Freethought & Rationalism Archive

Vanderzyden · 10-25-2002, 05:17 PM

Ladies & Gentleman,

To avoid fragmenting this <a href="http://iidb.org/cgi-bin/ultimatebb.cgi?ubb=get_topic&f=58&t=001531" target="_blank">thread</a>, I want to advance a challenge into this forum.

Can anyone provide conclusive evidence on just one beneficial genetic mutation.

I search the web and the first few hits link me to vacuous claims like "we only see the results of beneficial mutations" or "good mutations are extremely rare".

The best I could find here at Infidels is Coragyps' <a href="http://iidb.org/cgi-bin/ultimatebb.cgi?ubb=get_topic&f=3&t=001535" target="_blank">archived discussion</a> of Hemoglobin C:

Where the main point seems to be:

Quote:

Hemoglobin C (take that, you brits!) is a variant form of the "standard" hemoglobin A. It differs from A in having the amino acid lysine instead of glutamate at position 6 of the beta chain. The better known hemoglobin S, of sickle-cell anemia fame, has valine at this position. Note, though, that the DNA codon in hemoglobin A is GAA, that for HbC is AAA, and that for HbS is GUA. In other words, Occam's razor would much prefer that C and S arose independently from A, and not from each other: two point mutations would be required to interconvert C and S.

What here may be construed as a mutation?

NOTE: Please don't bother to reply if you do not have substantial references (web or otherwise) to support your answer.

Thanks!

John

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

Nat · 10-25-2002, 05:49 PM

I will answer, but only if you first show me that you understand what the terms being used mean. My experience in the other tread has taught me that you might not have a strong grasp of these terms. If I am mistaken I apologize.

Please define what you mean by "mutation." Also, please define what you mean by "beneficial."

Thanks

Jesus Tap-Dancin' Christ · 10-25-2002, 10:27 PM

The whole fucking protein is a mutation on the original. But this is moot. You refuse to allow any thing that IS a mutation to be called as such when it's beneficial, but when it ain't, you will jump all over it claiming no beneficial mutations.

Do NOT Feed the Troll.

Itzpapalotl · 10-26-2002, 02:27 AM

How about these mutations that happened in a ribonuclease enzyme:

"substitutions at two interacting sites (Arg-64-->Ser and Thr-132-->Arg) resulted in a 13-fold enhancement of the ribonucleolytic activity"

The gene in question is a duplicate of another gene so its possible to tell where mutations have happened.

The reference is: J. Zhang and H. F. Rosenberg. Complementary advantageous substitutions in the evolution of an antiviral RNase of higher primates. Proc.Natl.Acad.Sci.U.S.A 99 (8):5486-5491, 2002.

[ October 26, 2002: Message edited by: Itzpapalotl ]

scigirl · 10-26-2002, 08:32 AM

I too want an example of what vanderzyden means by "good."

What would a "good" immune system do, as opposed to a bad immune system?

I wonder if creationists get hung up on the words "good" and "bad" because of their Christian thinking. They aren't very useful terms when talking about biology, however. "Mutations that confer adaptations that suit a particular environment" MAYBE is a better term than "good."

scigirl

scigirl · 10-26-2002, 09:19 AM

In non-humans:

<a href="http://www.gate.net/~rwms/EvoEvidence.html" target="_blank">http://www.gate.net/~rwms/EvoEvidence.html</a>

One example:

Quote:

Evidence of genetic divergence and beneficial mutations in bacteria after 10,000 generations
Molecular methods are used widely to measure genetic diversity within populations and determine relationships among species. However, it is difficult to observe genomic evolution in action because these dynamics are too slow in most organisms. To overcome this limitation, we sampled genomes from populations of Escherichia coli evolving in the laboratory for 10,000 generations. We analyzed the genomes for restriction fragment length polymorphisms (RFLP) using seven insertion sequences (IS) as probes; most polymorphisms detected by this approach reflect rearrangements (including transpositions) rather than point mutations. The evolving genomes became increasingly different from their ancestor over time. Moreover, tremendous diversity accumulated within each population, such that almost every individual had a different genetic fingerprint after 10,000 generations. As has been often suggested, but not previously shown by experiment, the rates of phenotypic and genomic change were discordant, both across replicate populations and over time within a population. Certain pivotal mutations were shared by all descendants in a population, and these are candidates for beneficial mutations, which are rare and difficult to find. More generally, these data show that the genome is highly dynamic even over a time scale that is, from an evolutionary perspective, very brief.

One thing I keep thinking is that any evolutionary mechanism that increases diversity is a good thing. Stagnancy is bad, especially in a changing environment.

In humans: This site has 6 clinical examples of beneficial mutations found in humans.

<a href="http://www.gate.net/~rwms/EvoEvidence.html" target="_blank">http://www.gate.net/~rwms/EvoEvidence.html</a>

I found one I would like to focus on, because it's the one I know the most about!

Quote:

Enhanced fMLP-stimulated chemotaxis in human neutrophils from individuals carrying the G protein beta3 subunit 825 T-allele.
We have recently described a C825T polymorphism in the gene encoding for the Gbeta3 subunit of heterotrimeric G proteins. The 825T allele is associated with a novel splice variant (Gbeta3-s) and enhanced signal transduction via pertussis toxin (PTX)-sensitive G proteins. fMLP-induced chemotaxis, but not O2- generation, was increased in neutrophils with the TC/TT (EC50 = 1.5 +/- 1.3 nM) genotypes compared to the CC genotype (EC50 = 5.9 +/- 1.5 nM). Maximal fMLP-induced increase in [Ca2+]i was significantly reduced in neutrophils from individuals with TC/TT genotype vs. CC genotype (212.9 +/- 10.1 nM vs. 146.4 +/- 24.2 nM). Gbeta3-s appears to be associated with enhanced immune cell function in humans.

Neutrophils are really cool cells (I worked on them for my master's thesis). They are important in fighting off bacterial and fungal infections.

fMLP is a chemical produced by gram-negative bacteria. Neutrophils recognize that signal (by binding to it) and then turn on a host of defense systems. In the above paper, scientists identified individuals whose neutrophils responded better in a functional test to fMLP, compared to individuals who did not have that same "mutation." This function is chemotaxis, which is the ability of the neutrophil to sense there's a problem while it's in the bloodstream and extravasate to the infected tissue. Interestingly, the neutrophils did not have an increase in oxidant production.

It's funny that I asked you "What would a "good" immune system do, as opposed to a bad immune system?" then I found this exact example.

A good immune system must carefully balance the following roles:
1) Recognize foreign pathogens and destroy them.
2) Not recognize normal tissue so it doesn't destroy it.

A mutation which makes a neutrophil better at #1 a lot of times makes it worse at #2. If you have non-functioning neutrophils, you get very sick and die young. However, if you have over-active neutrophils, you get things like arthritis, COPD and a bunch of other nasty inflammatory conditions.

Keep in mind that the bacteria are constantly evolving too. They have to balance these two roles:
1) Become good invaders.
2) Don't completely destroy the host.

Our complex immune system is evidence of a giant "arms race". Think about the complex technology we have today thanks to the cold war. Our "enemy" builds a missile, we build a better one. Etc etc.

When we talk about things like "selective pressure" or "beneficial mutations," I think we get hung up on semantics, which is really too bad. Let's think about it in another way.

Animals are bombarded with bugs all the time. Bugs were of course around first, but then once animals evolved, bugs figured out that they could take advantage of their warm fuzzy tissues full of nutrients. They evolved to invade the host, but the host in turn evolved ways to fight them off. As the bugs got better, the immune systems got better too. If you look at more "primitive" organisms, you will find rudimentary counterparts to our amazingly complex (but not irreducibly complex!) immune system. You can find animals with 'half' a thymus, or a 'sort-of' neutrophil.

You may not buy this story, but the evidence above, about the neutrophils, tells us something: We are currently capable of producing genetic variations that change our ability to evade bacterial intrusion. That is clear from the abstract. Does this mean we evolved? No. But it sure lends credence to the idea, correct?

Another sort of philosophical evidence for evolution is the fact that the very concept of 'mutation' is elusive! You may think it's insane that you asked what (to you) is a very simple question - "Good mutations anyone?" and we all go, "uh define mutation" and "weasel" out of the question! (well then we anwered it with pubmed examples...)

Why can't we just tell you what the difference is between a mutation and a variant? Shouldn't it be easy? Did we all, like, fail genetics or something?

I say, yes it should be an easy question to answer - if intelligent design is true. We were created perfectly and any change in our DNA will be a "mutation" and hurt us.

However, what is the truth about DNA variation?
There is bitter debate right now about whether we should call changes in our genetic code "mutations" or "polymorphisms." Why do you think that is? Because scientists are argumentative? Sure that's part of it.

But if evolution is true, then you would expect the definition of mutation to be elusive. In one context, the genetic change confers a survival advantage, in another context it does not. 'Benefical mutations' in our genome that guaranteed us offspring in the ancestral environment are suddenly causing us problems in the modern day environment. Our diet is different, our pathogen repertoire is different. One hypothesis about allergies is that we see them more in the western world because we no longer fight off parasites. Back in the "good old days," we had to fight off those nasty parasites like tapeworms that even gross me out!

So we evolved mechanisms to fight them off which included IgE antibodies and eosinophils. Then pesky humans also evolved a brain, which afforded them the ability to get rid of parasites through means such cooking food. Now our eosinophils are a pain, because they cause allergies.

There are so many human diseases that make sense in the context of evolution - we have genes that helped us survive in a fundamentally different environment than we live in today.

Now think about the term "mutation" in terms of intelligent design. You would expect (or rather I would expect) that we were made ideally by an "intelligent designer," that all genetic changes would be harmful. Mutations would be mutations - and there would be no gray areas. However, that is not what we see at all.

Then if you go even further and put a description on this designer, it is clear from the evidence that this designer does not necessarily favor humans. If there is a designer, he (she, it) prescribes to Aristotle's adage that (paraphrased) says something like "the extremes are bad, the middle is good." Even if you were to convince me of a designer, I just don't see it being the Hebrew War god described in the old testament. Rather, it is someone who has an inordinate fondness for wasted DNA, beetles, and viruses.

scigirl

[ October 26, 2002: Message edited by: scigirl ]

Nickle · 10-26-2002, 09:31 AM

Quote:

Back in the "good old days," we had to fight off those nasty parasites like tapeworms that even gross me out!

I'll second that. I dissected one last week.

RufusAtticus · 10-26-2002, 09:57 AM

Vander here are the sequences of HBB, HBB-S, and HBB-C.

This is retrieved from LocusLink [1], the only difference occurs in the 7th codon (6th amino acid because the first one, 'm,' gets cut off). The letters refer to amino acids [2].
[code]
Human Beta-hemoglobin (HBB)
1 mvhltpeeks avtalwgkvn vdevggealg rllvvypwtq rffesfgdls tpdavmgnpk
61 vkahgkkvlg afsdglahld nlkgtfatls elhcdklhvd penfrllgnv lvcvlahhfg
121 keftppvqaa yqkvvagvan alahkyh

HBB-S
1 mvhltpveks avtalwgkvn vdevggealg rllvvypwtq rffesfgdls tpdavmgnpk
61 vkahgkkvlg afsdglahld nlkgtfatls elhcdklhvd penfrllgnv lvcvlahhfg
121 keftppvqaa yqkvvagvan alahkyh

HBB-C
1 mvhltpkeks avtalwgkvn vdevggealg rllvvypwtq rffesfgdls tpdavmgnpk
61 vkahgkkvlg afsdglahld nlkgtfatls elhcdklhvd penfrllgnv lvcvlahhfg
121 keftppvqaa yqkvvagvan alahkyh
</pre>[/quote]

Sequences Aligned (* marks differences)

[code]
HBB 1 mvhltpeeks avtalwgkvn vdevggealg rllvvypwtq rffesfgdls tpdavmgnpk
HBB-S 1 mvhltpveks avtalwgkvn vdevggealg rllvvypwtq rffesfgdls tpdavmgnpk
HBB-C 1 mvhltpkeks avtalwgkvn vdevggealg rllvvypwtq rffesfgdls tpdavmgnpk
*

HBB 61 vkahgkkvlg afsdglahld nlkgtfatls elhcdklhvd penfrllgnv lvcvlahhfg

HBB-S 61 vkahgkkvlg afsdglahld nlkgtfatls elhcdklhvd penfrllgnv lvcvlahhfg

HBB-C 61 vkahgkkvlg afsdglahld nlkgtfatls elhcdklhvd penfrllgnv lvcvlahhfg

HBB 121 keftppvqaa yqkvvagvan alahkyh
HBB-S 121 keftppvqaa yqkvvagvan alahkyh
HBB-C 121 keftppvqaa yqkvvagvan alahkyh
</pre>[/quote]

Each allele does not encode the same information since each one produces a distinctly different product. A single point mutation has enough effect on the information contained in the genome that it can determine whether an individual dies from malaria or not. In the presence of malaria, HBB-S is maintained because of heterozygote advantage. However, HBB-C also offers resistance to malaria, but the most fit genotype is the homozygote.[3] It is expected to become the most common allele in parts of Africa if the environment stays the same. These mutations have clearly added new information to the population. Selection then acts on this new information, changing the make up of the population. Thus, evolution happens.

1. <a href="http://www.ncbi.nlm.nih.gov/LocusLink/" target="_blank">http://www.ncbi.nlm.nih.gov/LocusLink/</a>
2. <a href="http://www.chem.qmul.ac.uk/iupac/AminoAcid/AA1n2.html" target="_blank">http://www.chem.qmul.ac.uk/iupac/AminoAcid/AA1n2.html</a>
3. Modiano D. et al. (2001) Haemoglobin C protects against clinical plasmodium falciparum malaria. Nature: 414 pp 305-308

~~RvFvS~~

[ October 26, 2002: Message edited by: RufusAtticus ]

Daggah · 10-26-2002, 06:38 PM

So far I see several examples of beneficial mutations in this thread. I wonder how Vander will weasel his way out of them? I'm sure he'll find a way.

What I wonder is: does Vander actually think anyone takes him seriously at this point?

Jesus Tap-Dancin' Christ · 10-26-2002, 09:22 PM

Quote:

Originally posted by Daggah:
So far I see several examples of beneficial mutations in this thread. I wonder how Vander will weasel his way out of them? I'm sure he'll find a way.

Denial ain't a river in Egypt.

10-26-2002, 02:27 AM	#4
Itzpapalotl Junior Member Join Date: Oct 2002 Location: UK Posts: 12	How about these mutations that happened in a ribonuclease enzyme: "substitutions at two interacting sites (Arg-64-->Ser and Thr-132-->Arg) resulted in a 13-fold enhancement of the ribonucleolytic activity" The gene in question is a duplicate of another gene so its possible to tell where mutations have happened. The reference is: J. Zhang and H. F. Rosenberg. Complementary advantageous substitutions in the evolution of an antiviral RNase of higher primates. Proc.Natl.Acad.Sci.U.S.A 99 (8):5486-5491, 2002. [ October 26, 2002: Message edited by: Itzpapalotl ]</p>

10-26-2002, 09:57 AM	#8
RufusAtticus Veteran Member Join Date: Nov 2001 Location: NCSU Posts: 5,853	Vander here are the sequences of HBB, HBB-S, and HBB-C. This is retrieved from LocusLink [1], the only difference occurs in the 7th codon (6th amino acid because the first one, 'm,' gets cut off). The letters refer to amino acids [2]. [code] Human Beta-hemoglobin (HBB) 1 mvhltpeeks avtalwgkvn vdevggealg rllvvypwtq rffesfgdls tpdavmgnpk 61 vkahgkkvlg afsdglahld nlkgtfatls elhcdklhvd penfrllgnv lvcvlahhfg 121 keftppvqaa yqkvvagvan alahkyh HBB-S 1 mvhltpveks avtalwgkvn vdevggealg rllvvypwtq rffesfgdls tpdavmgnpk 61 vkahgkkvlg afsdglahld nlkgtfatls elhcdklhvd penfrllgnv lvcvlahhfg 121 keftppvqaa yqkvvagvan alahkyh HBB-C 1 mvhltpkeks avtalwgkvn vdevggealg rllvvypwtq rffesfgdls tpdavmgnpk 61 vkahgkkvlg afsdglahld nlkgtfatls elhcdklhvd penfrllgnv lvcvlahhfg 121 keftppvqaa yqkvvagvan alahkyh </pre>[/quote] Sequences Aligned (* marks differences) [code] HBB 1 mvhltpeeks avtalwgkvn vdevggealg rllvvypwtq rffesfgdls tpdavmgnpk HBB-S 1 mvhltpveks avtalwgkvn vdevggealg rllvvypwtq rffesfgdls tpdavmgnpk HBB-C 1 mvhltpkeks avtalwgkvn vdevggealg rllvvypwtq rffesfgdls tpdavmgnpk * HBB 61 vkahgkkvlg afsdglahld nlkgtfatls elhcdklhvd penfrllgnv lvcvlahhfg HBB-S 61 vkahgkkvlg afsdglahld nlkgtfatls elhcdklhvd penfrllgnv lvcvlahhfg HBB-C 61 vkahgkkvlg afsdglahld nlkgtfatls elhcdklhvd penfrllgnv lvcvlahhfg HBB 121 keftppvqaa yqkvvagvan alahkyh HBB-S 121 keftppvqaa yqkvvagvan alahkyh HBB-C 121 keftppvqaa yqkvvagvan alahkyh </pre>[/quote] Each allele does not encode the same information since each one produces a distinctly different product. A single point mutation has enough effect on the information contained in the genome that it can determine whether an individual dies from malaria or not. In the presence of malaria, HBB-S is maintained because of heterozygote advantage. However, HBB-C also offers resistance to malaria, but the most fit genotype is the homozygote.[3] It is expected to become the most common allele in parts of Africa if the environment stays the same. These mutations have clearly added new information to the population. Selection then acts on this new information, changing the make up of the population. Thus, evolution happens. 1. <a href="http://www.ncbi.nlm.nih.gov/LocusLink/" target="_blank">http://www.ncbi.nlm.nih.gov/LocusLink/</a> 2. <a href="http://www.chem.qmul.ac.uk/iupac/AminoAcid/AA1n2.html" target="_blank">http://www.chem.qmul.ac.uk/iupac/AminoAcid/AA1n2.html</a> 3. Modiano D. et al. (2001) Haemoglobin C protects against clinical plasmodium falciparum malaria. Nature: 414 pp 305-308 ~~RvFvS~~ [ October 26, 2002: Message edited by: RufusAtticus ]</p>

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10-25-2002, 05:49 PM	#2
Nat Regular Member Join Date: May 2002 Location: USA Posts: 100	I will answer, but only if you first show me that you understand what the terms being used mean. My experience in the other tread has taught me that you might not have a strong grasp of these terms. If I am mistaken I apologize. Please define what you mean by "mutation." Also, please define what you mean by "beneficial." Thanks

10-25-2002, 10:27 PM	#3
Jesus Tap-Dancin' Christ Veteran Member Join Date: Apr 2001 Location: Heaven Posts: 6,980	The whole fucking protein is a mutation on the original. But this is moot. You refuse to allow any thing that IS a mutation to be called as such when it's beneficial, but when it ain't, you will jump all over it claiming no beneficial mutations. Do NOT Feed the Troll.

10-26-2002, 08:32 AM	#5
scigirl Veteran Member Join Date: Jul 2001 Location: Seattle Posts: 4,261	I too want an example of what vanderzyden means by "good." What would a "good" immune system do, as opposed to a bad immune system? I wonder if creationists get hung up on the words "good" and "bad" because of their Christian thinking. They aren't very useful terms when talking about biology, however. "Mutations that confer adaptations that suit a particular environment" MAYBE is a better term than "good." scigirl

10-26-2002, 06:38 PM	#9
Daggah Banned Join Date: Feb 2001 Location: Deployed to Kosovo Posts: 4,314	So far I see several examples of beneficial mutations in this thread. I wonder how Vander will weasel his way out of them? I'm sure he'll find a way. What I wonder is: does Vander actually think anyone takes him seriously at this point?

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