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Author Topic:   How well do we understand DNA?
crashfrog
Inactive Member


Message 31 of 98 (179915)
01-23-2005 11:06 AM
Reply to: Message 28 by Ben!
01-23-2005 6:56 AM


In fact, isn't the whole neo-evolutionary theory predicated on the fact that (in super simple terms) mutations can occur to change the function of a gene?

Genes have, at most, one of two functions. They either regulate the expression of other genes; or they encode amino acid sequences for protein expression. Or they may have no function at all.

It's proteins you're thinking of whose functions may change due to mutation.

Or to determine that there are no proteins being transcribed from this sequence in another way.

Proteins only get expressed in one way; the transcription mechanism you're probably already familiar with. And because we can read the genetic code we can read which sequences will generate proteins and which have "stop" codons right in the middle.


This message is a reply to:
 Message 28 by Ben!, posted 01-23-2005 6:56 AM Ben! has responded

Replies to this message:
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TheLiteralist
Inactive Member


Message 32 of 98 (179951)
01-23-2005 2:11 PM
Reply to: Message 28 by Ben!
01-23-2005 6:56 AM


Re: Broken Genes
Hi Ben!,

Or am I way off? I'm kind of out of the loop here.

I don't think you're way off, and I started the thread. I think that you have made a very honest observation.

--TL


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Wounded King
Member (Idle past 2137 days)
Posts: 4149
From: Edinburgh, Scotland
Joined: 04-09-2003


Message 33 of 98 (180151)
01-24-2005 9:27 AM
Reply to: Message 31 by crashfrog
01-23-2005 11:06 AM


Genes have, at most, one of two functions. They either regulate the expression of other genes; or they encode amino acid sequences for protein expression. Or they may have no function at all.

It's proteins you're thinking of whose functions may change due to mutation.

Eh, What on Earth are you trying to say? If you are allowing a gene to be defined as a regulatory element then how can you argue that they can't undergo mutations changing their function? If a given sequence is associated with expression in a particular tissue and that sequence is mutated abolishing expression in that tissue, then how has that 'Gene' not had its 'function' changed?

Were you thinking particularly of proteins producing functional RNAs maybe, or perhaps this is a third funtion you neglected? At the moment as your statement stands it doesn't make much sense. It would be fine if you only meant protein coding 'genes', but having broadened the focus your argument against Ben's suggestion is not valid.

Proteins only get expressed in one way; the transcription mechanism you're probably already familiar with. And because we can read the genetic code we can read which sequences will generate proteins and which have "stop" codons right in the middle.

You won't neccessarily be able to detect all the possible splice variants of a protein, although that sort of predictive analysis is getting better all the time. I realise that what Ben seems to be talking about seems a bit more radical that different splice forms however.

To take a hypothetical possibility, a promoter site could be generated by mutation leading to the production of an antisense mRNA transcript complementary to that in a closely related gene, effectively producing a naturally occurring antisense oligonucleotide downregulating the translation of the targetted transcript. Maybe this is more similar to the sort of thing Ben was thinking of?

TTFN,

WK


This message is a reply to:
 Message 31 by crashfrog, posted 01-23-2005 11:06 AM crashfrog has responded

Replies to this message:
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crashfrog
Inactive Member


Message 34 of 98 (180185)
01-24-2005 10:40 AM
Reply to: Message 33 by Wounded King
01-24-2005 9:27 AM


If you are allowing a gene to be defined as a regulatory element then how can you argue that they can't undergo mutations changing their function? If a given sequence is associated with expression in a particular tissue and that sequence is mutated abolishing expression in that tissue, then how has that 'Gene' not had its 'function' changed?

It may have lost a function, I guess, is that a change?

If a gene that codes for a protein that (say) metabolizes chemical A mutates, and the resulting protein now metabolizes chemical B, the function of the gene hasn't really changed; it still just codes for proteins. What changed, to my mind, was the function of the protein.

It's common to conflate, in conversation or explanation, the function of genes and their resulting products; I think it's important to at least consider the fact that the function is all in the protein.

For genes that make proteins, anyway.

It would be fine if you only meant protein coding 'genes', but having broadened the focus your argument against Ben's suggestion is not valid.

That's a very good point. I thought I had covered all my bases but I see that I had not.

To take a hypothetical possibility, a promoter site could be generated by mutation leading to the production of an antisense mRNA transcript complementary to that in a closely related gene, effectively producing a naturally occurring antisense oligonucleotide downregulating the translation of the targetted transcript. Maybe this is more similar to the sort of thing Ben was thinking of?

Maybe I'll just bow out now and let the smart folks talk about this now. :)


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TheLiteralist
Inactive Member


Message 35 of 98 (182019)
01-31-2005 8:43 AM
Reply to: Message 30 by crashfrog
01-23-2005 10:58 AM


CrashFrog,

I do wish to clarify that I have not said that random mutations could not or do not occur. What I am proposing is that the DNA somehow codes for most variations (random changes in DNA structure). Such changes being, according to my beliefs, intelligently programmed would not affect certain key areas of the DNA. However, any number of non-DNA influences could cause random mutations. These non-DNA influenced changes (i.e., random mutations) would, in most cases, though, be deleterious.

In my programming analogy, the computer code commands random changes to occur in certain areas but not others. However, power spikes, faulty processors, etc. could cause the program to change anywhere, anyway, in any module..but this would not result in any planned for changes and would in most, if not all, circumstances cause the program to run inefficiently if at all.

Don't know if that clarifies what I'm trying to say or not.

--TL


This message is a reply to:
 Message 30 by crashfrog, posted 01-23-2005 10:58 AM crashfrog has responded

Replies to this message:
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crashfrog
Inactive Member


Message 36 of 98 (182046)
01-31-2005 11:16 AM
Reply to: Message 35 by TheLiteralist
01-31-2005 8:43 AM


What I am proposing is that the DNA somehow codes for most variations (random changes in DNA structure).

By what mechanism?

However, any number of non-DNA influences could cause random mutations.

If random mutation is still happening, then you have evolution. I don't understand how your model is fundamentally different than the evolutionary one. At best you have a sort of add-on theory that posits additional evolutionary change.

Don't know if that clarifies what I'm trying to say or not.

Maybe you could explain how your model prevents macroevolution from occuring, because that would be the inevitable outcome of truly random mutations.


This message is a reply to:
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Replies to this message:
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TheLiteralist
Inactive Member


Message 37 of 98 (182111)
01-31-2005 4:52 PM
Reply to: Message 36 by crashfrog
01-31-2005 11:16 AM


By what mechanism?

I wouldn't really know the mechanisms involved. I get this whole idea from some reading about how the immune system works (in Michael Behe's book, Darwin's Black Box--his point was the irreducible complexity of the system, but that is not my point here). The t-cells or b-cells (or some kind of cells) can do some neat DNA shuffling just to try out different binding sites (if I remember how it works...forgive the vagueness). I don't know how the cells do that, but however they do, perhaps a similar mechanism would be what I am proposing (I think they even only use certain segments of DNA to arrive at the random sequence they will use for binding sites.) So I find myself wondering if cells in general are using something to make variation a normal mode of life, and we have incorrectly thought they are copying errors (i.e., sort of like the code demands a "copying error" to be made in certain places). In such a case I would expect the code to prevent (don't know how) certain areas of the genome from being affected.

Please understand that this is not something I've gotten off AIG or ICR, this is my own wondering. (So, if it turns out to be completely wrong, don't think this is mainstream (or any kind of stream) creationism). It's an idea born in a person with a high school level of understaning of biology, who's read Darwin's Black Box, and is just wondering about the random mutations thing. It is my understanding that most creationists accept the random mutations idea to some extent, but I am wondering how we can know that's what we are seeing.

Maybe you could explain how your model prevents macroevolution from occuring, because that would be the inevitable outcome of truly random mutations.

Yes. The code would not cause variation just anywhere or everywhere but would target only certain areas. Certain areas would be key for that particular kind (whatever God considers to be the kind--our own classification systems not necessarily being the same as His) and, therefore, would not be targetted by the code for variation. Random mutations could occur anywhere or everywhere, but I am proposing that truly random mutations (actual copying errors, radiation, etc.) would be useless or, most likely, harmful in some way and would quickly be selected out--perhaps ending with mutant organism itself.

Actually, to me, if all variants are due to truly random mutations, particularly in unicellular organisms, I find it difficult to believe that we could classify them (the bacteria and algae, etc) very easily...as they'd be changing significantly rather frequently I'd think. OTOH, if it is a pre-programmed, DNA controlled process, that could be the reason that the variants are numerous but the basic types of algae or bacteria, etc. stays the same.

If random mutation is still happening, then you have evolution. I don't understand how your model is fundamentally different than the evolutionary one. At best you have a sort of add-on theory that posits additional evolutionary change.

Well, in my "model" (if it can be called that), the DNA controlled variations are the main source of variations and, in general, are useful or useless and almost never harmful (and, therefore, may be selected). OTOH, truly random mutations would generally be useless or harmful (and, therefore, would generally be selected out quickly).

--TL

This message has been edited by TheLiteralist, 01-31-2005 17:00 AM


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crashfrog
Inactive Member


Message 38 of 98 (182113)
01-31-2005 5:11 PM
Reply to: Message 37 by TheLiteralist
01-31-2005 4:52 PM


In such a case I would expect the code to prevent (don't know how) certain areas of the genome from being affected.

But since we both agree this doesn't happen, I'm not sure what you're arguing.

It is my understanding that most creationists accept the random mutations idea to some extent, but I am wondering how we can know that's what we are seeing.

Well, we detect the formation of certain traits through mutation that there are no selection pressures for. For instance:

quote:
A reinterpretation by Kubitschek (1974) of work by Novick and Szilard (1956) suggests that the argument above was reasonable. In this study resistance to a bacterial virus was used as a marker to follow the appearance of some mutations in a chemostat culture. Novick and Szilard grew E. coli in a chemostat at a steady-state density of about 3 108 cells per ml. Periodically they assayed cells sampled from the chemostat for resistance to infection by bacteriophage T5 and calculated the density of T5 resistant cells in the culture. At no time was phage T5 present in the chemostat nor had the cells in the chemostat been exposed to phage T5. They found that there was always a fraction of cells in the culture that was resistant to T5. The density of resistant cells fluctuated betweeen 102 and 103 per ml. It followed a pattern like the one drawn below:


2,000 per ml
| *
R | *
e | *
s | * *
i | * * *
s | * * * *
t | * * * * *
a | * * * * * * * * *
n | * * *
t | * * * *
| * * * * *
c | * * * * * *
e | * * * *
l | *
l | *
s |___________________________________________________________
0
0 Generations 700

quote:
The increases and decreases reflect the occurrance of mutations within strains in the chemostat. The initial increase in the frequency of resistant cells occurs because a mutation occurs within a T5 resistant strain that makes it (and its descendents) the fastest growing cells in the culture. As long as this strain remains the fastest growing one its representation in the population will increase. Eventually different favorable mutation occurs in a cell that is sensitive to T5 that makes it (and its descendents) the fastest growing cells in the culture. This causes the frequency of T5 resistance to decline. Later a different mutation occurs in a T5 resistant strain that makes it the fastest growing strain. Its frequency increases, and so on.

It is important to note here that in this environment sensitivity and resistance to infection by T5 is a neutral trait here. Because there is no T5 in the environment, resistance does not provide an advantage. But it doesn't seem to provide much disadvantage either. If it provided a disadvantage, the resistant cells would washout of the chemostat. In this environment, it is selectively neutral. Mutations in other genes cause some cells to have a higher growth rate. It is just a matter of whether these mutations occur first in resistant or sensitive cells that determines whether the frequency of T5 resistant cells increases or decreases. It's a hitchhiking effect - the T5 resistance gene just goes along for the ride with the genes causing the fluctuations.


If you're at all math-minded, you should recognize that figure as a "random walk". And remember too that this is a chemostat monoculture, so there was no variation present in the inital population (bacteria are haploid so an individual has at most one allele per gene).

We know that these mutations are occuring randomly and not in response to circumstance, because they occur in a random distribution, and occur in all circumstances.

Random mutations could occur anywhere or everywhere, but I am proposing that truly random mutations (actual copying errors, radiation, etc.) would be useless or, most likely, harmful in some way and would quickly be selected out--perhaps ending with mutant organism itself.

But we know that isn't true. Your model needs to work with the reality that some random mutations are, in fact, beneficial. Otherwise all you have is an ad-hoc rationalization of all beneficial mutations being created by your unknown mutagenic-on-purpose mechanism, without any actual evidence that this is so.

We know that some random mutations can be beneficial. You can't simply ignore this.

Actually, to me, if all variants are due to truly random mutations, particularly in unicellular organisms, I find it difficult to believe that we could classify them (the bacteria and algae, etc) very easily...as they'd be changing significantly rather frequently I'd think.

It's not as hard as you think. We classify species into "clades" based on their heredity. Family trees, if you will. No matter how much you change, you're always related to your relatives. So classification isn't that hard, thanks to genetics. (I say "not that hard" but it's actually a pretty involved procedure, one I'm lucky enough to be somewhat familiar with, due to my wife currently engaged in a line of research to establish the phylogenetics of several local species of an insect corn pest.)

OTOH, if it is a pre-programmed, DNA controlled process, that could be the reason that the variants are numerous but the basic types of algae or bacteria, etc. stays the same.

I don't know, exactly, what you mean by "stay the same." All individuals are variants, and populations are always changing. Nothing "stays the same" in biology; change and diversity are the rule.

Well, in my "model" (if it can be called that), the DNA controlled variations are the main source of variations and, in general are useful or useless and almost never harmful (and, therefore, may be selected).

And what process, at the DNA level, is going to be able to predict which changes are going to be beneficial and which are not?

Pop quiz: which is the beneficial mutation? Lots of fur and a squat, short body type, or no fur and a long, svelte form?

Kind of depends on whether or not you live in Antarctica or the Sahara desert, doesn't it? Since the benefit of a mutation is inextricably linked to environment, natural selection is the only thing that determines whether or not a mutation is beneficial. At the DNA level, all mutations are equivalent.

I simply don't see how your model can work, and it's based ont he faulty premise that you can simply ignore the fact that random mutations are occasionally beneficial. In fact, you can't determine the fitness outcome of a mutation short of its interaction with the environment, which your model doesn't even begin to take into account.


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 Message 37 by TheLiteralist, posted 01-31-2005 4:52 PM TheLiteralist has not yet responded

  
Jazzns
Member (Idle past 1954 days)
Posts: 2657
From: A Better America
Joined: 07-23-2004


Message 39 of 98 (182314)
02-01-2005 11:47 AM
Reply to: Message 37 by TheLiteralist
01-31-2005 4:52 PM


Carry over from another thread.
TL seemed to say that he/she would rather discuss this here.

Jazzns writes:


Disclaimer: Not a biologist

From what I understand, when an experiment is done with antibiotic resistant bacteria, scientists can look at the genome of the bacteria before and after the experiment to see what genetic changes in particular are responsible for causing the resistence.

If the reason for this change is due to true random mutation or some kind of programmed random mutation then how would we be able to tell the difference?

In particular, I think we have actually been able to watch mutations happen when cells divide. Given that we can actually see a cause for change in the genome that is not caused by the genome but rather the process of dividing, why should we suspect programmed mutation rather than random ones?

Also, in regards to your claim that the organelles of a cell are BELIEVED to be a result of evolution, what other objective conclusion would you have science hold. Given that they act like independent cells, are disjoint, and have characteristics of a cell such as DNA, why would you consider that a "belief" rather than simply the best objective theory we can come up with given what we know. It is not as if scientists hold this "belief" true in their hearts in the same way people of faith hold true to belief in God.

In general, it seems to me that you think DNA has to be a certain way for God to have shown his fingerprint. For me, God's fingerprint is what it is and it is a personal choice to see it as such or not. Also, that belief that I feel we share has nothing to do with science.

God made "junk DNA" and it serves a purpose as can be understood by the many posts made by people much more knowledgeable than I in different threads. God made the system such that variety is produced intrinsically by the rules that govern existence rather than by some hopefull notion of perfection as we percieve.

It just seems that you are trying to pidegon hole reality into some ideal of perfection that must exist for God to be real (i.e. there should be no junk DNA, guided/prescribed mutation, etc). Why can't DNA as a part of the creation just be what it is and we can glorify God based on our faith that he created it rather than the justification that something worldly must show signs of perfection in order to be the hand of God.


By the way, for a fun second-term drinking game, chug a beer every time you hear the phrase, "...contentious but futile protest vote by democrats." By the time Jeb Bush is elected president you will be so wasted you wont even notice the war in Syria.
-- Jon Stewart, The Daily Show
This message is a reply to:
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Loudmouth
Inactive Member


Message 40 of 98 (182343)
02-01-2005 1:08 PM
Reply to: Message 37 by TheLiteralist
01-31-2005 4:52 PM


quote:
I wouldn't really know the mechanisms involved. I get this whole idea from some reading about how the immune system works (in Michael Behe's book, Darwin's Black Box--his point was the irreducible complexity of the system, but that is not my point here). The t-cells or b-cells (or some kind of cells) can do some neat DNA shuffling just to try out different binding sites (if I remember how it works...forgive the vagueness).

Ok, I think I know where you are trying to go with this.

The b-cells are responsible for producing antibodies. When a b-cell matures it rearranges a set of genes. Those genes make up the antigen binding portion (ie the portion that binds to the germs) of the antibody. That mature b-cell can only express that antibody for the entirety of it's life span. The immune system works by creating a bank of these b-cells that all have a randomly created antigen binding site. During an infection, the b-cells that bind antigen are turned on. They then start dividing and pumping out large volumes of this antibody. In some ways, the immune system uses the mechanisms of mutation and natural selection to produce antibodies that are specific to certain antigens. There is absolutely no foresight into which combination of genes goes into each antibody. Rather, the b-cells are selected for by the ability to bind antigen.

This is very similar to how evolution occurs, where the mutations are not created with foresight but are actually selected for by the environment. In the same way, the DNA replication system is allowed to be somewhat sloppy to allow for mutations to occur, although mutations will always happen. For example, humans have mutated the enzymes involved in DNA replication and some of those mutants are actually better at copying DNA without errors. There are also bacteria that live on x-ray equipment. These bacteria have extensive DNA repair mechanisms. From this we know that the DNA repair mechanisms and DNA replication systems are allowed to be a little less accurate than they could be.

However, this is a trait that would be selected for. If mutations were not allowed to happen, or were extremely rare, that species would not be able to adapt to new environments as quickly as they do now. It is always a balancing act between the production of detrimental mutations and the production of beneficial mutations. There is a "sweet spot" where the mutation rate produces detrimental mutations at a rate where natural selection can remove them without harming the overall population.

I always like analogies, so I thought up one for this situation. Let's equate the mutation rate with highway speed limits. On the highways we always balance two things, the ability to get somewhere fast and safety. The faster you can travel the quicker you get somewhere, but there is also an increase in the chances of serious car accidents. The speed is the mutation rate. The ability to get somewhere quickly is the occurrence of beneficial mutations. The accident rate is the occurrence of detrimental mutations. So the balancing act is having a "highway speed" that is both beneficial and poses an acceptable rate of accidents.

This "highway speed" is then selected for by the environment, no need for a intelligent designer to program it in. Those species that do not mutate quickly enough will be outcompeted for new niches. Those species that mutate too quickly will be too unhealthy to adapt to new environments because of the occurrence of too many detrimental mutations. The "Goldylocks" species will have a mutation rate that is "just right".

So random mutations can arise naturally without the need for an intelligent designer to insert the mechanism for creating them. The pattern of mutations shows us that no foresight is involved, even in the case of b-cells and the immune system. For me, we could conclude that a Designer was possibly involved if the same mutation appeared in 10% of the population in one generation. This would show that mutations are not random and that they are produced through foresight. However, this is not seen.


This message is a reply to:
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TheLiteralist
Inactive Member


Message 41 of 98 (182467)
02-02-2005 2:15 AM
Reply to: Message 40 by Loudmouth
02-01-2005 1:08 PM


Foresight
Hi Loudmouth,

You being a biologist, I will consider much of what you say, much as I will give consideration to what Quetzal or Wounded King says--about this idea of mine at least. I am speaking mainly about the mechanics of it all, and not so much the interpretation as to whether it was intelligently designed or evolved or whatnot (though we'll certainly be sharing opinions on that as well, I'm sure--I mean, it IS EvC.)

I wish everyone to understand two things:


  1. I am NOT saying that this is the way DNA operates
  2. my "model" does NOT involve forsight of any sort (just as the immune system does not)

It is just an idea that I had, and I wouldn't be surprised if it turned out to work this or some similar way based on the idea that the genetic code is of intelligent design. However, if my idea is incorrect, that doesn't mean the code isn't of intelligent origin.

It'd be neat if I, a fast-food cook and college drop-out, had an idea that turned out to be the next great discovery that unlocks heretofore unknown genetic secrets, that sends shock waves through the scientific world...I'm not getting my hopes up about it, though.

It is obvious, to us creationists, that the Creator has created the code to allow for tremendous variation while maintaining, to an amazing degree (considering the changes that apparently occur at the genetic level), the stability of the various types of organisms.

--TL


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TheLiteralist
Inactive Member


Message 42 of 98 (182469)
02-02-2005 2:23 AM
Reply to: Message 40 by Loudmouth
02-01-2005 1:08 PM


Mechanism?
Loudmouth,

I don't know much about DNA...looking at my "model" would you say that the mechanism that allows the immune system to be "sloppy on purpose" couldn't have a similar counterpart in the DNA replication of most any cell? Not necessarily exactly the same, but similar?

If there is, wouldn't you say that we could possibly be calling things random mutations, when in fact they are "on-purpose mistakes."

Once again, I re-iterate, I am not saying that my idea is true...I'd really like to know how plausible it is, though.

--TL

This message has been edited by TheLiteralist, 02-02-2005 02:24 AM


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TheLiteralist
Inactive Member


Message 43 of 98 (182471)
02-02-2005 2:32 AM
Reply to: Message 39 by Jazzns
02-01-2005 11:47 AM


I Am Not Trying To Prove God Is Real
Jazzns,

I can understand you and others thinking this, but it isn't so. I believe God is real no matter how the DNA works. This is just an idea I had that was inspired by the fact that I believe God is real (i.e., the code is of intelligent design).

My "model" could be wrong or need to be modified or highly modified for all kinds of reasons...especially considering my low-level of biological knowledge (particularly of DNA). And my awareness of how little I know of biology and genetics is becoming clearer the more Wounded King and Quetzal type.

The reason I wanted to discuss this issue in this thread was because this thread is more focussed and because the other was getting near closing (and now has been closed).

Thanks for joining in.

--TL


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Wounded King
Member (Idle past 2137 days)
Posts: 4149
From: Edinburgh, Scotland
Joined: 04-09-2003


Message 44 of 98 (182482)
02-02-2005 4:20 AM
Reply to: Message 41 by TheLiteralist
02-02-2005 2:15 AM


Re: Foresight
Dear Literalist,

The major problem I see is that there already is a lot of evidence pointing towards the evolution of 'mutator' strategies, at least in unicellular organisms. Such strategies lead to increased amounts of mutation and genomic rearrangement when the bacteria are stressed.

See for instance...

Stress-directed adaptive mutations and evolution.
Wright BE.
Mol Microbiol. 2004 May;52(3):643-50

Comparative biochemistry demonstrates that the metabolites, complex biochemical networks, enzymes and regulatory mechanisms essential to all living cells are conserved in amazing detail throughout evolution. Thus, in order to evolve, an organism must overcome new adverse conditions without creating different but equally dangerous alterations in its ongoing successful metabolic relationship with its environment. Evidence suggests that stable long-term acquisitive evolution results from minor increases in mutation rates of genes related to a particular stress, with minimal disturbance to the balanced and resilient metabolism critical for responding to an unpredictable environment. Microorganisms have evolved specific biochemical feedback mechanisms that direct mutations to genes derepressed by starvation or other stressors in their environment. Transcription of the activated genes creates localized supercoiling and DNA secondary structures with unpaired bases vulnerable to mutation. The resulting mutants provide appropriate variants for selection by the stress involved, thus accelerating evolution with minimal random damage to the genome. This model has successfully predicted mutation frequencies in genes of E. coli and humans. Stressed cells observed in the laboratory over hundreds of generations accumulate mutations that also arise by this mechanism. When this occurs in repair-deficient mutator strains with high rates of random mutation, the specific stress-directed mutations are also enhanced.

The existence of such sytems is not evidence for intelligent design since these systems can themselves evolve if they provide an advantage to the organism.

TTFN,

WK


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Quetzal
Member (Idle past 3915 days)
Posts: 3228
Joined: 01-09-2002


Message 45 of 98 (182555)
02-02-2005 11:52 AM
Reply to: Message 41 by TheLiteralist
02-02-2005 2:15 AM


Re: Foresight
Hi TheLit,

Too bad about the other thread, but feel free to start a new topic with whatever questions or comments you might have. I probably won't start one unless you indicate you're interested in continuing the island biogeography discussion or have any questions concerning endosymbiosis, etc.

I would, however like to add a little bit to WK's explanation above. An interesting area of active research involves the "evolution of evolvability". IOW, there are indications in some organisms that high mutation rates in certain segments of the genome are actually adaptive. There's an excellent review article available on-line by Metzgar and Wills (full citation: Cell, Vol. 101, 581584, June 9, 2000) called Evidence for the Adaptive Evolution of Mutation Rates that discusses the theoretical and logical basis for why this concept makes sense. Although the technical details may get a bit beyond where you're at currently, the general discussion should be accessible and understandable. Let me know if you have any questions on the article or its conclusions.

In addition, hypervariability has been studied in certain organisms, including yeast and cone shells, that show what appears to be an adaptive (i.e. selective advantage) for increasing mutation rates to produce large degrees of variability in these organisms. For example, Conticello SG, Gilad Y, Avidan N, Ben-Asher E, Levy Z, and Fainzilber M, 2001, "Mechanisms for Evolving Hypervariability: The Case of Conopeptides", Mol. Biol. Evol. 18:120131.

quote:
Hypervariability is a prominent feature of large gene families that mediate interactions between organisms, such as venom-derived toxins or immunoglobulins. In order to study mechanisms for evolution of hypervariability, we examined an EST-generated assemblage of 170 distinct conopeptide sequences from the venoms of five species of marine Conus snails. These sequences were assigned to eight gene families, defined by conserved elements in the signal domain and untranslated regions. Order-of-magnitude differences were observed in the expression levels of individual conopeptides, with five to seven transcripts typically comprising over 50% of the sequenced clones in a given species. The conopeptide precursor alignments revealed four striking features peculiar to the mature peptide domain: (1) an accelerated rate of nucleotide substitution, (2) a bias for transversions over transitions in nucleotide substitutions, (3) a position-specific conservation of cysteine codons within the hypervariable region, and (4) a preponderance of nonsynonymous substitutions over synonymous substitutions. We propose that the first three observations argue for a mutator mechanism targeted to mature domains in conopeptide genes, combining a protective activity specific for cysteine codons and a mutagenic polymerase that exhibits transversion bias, such as DNA polymerase V. The high Dn/Ds ratio is consistent with positive or diversifying selection, and further analyses by intraspecific/interspecific gene tree contingency tests weakly support recent diversifying selection in the evolution of conopeptides. Since only the most highly expressed transcripts segregate in gene trees according to the feeding specificity of the species, diversifying selection might be acting primarily on these sequences. The combination of a targeted mutator mechanism to generate high variability with the subsequent action of diversifying selection on highly expressed variants might explain both the hypervariability of conopeptides and the large number of unique sequences per species.

Although again the details are technical, the conclusion is that a high degree of variability provides a distinct selective advantage to this organism, and hence elevated mutation rates, rather than being a negative for the species, is actually a benefit (in this case the production of toxins this predator uses).


This message is a reply to:
 Message 41 by TheLiteralist, posted 02-02-2005 2:15 AM TheLiteralist has not yet responded

  
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