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Author Topic:   Mutations Made Easy
Hyroglyphx
Member
Posts: 5863
From: Austin, TX
Joined: 05-03-2006
Member Rating: 2.2


Message 16 of 52 (310463)
05-09-2006 9:02 AM
Reply to: Message 13 by Quetzal
05-08-2006 5:26 PM


Re: Gene transfer
You stated, as if I was differing in my statements:

quote:
Good thing you weren't trying to compare the two of you. However, let me refresh your memory of what you stated:

I said:

quote:
One of his peeves is for people to assert that life originated at random.

quote:
That's just to arrive at any lifeforms at all.

I'm not seeing the apparent contradiction. I even went on to say that its in referrence to abiogenesis and that I was specifically barred from mentioning it because the Admins said I was OT.

quote:
Unfortunately for your argument on Chiro's thread, both of these two points completely refute your arguments using them on that thread.

How does it refute my argument when everyone in here mentions that entropy only exists in closed systems? Is the principle of entropy existent in open systems as well, or not?

quote:
The fact is most mutations are silent. They are mostly benign deletions from copying errors in the genes (FALSE: There are multiple types of mutation, from frame shift to substitution).

The fact is, most mutations are silent. That's true. I never said there weren't multiple types of mutations or that there weren't multiple causes for it. I didn't even go into that. How you arrived at that conclusion is anyone's guess. I didn't even infer it. I did, however, reference three types of repair on the cellular level. From this I'm assuming that you think most mutations are either harmful or beneficial. If so, is that your official stance?

quote:
Its important to note, however, that the only reason most mutations are benign is because of specific cells that serve to repair mutations.(FALSE: Enzymes are the repair mechanisms. They are found within the cell. They are not cells.) In fact, it is their only function.

Okay, my apologies. You're right. Its specific enzymes which is the vehicle behind the cell in its repair mechanism. I can split hairs down to nanoparticles if you need me to.

quote:
The "false" statements are what I addressed with my "mini primer". Do you understand the 2 points I raised? If not, I'll be happy to explain them further.

I'm actually lost as to what we are even arguing about.

quote:
In the first place, "free radicals" aren't mutations.

No, but they [free radicals] are the cause of some mutation, which left unchecked, can lead to more mutations. Nonetheless, I don't see the problem with my statement. Its almost as if you're stating that free radicals have nothing to do with mutations. I guess I'm asking you: What are you even arguing about? Free radicals can cause mutation. True or false?

quote:
You're again contradicting yourself in the same way. Either mutations are mostly neutral, or they're mostly detrimental.

I said the majority of mutations are benign. Out of the total sum of mutations, a large (not majority) are detrimental. I didn't give two majorities. If, say, 68% of mutations are benign, and 31.5% are detrimental, and .5% are beneficial, then once again, there is no contradiction. 68% would be the majority figure. 31.5% would be a large figure of the overall summation of 100%, but it isn't the majority. And for the record, no, that isn't an official figure. I'm just using it to get my point across.

quote:
This is a response to my question? For future reference, I never debate websites.

Okay, so on that note I'm assuming that I'm not required to respond to your websites in order to clarify your answers. Is that a good assumption?

quote:
Plaisted is wrong. His spurious equations and hypothetical population show absolutely nothing. He neglects the action of purifying selection on mutation, neglects the fact not all of his "mutant" offspring will reproduce thus reducing the population's overall mutational load, and he fails to take into consideration gene flow from other populations. In other words, he plays mathematical games to buffalo the incredulous. Sort of like his partner in crime Dembski.

His thesis was very clear and eloquent. I suspect that you simply disagree with him on grounds that his cohort is William Dembski or that you don't like the implications of his thesis. In either case, your incredulity is suspect.

quote:
A lot of other people have already picked up on this. Saves me from trying to draw a Venn diagram on a message board. Any part of their responses you didn't understand?

If anyone likes one in four odds, that's on them. Those are horrible odds. Its miraculous that anyone would scoff at such a figure. If I presented a 4 prospective wives to you, but told you that one of them has AIDS, would you choose wisely or opt not to choose at all?

"When both parents have the genetic defect that causes sickle cell disease, there's a 25% chance that a child will be born with the disease. Children who inherit the defective gene from only one parent run a 50% chance of carrying the sickle cell trait. People who just carry the sickle cell trait usually don't get the disease, but they can pass the defective gene on to their children."

http://healthlink.mcw.edu/article/1031002383.html

So, if more and more carriers of the trait procreate, the frequency increases and the odds of developing said Anemia will become more likely. In any case, my original point has been completely undermined. Many evolutionists assert that Sickle Cell Anemia developed in the malaria stricken continent of Africa to combat malaria. So, why are we detracting from the initial argument?


This message is a reply to:
 Message 13 by Quetzal, posted 05-08-2006 5:26 PM Quetzal has responded

Replies to this message:
 Message 18 by Quetzal, posted 05-09-2006 9:59 AM Hyroglyphx has responded

  
Quetzal
Member (Idle past 4208 days)
Posts: 3228
Joined: 01-09-2002


Message 17 of 52 (310464)
05-09-2006 9:07 AM
Reply to: Message 15 by Wounded King
05-09-2006 5:58 AM


Re: Gene transfer
That's what I meant.

This message is a reply to:
 Message 15 by Wounded King, posted 05-09-2006 5:58 AM Wounded King has not yet responded

  
Quetzal
Member (Idle past 4208 days)
Posts: 3228
Joined: 01-09-2002


Message 18 of 52 (310471)
05-09-2006 9:59 AM
Reply to: Message 16 by Hyroglyphx
05-09-2006 9:02 AM


Re: Gene transfer
How does it refute my argument when everyone in here mentions that entropy only exists in closed systems? Is the principle of entropy existent in open systems as well, or not?

Of course. However, this "principle" has no functional bearing on evolution (your contention in the other thread) as long as the sun is shining. Entropy can decrease in an open system as long as entropy increases somewhere else (from energy transfer). This is the bit you seem to be missing.

I never said there weren't multiple types of mutations or that there weren't multiple causes for it. I didn't even go into that. How you arrived at that conclusion is anyone's guess. I didn't even infer it.

No. You made an erroneous statement, which I corrected. Here it is again: "They are mostly benign deletions from copying errors in the genes." This is incorrect. All you need to do is admit the error, and we can go on.

I did, however, reference three types of repair on the cellular level. From this I'm assuming that you think most mutations are either harmful or beneficial. If so, is that your official stance?

No you didn't - you made some statement to the effect that cells repair cells, which is patently incorrect. Whatever repair mechanism you thought you referred to is wrong. That's not how repair operates. Admit you were incorrect, and we can move on.

As far as my "assumptions" go, I think I have stated fairly consistently that the majority of mutations are neutral with respect to fitness. Of the ones that aren't neutral, most are deleterious. The rare remainder are beneficial. Selection removes the deleterious ones (with minor exceptions in unusual cases such as sickle cell, which I've explained), leaving the neutral and beneficial ones in the population. Since selection can only operate on expressed traits, beneficial mutations can - not always - become fixed. Do you follow me here?

Okay, my apologies. You're right. Its specific enzymes which is the vehicle behind the cell in its repair mechanism. I can split hairs down to nanoparticles if you need me to.

It wasn't splitting hairs. You made severely incorrect statements, which I addressed. We're not arguing over the definition of "is", here. I'm trying to correct your misapprehensions concerning basic genetics. Once we get past all that, I'm hoping we can get to the meat of the argument concerning macroevolution. However, until we can get some of the foundation out of the way, I don't see how any kind of useful discussion can take place.

I'm actually lost as to what we are even arguing about.

Not arguing - correcting.

No, but they [free radicals] are the cause of some mutation, which left unchecked, can lead to more mutations. Nonetheless, I don't see the problem with my statement. Its almost as if you're stating that free radicals have nothing to do with mutations. I guess I'm asking you: What are you even arguing about? Free radicals can cause mutation. True or false?

Yeah, but that's not what you said. You talked about free radicals "corrupting cells" as though they could cause some kind of chain reaction - like a virus. You even called them mutations. Ain't what happens. Ain't what they are. IOW, you were incorrect. Acknowledge your mistake and we can move on.

Okay, so on that note I'm assuming that I'm not required to respond to your websites in order to clarify your answers. Is that a good assumption?

If I ever do that, you are of course free to ignore it. The papers I reference are supportive of points I actually make in the message text. It's not a requirement that you address them specifically unless you feel that they are either not germane or that I have misinterpreted them somehow (which has happened in the past). On the other hand, addressing my actual points would be appropriate.

What you did, posting a bare link with no discussion, is not only frowned upon here but doesn't help your credibility much or advance the discussion. If you think Plaisted's argument is so compelling, explain it in your own words, using his essay as support, as I have done with the papers I referenced. You can start by addressing my (short) criticism:

quote:
Quetzal: He neglects the action of purifying selection on mutation, neglects the fact not all of his "mutant" offspring will reproduce thus reducing the population's overall mutational load, and he fails to take into consideration gene flow from other populations.

And then going on to explain why the essay supports your point that beneficial mutations are a bad thing. See how it works?

So, if more and more carriers of the trait procreate, the frequency increases and the odds of developing said Anemia will become more likely. In any case, my original point has been completely undermined. Many evolutionists assert that Sickle Cell Anemia developed in the malaria stricken continent of Africa to combat malaria. So, why are we detracting from the initial argument?

However, my point (and that of the others who addressed this) is that the odds of developing full blown anemia will NOT increase. They will always be the same - one in four. Stabilizing selection eliminates both the anemic and many non-malaria-resistant offspring. The sickle cell allele is maintained in the population through this process. The allele did not "develop" in order to combat malaria. It is a deleterious mutation - a single substitution of a thymine for an adenine in one triplet - that screws up HbA. The only reason that this allele is still in existence in the population is because non-carriers tend to die off before reproducing. Because of stabilizing selection, the frequency of the trait does NOT increase. Which fact falsifies your rather confused statements about immunity. Which is the whole point of this part of the discussion.


This message is a reply to:
 Message 16 by Hyroglyphx, posted 05-09-2006 9:02 AM Hyroglyphx has responded

Replies to this message:
 Message 19 by Hyroglyphx, posted 05-09-2006 12:10 PM Quetzal has responded

  
Hyroglyphx
Member
Posts: 5863
From: Austin, TX
Joined: 05-03-2006
Member Rating: 2.2


Message 19 of 52 (310493)
05-09-2006 12:10 PM
Reply to: Message 18 by Quetzal
05-09-2006 9:59 AM


Re: Gene transfer
However, this "principle" has no functional bearing on evolution

This brings me back to the two reasons why I mentioned Morowitz. He says it does and apparently a large numer of reputable scientists agree. Its our definition of 'entropy,' that is causing this ambiguity. There is more than one kind of entropy. Classical entropy deals with 2LoT. That's unquestionable. This is one objections to the Big Bang that I have. But I won't go into that because its OT. But there are also theorems on logical entropy. To clarify what I'm referring to, let me pull up the Dictionary version. The definitions are as follows:

1. Symbol S For a closed thermodynamic system, a quantitative measure of the amount of thermal energy not available to do work.
2. A measure of the disorder or randomness in a closed system.
3. A measure of the loss of information in a transmitted message.
4. The tendency for all matter and energy in the universe to evolve toward a state of inert uniformity.
5. Inevitable and steady deterioration of a system or society

1 and 2 deal with classical entropy as they relate to 2LoT. 3-5 deal with something closely related with 2LoT, but recognizes that all systems, whether open or closed, will always tend toward disorder w/o the intervention of newly introduced energy. Hot things become cold things with no intervention, but cold things never become hot for no apparent reason. Living things become dead things, always, but dead things never become living things. That is simplistic as I could put it. As it relates to biology, the constant transferring of genes would not lead to an upgrade of information, but a steady, gradual decline. I believe we are becoming less and less pure, genetically speaking, which is clearly the opposite. Does natural selection exist? Yes. And it does help in slowing this inevitable process down. But nonetheless, ultimate corruption is an inevitable outcome. Do you understand now my mentioning for entropy?

"They are mostly benign deletions from copying errors in the genes." This is incorrect. All you need to do is admit the error, and we can go on.

What's wrong with that? Copying errors occur that lead to the steady degradation of information. Seriously, what's unfactual about that?

No you didn't - you made some statement to the effect that cells repair cells, which is patently incorrect. Whatever repair mechanism you thought you referred to is wrong.

I gave you three referrences to what mechanisms correct mutations. It happens all the time in our body, unbeknownst to us. And if these enzymes didn't do their job, we'd succomb to cancer at a much more prevelant rate than we do.

http://en.wikipedia.org/wiki/DNA_repair

This site even provides on information of nucleotide, base pair, and mismatch repair.

Since selection can only operate on expressed traits, beneficial mutations can - not always - become fixed. Do you follow me here?

I'm not suggesting that mutations are always fixed. That's so blatantly obvious that's not even worth mentioning, being that cancer and Down Syndrome. How could you think that I was saying anything counter to that?

It wasn't splitting hairs. You made severely incorrect statements

Severely incorrect statements? Lets not get carried away. I've already conceded that I should have said enzymes. The point was clear, however, that these enzymes aid in the repair of certain mutations.

Yeah, but that's not what you said. You talked about free radicals "corrupting cells" as though they could cause some kind of chain reaction - like a virus.

Without certain enzymes, free radicals can affect cellular activity. They can corrupt the integrity of any cell by carcinogenesis if left to proliferate. They can and do accumulate when left unchecked. You keep breaking things down to subatomc particles when it isn't necessary to do so. We might just as well speak about quarks if we were going to reduce things into nanoparticles.

What you did, posting a bare link with no discussion, is not only frowned upon here but doesn't help your credibility much or advance the discussion. If you think Plaisted's argument is so compelling, explain it in your own words, using his essay as support, as I have done with the papers I referenced. You can start by addressing my (short) criticism:

quote:
--------------------------------------------------------------------------------
Quetzal: He neglects the action of purifying selection on mutation, neglects the fact not all of his "mutant" offspring will reproduce thus reducing the population's overall mutational load, and he fails to take into consideration gene flow from other populations.

Well, then I should thank you on clarifying the ettiquate of EvC. Thank you. I will make a mental note of that.
1. I'm not sure what you mean by 'purifying' selection on mutation. Can you elaborate?
2. Not all organisms live until the chance for reproduction, this is true. However, he obviously is speaking about the ones that do survive in a population. Therefore, there is no need to distinguish the ones that do not survive because they bear no relevance to his equation.
3. What do you mean by 'gene flow from other populations'? By population, do you mean a specific specie or a specific classification? IOW, lets take Darwins classic Finches as an example. Do you mean how one specie of Finches can effect another? Or do you mean how one type of bird can corrupt or benefit another?

However, my point (and that of the others who addressed this) is that the odds of developing full blown anemia will NOT increase. They will always be the same - one in four. Stabilizing selection eliminates both the anemic and many non-malaria-resistant offspring.

I disagree. The majority of affected people come from African decent. Lets say we have 100 carriers, 50 male, 50 female. Then we have 100 with full-blown SCA, 50 male, 50 female. All it takes is for these people to get it is to procreate in order for it to proliferate in their progeny. Heterozygous becomes homozygous in the offspring and that's when people start dying. I'm not saying its a pandemic, I'm just saying that if people from African, Hispanic, and certain Meditteranean decent continue to procreate in that specific group, it has a much greater chance of at least bcoming a significant problem.


This message is a reply to:
 Message 18 by Quetzal, posted 05-09-2006 9:59 AM Quetzal has responded

Replies to this message:
 Message 20 by NosyNed, posted 05-09-2006 12:15 PM Hyroglyphx has not yet responded
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 Message 22 by Coragyps, posted 05-09-2006 12:46 PM Hyroglyphx has not yet responded
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 Message 25 by Quetzal, posted 05-09-2006 1:08 PM Hyroglyphx has responded
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NosyNed
Member
Posts: 8868
From: Canada
Joined: 04-04-2003
Member Rating: 6.5


Message 20 of 52 (310494)
05-09-2006 12:15 PM
Reply to: Message 19 by Hyroglyphx
05-09-2006 12:10 PM


Carriers and SCA
Lets say we have 100 carriers, 50 male, 50 female. Then we have 100 with full-blown SCA, 50 male, 50 female.

This is incorrect. A "carrier" is one who is heterozygotic for the trait. That is they carry only 1 copy of the SCA gene and do NOT get full blown SCA. They do, however, do better in a malarial enviroment.

ABE

Heterozygous becomes homozygous in the offspring and that's when people start dying. I'm not saying its a pandemic, I'm just saying that if people from African, Hispanic, and certain Meditteranean decent continue to procreate in that specific group, it has a much greater chance of at least bcoming a significant problem.

In a non malarial environment people do start dying (without medical treatment). However in a malarial environment a balance is reached. The proportion that carry the SCA gene depends on the selective pressure of the malaria (it is rather high).

You are mixing up the two different environments. In a malarial environment the facts show that you are wrong about what happens.

This message has been edited by NosyNed, 05-09-2006 12:23 PM


This message is a reply to:
 Message 19 by Hyroglyphx, posted 05-09-2006 12:10 PM Hyroglyphx has not yet responded

  
Modulous
Member (Idle past 440 days)
Posts: 7789
From: Manchester, UK
Joined: 05-01-2005


Message 21 of 52 (310496)
05-09-2006 12:42 PM
Reply to: Message 19 by Hyroglyphx
05-09-2006 12:10 PM


Information corruption isn't always a bad thing
As it relates to biology, the constant transferring of genes would not lead to an upgrade of information, but a steady, gradual decline

This is where things get confused. We have a tendency to see a loss of information as a bad thing because we usually intend to send a specific message. From this point of view, the original message (in the first DNA lifeforms) is horribly twisted and corrupted.

However, the 'goal' of this message isn't to pass a specific message, but a general message "replicate". The message itself creates a replicating machine. If the message gets corrupted so that it creates a machine that cannot replicate the message, it gets selected out. If the message gets corrupted so that it creates a machine which replicates slightly better than others, the frequency of occurance of that corrupted section will increase.

From the point of view of sending the original message - this is a disaster. The information has been corrupted and is now becoming the new gospel, soon the original pure message will be lost forever. However, a population which is better at replicating will be the result.


This message is a reply to:
 Message 19 by Hyroglyphx, posted 05-09-2006 12:10 PM Hyroglyphx has not yet responded

  
Coragyps
Member
Posts: 5410
From: Snyder, Texas, USA
Joined: 11-12-2002
Member Rating: 5.9


Message 22 of 52 (310498)
05-09-2006 12:46 PM
Reply to: Message 19 by Hyroglyphx
05-09-2006 12:10 PM


Re: Gene transfer
Heterozygous becomes homozygous in the offspring and that's when people start dying.

I think you may just be babbling here. Can you explain what this is intended to mean?

This message is a reply to:
 Message 19 by Hyroglyphx, posted 05-09-2006 12:10 PM Hyroglyphx has not yet responded

  
Wounded King
Member (Idle past 2431 days)
Posts: 4149
From: Edinburgh, Scotland
Joined: 04-09-2003


Message 23 of 52 (310502)
05-09-2006 1:00 PM
Reply to: Message 19 by Hyroglyphx
05-09-2006 12:10 PM


Corruption and entropy
Hot things become cold things with no intervention, but cold things never become hot for no apparent reason. Living things become dead things, always, but dead things never become living things.

Perhaps you should similarly caveat that "dead things never become living things [for no apparent reason]", the reason would be due to chemical reactions driven by energy flow within the system.

As it relates to biology, the constant transferring of genes would not lead to an upgrade of information, but a steady, gradual decline.

This seems like a straw-man, if it were only the constant transfer of stable genes or the only mutations were losses then you might have a case, but as it is you are merely creating a nonsensical case to argue against.

"Ultimate corruption" may be the logical consequence of entropy but it doesn't mean that ther must be continuous corruption or only corruption of any specific open component system.

Merely recognising that entropy applies to both open and closed systems doesn't mean that claims that the 2LOT somehow bars either abiogenesis or the gain of 'information' are somehow supported.

What's wrong with that? Copying errors occur that lead to the steady degradation of information. Seriously, what's unfactual about that?

This assumes that there was some sort of original platonic message encoded in the DNA which is being diverged from. In the absence of such a platonic message it is pointless to speak about the degradation of information. Copying errors lead to a vast variety of different changes in the DNA and, by a number of measures, in the information content of the DNA.

Heterozygous becomes homozygous in the offspring and that's when people start dying

Why didn't the 100 adults with full blown SCA start dying before reaching reproductive age then? If you intentionally mess about the the figures beforehand to front load them to give you the answer you want then I doubt anyone is going to be impressed when you do in fact get that answer.

3. What do you mean by 'gene flow from other populations'? By population, do you mean a specific specie or a specific classification? IOW, lets take Darwins classic Finches as an example. Do you mean how one specie of Finches can effect another? Or do you mean how one type of bird can corrupt or benefit another?

Gene flow refers to the changes in genetic variance, and possibly variation, when members of the same species from another population or sub-population are introduced to a population. In the case of Darwin's finches it would be if the odd one or 2 finches from an island flew to other islands every generation. The islands the finches flew to might gain more varianc if the migrants can breed with the native populations.

To take your SCA example, if a group of scandinavians settled and interbred in an African population then they might increase the variance at the sickle cell locus.

TTFN,

WK


This message is a reply to:
 Message 19 by Hyroglyphx, posted 05-09-2006 12:10 PM Hyroglyphx has not yet responded

  
PaulK
Member
Posts: 15627
Joined: 01-10-2003
Member Rating: 2.8


Message 24 of 52 (310505)
05-09-2006 1:05 PM
Reply to: Message 19 by Hyroglyphx
05-09-2006 12:10 PM


Entropy and thermodynamics
quote:

As it relates to biology, the constant transferring of genes would not lead to an upgrade of information, but a steady, gradual decline. I believe we are becoming less and less pure, genetically speaking, which is clearly the opposite. Does natural selection exist? Yes. And it does help in slowing this inevitable process down. But nonetheless, ultimate corruption is an inevitable outcome. Do you understand now my mentioning for entropy?

What you are talking about is not thermodynamic entropy which makes your reference to Morowitz irrelevant. It isn't really the entropy of information theory either (and it wouldbe no good for your argument even if it was - there is no equicalent of the 2LoT for information theory).

So again, it seems that you have made a mistake.s


This message is a reply to:
 Message 19 by Hyroglyphx, posted 05-09-2006 12:10 PM Hyroglyphx has not yet responded

  
Quetzal
Member (Idle past 4208 days)
Posts: 3228
Joined: 01-09-2002


Message 25 of 52 (310507)
05-09-2006 1:08 PM
Reply to: Message 19 by Hyroglyphx
05-09-2006 12:10 PM


Re: Gene transfer
This brings me back to the two reasons why I mentioned Morowitz. He says it does and apparently a large numer of reputable scientists agree.

Actually, no. Morowitz explains abiogenesis in thermodynamic terms - making it quite clear that thermodynamics not only permits but actually energizes the formation of biologically significant macromolecules. He also uses thermodynamics as his basis for his "membrane-first" counter-hypothesis to other researchers' "RNA-first" hypothesis. That's all.

1 and 2 deal with classical entropy as they relate to 2LoT. 3-5 deal with something closely related with 2LoT, but recognizes that all systems, whether open or closed, will always tend toward disorder w/o the intervention of newly introduced energy.

Right. Which is where the sun comes in - providing energy to overcome local entropy. Therefore thermodynamics has no negative implications for evolution. Enough, already.

Seriously, what's unfactual about that?

"Mostly...deletions from the genome" is what's unfactual. Substitutions are actually the most common form (i.e., "mostly") of mutation. These represent a change in the information content (and let's not go down the information road, there are a lot of other threads open for that), but not a "steady degradation". Insertions, translocations, deletions, etc, are other types of mutation. Your statement is factually incorrect. It is possible that this misunderstanding on your part is why you think only in terms of "loss of information".

I gave you three referrences to what mechanisms correct mutations. It happens all the time in our body, unbeknownst to us. And if these enzymes didn't do their job, we'd succomb to cancer at a much more prevelant rate than we do.

No, you didn't. But as long as you acknowledge that cells don't repair cells, we're golden.

I'm not suggesting that mutations are always fixed. That's so blatantly obvious that's not even worth mentioning, being that cancer and Down Syndrome. How could you think that I was saying anything counter to that?

You seem to have missed the entire point of my statement. Let me refresh your memory and try and clarify.

quote:
You stated: "From this I'm assuming that you think most mutations are either harmful or beneficial. If so, is that your official stance?"

My response: "As far as my "assumptions" go, I think I have stated fairly consistently that the majority of mutations are neutral with respect to fitness. Of the ones that aren't neutral, most are deleterious. The rare remainder are beneficial. Selection removes the deleterious ones (with minor exceptions in unusual cases such as sickle cell, which I've explained), leaving the neutral and beneficial ones in the population. Since selection can only operate on expressed traits, beneficial mutations can - not always - become fixed. Do you follow me here?"


I never said anything about your take on fixation, since that hadn't been discussed. I was clarifying my position. This is getting somewhat tedious - can we move on?

Without certain enzymes, free radicals can affect cellular activity. They can corrupt the integrity of any cell by carcinogenesis if left to proliferate. They can and do accumulate when left unchecked. You keep breaking things down to subatomc particles when it isn't necessary to do so. We might just as well speak about quarks if we were going to reduce things into nanoparticles.

Tell you what, if you stop making incorrect statements like "Therefore, in all actuality, all mutations are truly harmful, especially if these specific cells, themselves, are the product of a mutation. There would be nothing to stop these free radicals from culturing rogue, mutated cells without their assistance.", then I'll stop calling you on it. Parsing this it appears you are equivocating on free radical = specific cell = DNA repair mechanism. You couldn't be more wrong. I explained what free radicals were, explained how they can damage cells. None of which you've acknowledged. If this is the way you are going to be conducting this discussion, it's going to be a short conversation.

1. I'm not sure what you mean by 'purifying' selection on mutation. Can you elaborate?

Purifying selection refers to the elimination of deleterious mutations in a population by natural selection eliminating the individual organism that carries it. That's what deleterious means, more or less. This is the principle reason why mutational load doesn't become terminal in most populations. IOW, Plaisted's hypothetical population ignores the most critical factor that falsifies his contention: the action of natural selection. Even if a particular mildly deleterious mutation doesn't preclude the individual from reproducing, observations of natural populations show that that individual will have a lower absolute fitness than non-mutated members of the population. Meaning that eventually the deleterious mutation will be eliminated. There are, of course, exceptions. However, Plaisted ignoring this factor pretty much renders his entire exercise moot. Since he's a very intelligent individual, and therefore knows of what he speaks, the fact that he didn't take this into consideration indicates to me that the omission was deliberate. Hence my "spurious equation" comment.

2. Not all organisms live until the chance for reproduction, this is true. However, he obviously is speaking about the ones that do survive in a population. Therefore, there is no need to distinguish the ones that do not survive because they bear no relevance to his equation.

On the contrary, not taking into consideration the fact that deleterious mutations - and even neutral mutations, since carrying around all that garbage does have an energy impact, however slight - will have a negative impact on the individual's fitness, is once again ignoring the action of natural selection. IOW, causing the death of the organism or causing it to reproduce less than the non-mutants falsifies his hypothetical population equations since the mutants are less likely to leave their legacy in the population.

3. What do you mean by 'gene flow from other populations'? By population, do you mean a specific specie or a specific classification?

A species in nature is a collection of discrete populations distributed across the range of the species. Gene flow between these populations has a significant reduction effect on mutational load. Only in a small, completely isolated population does the cumulative effect of sequential mutations possibly cause the kind of inbreeding depression Plaisted refers to. Although this does occur (it's one of the reasons new colonists on isolated islands often go extinct rather than become established), it's the exception rather than the rule. Ignoring gene flow is another questionable premise in Plaisted's argument.

IOW, lets take Darwins classic Finches as an example. Do you mean how one specie of Finches can effect another? Or do you mean how one type of bird can corrupt or benefit another?

What? I'm sorry, this doesn't make any sense. What are you asking?

Edited to add the following:

disagree. The majority of affected people come from African decent. Lets say we have 100 carriers, 50 male, 50 female. Then we have 100 with full-blown SCA, 50 male, 50 female. All it takes is for these people to get it is to procreate in order for it to proliferate in their progeny. Heterozygous becomes homozygous in the offspring and that's when people start dying. I'm not saying its a pandemic, I'm just saying that if people from African, Hispanic, and certain Meditteranean decent continue to procreate in that specific group, it has a much greater chance of at least bcoming a significant problem.

Wow, this is so wrong I'm not sure where to begin. In the first place, it doesn't matter how many adult heterozygotes you've got. 25% of their offspring (no matter how many there are) are statistically likely to develop full-blown SCA. 50% will be heterozygotes, and 25% won't have the trait at all. In a malaria endemic area, this latter group are in trouble. In most other places, they're golden. If a carrier mates with a non-carrier, no full-blown SCA will occur (somebody check my genetics, here, please), and 50% of the offspring won't even be carriers. Eventually, with a small population of carriers and a really really large population of non-carriers (assuming random mating), the trait will either be swamped out of existence, or will persist in very low frequency. IOW, I don't think you need to worry about SCA becoming a pandemic. Only where most everyone is a carrier will the disease even persist.

This message has been edited by Quetzal, 05-09-2006 01:18 PM


This message is a reply to:
 Message 19 by Hyroglyphx, posted 05-09-2006 12:10 PM Hyroglyphx has responded

Replies to this message:
 Message 27 by Coragyps, posted 05-09-2006 1:55 PM Quetzal has responded
 Message 36 by Hyroglyphx, posted 05-15-2006 2:48 PM Quetzal has responded

  
PaulK
Member
Posts: 15627
Joined: 01-10-2003
Member Rating: 2.8


Message 26 of 52 (310512)
05-09-2006 1:16 PM
Reply to: Message 19 by Hyroglyphx
05-09-2006 12:10 PM


Sickle-Cell and genetics
quote:

I disagree. The majority of affected people come from African decent. Lets say we have 100 carriers, 50 male, 50 female. Then we have 100 with full-blown SCA, 50 male, 50 female. All it takes is for these people to get it is to procreate in order for it to proliferate in their progeny. Heterozygous becomes homozygous in the offspring and that's when people start dying.

How do you get your 100 individuals with full-blown SCA ? From the figures which you agreed with only 25% of the offspring would have full-blown SCA. Are you assuming that each couple has an average of 4 children ? If so why don't you mention that you should also have 200 new carriers and 100 people without the SCA gene at all ?

If you actually do a proper analysis you will see that if your initial population is entirely heterozygous for the SCA gene then the next generation will also have an average of 1 copy of the gene per individual (the distribution wills change so that many will have 2 copies or none). The only way for that to change is if the individuals with 2 copies are more successful at breeding ("fitter") then those with none. i.e. only if full-blown sickle-cell is better - or less bad - than the lack of malaria resistance in the "normal" population.

(And, of course, out of malarial areas the lack of resistance is not a disadvantage at all - while full-blown SCA is unambiguously bad).l


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Coragyps
Member
Posts: 5410
From: Snyder, Texas, USA
Joined: 11-12-2002
Member Rating: 5.9


Message 27 of 52 (310527)
05-09-2006 1:55 PM
Reply to: Message 25 by Quetzal
05-09-2006 1:08 PM


Re: Gene transfer
If a carrier mates with a non-carrier, no full-blown SCA will occur (somebody check my genetics, here, please), and 50% of the offspring won't even be carriers.

That's what my Punnett square says, too.

This message is a reply to:
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Replies to this message:
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Quetzal
Member (Idle past 4208 days)
Posts: 3228
Joined: 01-09-2002


Message 28 of 52 (310535)
05-09-2006 2:17 PM
Reply to: Message 27 by Coragyps
05-09-2006 1:55 PM


Squares are as Squares Do
Punnett square

Rub it in C. Rub it in. Would you like some lemon juice on that cut? :p


This message is a reply to:
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Brad McFall
Member (Idle past 3369 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 29 of 52 (310548)
05-09-2006 4:14 PM
Reply to: Message 7 by kalimero
05-08-2006 1:39 PM


does not the point depend on,
if the fluctuating mutations are different categorically than any other mutation?

Gould seems to insist in his structure book that that the difference of fluctuating and non-fluctuating mutations is not real as to mutational variation.

It seems to me that some traits artists attempt to draw on animals, of a pretended future, may not be real but it seems possible to me that the category we think of fluctuating mutations in, might be very well broadened. I subjectively think I thought so for fish in '86.

I wonder if the images presented in the Vonynich manuscript
http://www.voynich.nu/
might not eventually be found to be evidence of De Vries' idea
http://www.stephenjaygould.org/library/modern-science/chapter04.html

centuries before empircal science caught up with the observation


Click to enlarge

If I am correct the cylinder images on left in the manscript ( see example in thumbnail above) represent, non-fluctuating mutations (any kind of mutation from point mutations to delterious ones in general) that are serialized to the right. I have only just begun to look this intently at this work, but if I am correct the the text itself will represent the discontinuity or "saltation" of Gould's liking and the different series will premeditate actual mutation series DIFFERNENCES. Thus I will be possibly able to explain what Gould could not, namely, why De Vries added the crucial part of his idea near the end of a list, BEFORE he stated about the ALL DIRECTION of mutations. The reference to women and stars in the Vonyich script might simply be a an attempt to take the text out of the direction caused by the specific mutations or variations painted. Thus Gould's would have been possibly been found to have a fudamental error in giving algebra more to geneotypes than phenotypes AT THE SAME TIME he descripts the motivation to use geometry in biology.

In any event, I do not count the idea that fluctuating mutations only apply to the leaves to be particularly telling for Darwin's strategic discussion of flowers, as some "female" parts move past male "ones" that are in the process of inverting morphologically (amarillus).

This message has been edited by Brad McFall, 05-09-2006 04:27 PM


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Brad McFall
Member (Idle past 3369 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 30 of 52 (310549)
05-09-2006 4:15 PM
Reply to: Message 7 by kalimero
05-08-2006 1:39 PM


double post
sorry

This message has been edited by Brad McFall, 05-09-2006 04:18 PM


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