Freethought & Rationalism Archive

Nat · 10-25-2002, 03:43 PM

"4. In the chromosome fusion thread, you said that mutations would result in fusing and truncation. Please reconcile and/or distinguish your reasoning there with what you are saying here."

Different type of mutations. All mutation means is a change in the genome that is not apparent in the parent(s)'s genome but exists in the offspring's genome. You yourself contain a few mutations in your genome. Most are likely point mutations of non-coding parts of your genome.

"Note: It would seem that the software analogy is direct and strong, as I indicated, since we are discussing genetic code. Tell me, why precisely is unsuitable about the analogy?"

Because all analogies are fundamentally flawed, and it seems that discussions involving them simply result in arguments about the appropriateness of the analogy. You can agree that there are substantial differences between the genetic code and computer software and these differences are not relevant to the evolution debate, so by not using imprecise analogies we can keep the discussion on track.

monkenstick · 10-25-2002, 04:07 PM

Quote:

1. I notice that the same scientists have published the sequences (in a foreign journal) for the non-functional proteins in the apes/humans as well as the functional copy taken from the owl monkey. Are you aware of independent confirmation of their work?

there is independent verification of the human sequence - I think I mentioned it in the old thread. I am unaware of any independent verification of the other sequences. The human urate oxidase pseudogene they sequenced is accurate, so I see no reason to doubt the accuracy of the other sequences.

Quote:

2. Let assume that the work of these scientists is solidly affirmed. What makes this extant genetic characteristic
significantly different from other thousands (millions?) of other genetic homologies in the attempt to collect evidence for modified trans-species common descent?

The fact that this particular sequence shows homology in non-functional sequences, which cannot be explained by a "similar sequence - similar design" hypothesis, because design implies function

Quote:

3. Let assume that the BLAST pairwise alignment analysis (which, I understand, is highly statistical) is correct. Then the owl/monkey sequences are 94% similar. What assures you that the 6% difference is not functionally critical?

Blast lines the sequences up just as for the clustal alignment in my first post - the 6 percent difference is merely the percentage of nucleotides which differ between the two
e.g.
A C G T
A C T T
blast would say these sequences were 75 percent similar (it also factors in gaps, but there are none in the alignment in question)

The 6 percent is functionally critical vander, thats the whole point. The spider monkey version of urate oxidase is functional, it doesn't contain any premature stop codons. The human sequence on the other hand is non functional becuase it has a stop codon very early on in its transcript which truncates it.

Quote:

4. It would appear that the urate oxidase sequence contains only two (not "several") premature stop codons. What "evolutionary" event would cause the INSERTION of a terminal codon in the MIDDLE of a gene? (As you imply, the stop codon is directly and strongly analogous to an "exit", "end" or "terminate" in a computer program)

see the other guys posts on this, a single point mutation can cause a stop codon

Quote:

5. What prevents me from reasoning intelligibly that the Creator merely employed life-building blocks in the establishment of entirely new species, rendering some of the genes, or genetic components, inoperable?

nothing, except for the fact that the creator rendered the genes inoperable in exactly the same place in at least four closely related species. (evolutionary prediction: the bonobo will have exactly the same premature stop codon if its urate oxidase gene is sequenced)

I'm having a hard time understanding where you're coming from vander, do you believe in common descent, and that god is the force behind the "evolution" of new species, or do you believe in special creation? If its the latter, then I'm wondering why god would include a non-functional gene. If he didn't require that humans, chimps etc. have this gene, then why not just leave it out?

[ October 25, 2002: Message edited by: monkenstick ]

ps418 · 10-25-2002, 04:37 PM

Quote:

Vanderzyden: A mutation is a detrimental, passive, malfunctional event . . .

This is a very common, but false, claim. A mutation is simply a change in nucleotide sequence. The effect of the mutation can be neutral, detrimental, or even beneficial, depending upon, amongst other things, where it occurs in the genome. Even Answers in Genesis's article on Arguments we think creationists should not use says that the claim that "there are no beneficial mutations" is not true.

Vanderzyden · 10-25-2002, 04:50 PM

Quote:

Originally posted by Nat:
"3. What is a point mutation? Please distinguish it from other mutations."

A point mutation is a mutation that results in a single nucleotide being swapped out for another. Such mutations differ from insertions and deletions because they do not result in a fram-shift of the rest of the genome.

Nat,

You reply is quite short, and therefore more questions arise from your answer....

1. It seems strange that a single nucleotide could be replaced.

1a. What is the means of substitution for a single nucleotide?
1b. How is a single nucleotide extracted and replaced (or overwritten) by a stop codon nucleotide?

2. Scigirl answer very quickly and confidently with the "point mutation" answer. In contradiction, you answer that an insertion/deletion is the result of a different type of mutation.

2a. What would we call this mutation?
2b. How does this mutation work?
2c. Which is more likely, a point mutation or an insertion?

John

monkenstick · 10-25-2002, 04:53 PM

Quote:

1. Specifically, what in a mutation would cause the INSERTION of a stop codon? (A mutation is a detrimental, passive, malfunctional event, and yet you are saying that such events could be responsible for the active, specific placement of a terminal codon).

2. You say the answer is easy. Therefore, I think it's reasonable to ask for direct support for your response: What evidence do you have from which we may directly infer that mutations are responsible for the insertion of stop codons?

3. What is a point mutation? Please distinguish it from other mutations.

1) vanderzyden, if you'd looked at the sequences i'd posted you'd see the exact mutation that was responsible for the introduction of a premature stop codon

i.e.
CGA (encodes for arginine)
<point mutation>
TGA (encodes a stop codon)

2) evidence for stop codons arising via mutation;

Quote:

1: Gynecol Oncol 2002 Sep;86(3):375-8
Related Articles, Links

BRCA1-related malignancies in a family presenting with von Recklinghausen's disease.

Ceccaroni M, Genuardi M, Legge F, Lucci-Cordisco E, Carrara S, D'Amico F, Greggi S, Scambia G.

Department of Obstetrics and Gynecology, Catholic University of the Sacred Heart, Largo E. Gemelli 8, 00168 Rome, Italy.

BACKGROUND: The association between neurofibromatosis and gynecologic malignancies is rarely reported in the literature. Both BRCA1 and NF1 genes are located on the long arm of chromosome 17. CASE: We have observed a pedigree showing several individuals affected by both type 1 neurofibromatosis (NF1) and breast or coelomatic cancers. The number of individuals affected, their degree of relationship, and the early age at onset were suggestive of an hereditary breast/ovarian cancer syndrome. Linkage analysis was performed in order to establish whether markers in the chromosome 17 region containing the BRCA1 and NF1 loci were shared by affected individuals. Screening for BRCA1 mutations was performed by PTT and SSCP. Analysis of chromosome 17 DNA markers in the five family members tested show that three individuals affected by both NF1 and carcinomas share a common haplotype including the NF1 and BRCA1 loci on chromosome 17. Mutation analysis showed the presence of a nonsense mutation within BRCA1 exon 12 in two individuals, mother and daughter, affected by breast and peritoneal cancer, respectively, as well as in the son, who had rectal cancer at the early age of 27 years. All three subjects also had NF1. CONCLUSION: The concurrence of NF1 and hereditary breast/ovarian cancer in this family is likely due to the presence of two linked mutations at the NF1 and BRCA1 loci.

hint: nonsense mutation = introduction of a stop codon

lpetrich · 10-25-2002, 04:56 PM

Except that a codon is not a single nucleotide, but a triplet of nucleotides. And that a point mutation can result from miscopying or from damage to a nucleotide.

In translating from RNA to amino acids, each codon either gets translated into an amino acid, or is treated as a command to stop the translation. Thus being a stop codon.

S2Focus · 10-25-2002, 05:05 PM

Quote:

Originally posted by Nat:
"3. What is a point mutation? Please distinguish it from other mutations."

A point mutation is a mutation that results in a single nucleotide being swapped out for another. Such mutations differ from insertions and deletions because they do not result in a fram-shift of the rest of the genome.

[ October 25, 2002: Message edited by: Nat ]

I have to admire your forbearance with Vanderzyden here, but I can't help but wondering why someone who is so eager to take on the knowledgeable students/doctor/scientists in this forum doesn't want to take the trouble to learn the most rudimentary basics (i.e. definition of a "point mutation") first.

monkenstick · 10-25-2002, 05:13 PM

here vanderzyden, I found you a nice set of lecture notes on mutations:

<a href="http://ww2.mcgill.ca/neuromuscular/Lecture17202B2001.pdf" target="_blank">http://ww2.mcgill.ca/neuromuscular/Lecture17202B2001.pdf</a>

Vanderzyden · 10-25-2002, 05:19 PM

Quote:

Originally posted by ps418:

V: A mutation is a detrimental, passive, malfunctional event . . .

PS: This is a very common, but false, claim....

PS,

Please provide support for your response in this
<a href="http://iidb.org/cgi-bin/ultimatebb.cgi?ubb=get_topic&f=58&t=001596" target="_blank">thread</a>.

Thanks,

John

[ October 25, 2002: Message edited by: Vanderzyden ]

Nat · 10-25-2002, 05:39 PM

"1. It seems strange that a single nucleotide could be replaced."

Why? It happens all the time - we can actually observe changes in single nucleotides mutations in bacteria in the lab.

"1a. What is the means of substitution for a single nucleotide?"

Simply a copying error in the genome.

"1b. How is a single nucleotide extracted and replaced (or overwritten) by a stop codon nucleotide?"

It doesn't need to be extracted and overwritten - it happens during replication of the genome usually presemination of a zygote (i.e. the sperm or egg that later develops into you, had an error during meiosis).

"2. Scigirl answer very quickly and confidently with the "point mutation" answer. In contradiction, you answer that an insertion/deletion is the result of a different type of mutation. "

I did not see any contradiction in what we posted - can you point it out to me? Pretty sure she would agree with me. An insertion or a deletion results in a frameshift (i.e. if you add or substract a nucleotide all the others in the chain have been moved one way or the other), a point mutation, or substitution mutation, only changes a single nucleotide.

"2a. What would we call this mutation?"

Looks like a point/substitution mutation to me. The sequence after the new stop codon is the same as it is in the operable gene, so it looks a lot like a single nucleotide was switched as monken states.

"2b. How does this mutation work?"

As explained to you, a sinlge nucleotide is switched for another which can code for another amino acid, do nothing, or in this case, code for a stop codon.

"2c. Which is more likely, a point mutation or an insertion?"

I have no idea - I'm just a physicist not a molecular biologist, so I haven't really given it much thought. I would guess that error correction mechanisms are more likely to correct frameshift mutations as opposed to a single point mutation.

[ October 25, 2002: Message edited by: Nat ]

10-25-2002, 05:39 PM	#40
Nat Regular Member Join Date: May 2002 Location: USA Posts: 100	"1. It seems strange that a single nucleotide could be replaced." Why? It happens all the time - we can actually observe changes in single nucleotides mutations in bacteria in the lab. "1a. What is the means of substitution for a single nucleotide?" Simply a copying error in the genome. "1b. How is a single nucleotide extracted and replaced (or overwritten) by a stop codon nucleotide?" It doesn't need to be extracted and overwritten - it happens during replication of the genome usually presemination of a zygote (i.e. the sperm or egg that later develops into you, had an error during meiosis). "2. Scigirl answer very quickly and confidently with the "point mutation" answer. In contradiction, you answer that an insertion/deletion is the result of a different type of mutation. " I did not see any contradiction in what we posted - can you point it out to me? Pretty sure she would agree with me. An insertion or a deletion results in a frameshift (i.e. if you add or substract a nucleotide all the others in the chain have been moved one way or the other), a point mutation, or substitution mutation, only changes a single nucleotide. "2a. What would we call this mutation?" Looks like a point/substitution mutation to me. The sequence after the new stop codon is the same as it is in the operable gene, so it looks a lot like a single nucleotide was switched as monken states. "2b. How does this mutation work?" As explained to you, a sinlge nucleotide is switched for another which can code for another amino acid, do nothing, or in this case, code for a stop codon. "2c. Which is more likely, a point mutation or an insertion?" I have no idea - I'm just a physicist not a molecular biologist, so I haven't really given it much thought. I would guess that error correction mechanisms are more likely to correct frameshift mutations as opposed to a single point mutation. [ October 25, 2002: Message edited by: Nat ]</p>

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10-25-2002, 03:43 PM	#31
Nat Regular Member Join Date: May 2002 Location: USA Posts: 100	"4. In the chromosome fusion thread, you said that mutations would result in fusing and truncation. Please reconcile and/or distinguish your reasoning there with what you are saying here." Different type of mutations. All mutation means is a change in the genome that is not apparent in the parent(s)'s genome but exists in the offspring's genome. You yourself contain a few mutations in your genome. Most are likely point mutations of non-coding parts of your genome. "Note: It would seem that the software analogy is direct and strong, as I indicated, since we are discussing genetic code. Tell me, why precisely is unsuitable about the analogy?" Because all analogies are fundamentally flawed, and it seems that discussions involving them simply result in arguments about the appropriateness of the analogy. You can agree that there are substantial differences between the genetic code and computer software and these differences are not relevant to the evolution debate, so by not using imprecise analogies we can keep the discussion on track.

10-25-2002, 04:56 PM	#36
lpetrich Contributor Join Date: Jul 2000 Location: Lebanon, OR, USA Posts: 16,829	Except that a codon is not a single nucleotide, but a triplet of nucleotides. And that a point mutation can result from miscopying or from damage to a nucleotide. In translating from RNA to amino acids, each codon either gets translated into an amino acid, or is treated as a command to stop the translation. Thus being a stop codon.

10-25-2002, 05:13 PM	#38
monkenstick Regular Member Join Date: Jul 2002 Location: Australia Posts: 214	here vanderzyden, I found you a nice set of lecture notes on mutations: <a href="http://ww2.mcgill.ca/neuromuscular/Lecture17202B2001.pdf" target="_blank">http://ww2.mcgill.ca/neuromuscular/Lecture17202B2001.pdf</a>

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