or 4 nucleotides repeated over and over.

Huntington's Disease

In this disorder, the repeated trinucleotide is CAG, which adds a string of glutamines (Gln) to the encoded protein (called huntingtin). The abnormal protein increases the level of the p53 protein in brain cells causing their death by apoptosis.

Muscular Dystrophy

Some forms of muscular dystrophy that appear in adults are caused by tri- or tetranucleotide, e.g. (CTG)n and (CCTG)n, repeats where n may run into the thousands. The huge RNA transcripts that result interfere with the alternative splicing of other transcripts in the nucleus. Mutations
​

Notice that muscular dystrophy is from huge RNA transcripts that interfere with other transcripts?

The only point Steve really made was that a DNA copy error and a transcript error are not the same thing. The fact is I never thought nor tried to argue that they were. Now look at my response again:

A

transcript error is an error in the transcript (aka RNA). An error in the DNA error is not a transcript error even if it occurs during transcription and has nothing to do with mutations but the error is a mutation.​

It has nothing to do with mutations even though its a mutation? You've got to be putting me on.

Anything that destabilizes the DNA and is not corrected is a mutation. That is all there is to that and splitting semantical hairs between a DNA copy and an RNA transcript is absolutely meaningless since I never argued against it and that has nothing to do with what I have been saying.

 

[mark kennedy]

Scientists really didn't give creationism a second thought until creationists started insisting that it be taught to our children in science classes. Further, most people posting here are interested in the topic for theological as well as purely scientific reasons. We are all Christians here after all.

Do you know how I got into these debates? I posted to secular board about teaching Creationism in the public schools and said I agreed that it should not be taught because of strong feelings about separation of church an state. Near the end of the post that was not very long I said something to the order that I feel that way despite the fact that I am a young earth creationist. They went off.

I'm not pushing creationism, it's secular scientists that are pushing their naturalistic assumptions off on me.

I know religion and science have to be kept separated, that is why I am so adamantly opposed to Darwinism. The theological themata is unscientific, science has nothing to do with God but theology is a science.