Mutations cannot be the mechanism of Evolution., page 3
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reply posted on 2-6-2004 @ 08:20 AM by Byrd
Originally posted by BlackJackal
Alright lets think what will happen if natural selection is turned on at step two. If natural selection works like it is supposed to it will completely get rid of the non functioning gene since it serves no purpose and is just extra baggage.


Not necessarily true. Last I read, we do have inactive genetic material all over our chromosomes. And remember, that during mutations, genes may also get shifted around between chromosomes or to different locations. This modifies their function.

As for rate of mutation slowing as the genome increases it is very much a reality. The correlation was first discovered in 1987 and since that time several other studies have backed it up.
I agree that high energy photons dont care how large the genome is but the larger the genome the more likely that photon will mutate a needed gene not the target gene.


...but radiation is not the only source of mutation.

1. Beneficial Mutations- There have been a handful of these discovered but they have all been deletious and not one has ever added more information to the genetic code. For example in the BG Hall experiment pointed out by Amantine the mutated enzyme was already present.


A personal one, then: I'm immune to smallpox (no one else in my family is, however (we know this from vaccination scars, and my lack of them was explained to me by doctors... I'm immune, naturally.))

2. Junk DNA- the supposed left over from Eons of evolution aint junk but useful DNA


As far as I know, our genome isn't completely mapped out and we're not sure of the function of everything.

3. Gene duplication Theory has too many exceptions to work in the real world making it just a theory. Even if it was viable there simply isnt enough time in Earths history to make it work.

Not if you think the world is only 6,000 years old.

4. The original question posed as well has yet to be answered If Mutation is the mechanism of evolution then why does DNA work hard to repair mutations?

As far as I know, it doesn't. It works, or you're ill and frail, or it's not useful (tails on humans), or you're dead.


[Edited on 2-6-2004 by BlackJackal]


reply posted on 2-6-2004 @ 09:02 AM by SimpleTruth
Originally posted by Mxyztos
A virus mutates because when you administer a drug you kill most if not all of the virus and leave only the ones that are resistant to the drug. These then replicate and pass on the resistant traits they have to their offspring.


This is NOT mutation. This is natural selection. Just because some survive and most others die off doesn't mean squat about mutation. If 30 people get lost in the wilderness and only two survive, does that mean the two have a mutation like an extra limb lung, or eye that helped them?? No, just because they were a tougher version of the other people, but NOT fundamentally different, as a mutation would imply.

The strongest sperm that make it to the end of the journey to the egg have not had any mutations that caused them to persist. This is IMPOSSIBLE because they don't replicate or reproduce and therefore consist of only one generation. So many many many die out and don't make it. Few carry on. NOTHING to do with mutation.

If anything, the ones who make it, like in your example are probably the most NORMAL ones and consist of little or no faults/mutations, and therefore is why they survive. Take the sperm again. The reason why one may die in the beginning is because it is weak, can't swim right, is too slow, etc. But sperm are not supposed to be like that. But why is it slow? Because it's defective. And it's defective possibly because of MUTATION. Therefore mutation is a HINDRANCE, NOT a benefical event! It's very simple.

So let's touch back on the HIV virus now. Why is it becoming more potent? Because when it or other viruses are hit with treatments, the weakest or the ones not up to the task....die. Therefore what is left to replicate, is PURELY the best one's. This is natural selection. Therefore you have a better concentration of the tougher little punks and therefore it's harder to wipe out. But if you really want to fit mutation in there, it doensn't explain the strong ones, it explains why there are some that are messed up, and therefore separates and filters out those that are normal, from defective. Even if there is NO mutations present in a group, there will still be those that survive and those that don't.


reply posted on 2-6-2004 @ 02:29 PM by BlackJackal
Not necessarily true. Last I read, we do have inactive genetic material all over our chromosomes. And remember, that during mutations, genes may also get shifted around between chromosomes or to different locations. This modifies their function.


That inactive genetic material is currently being studied and being found not to be inactive but tied to the organism in some as yet unknown way (as pointed out by my earlier posts on Junk DNA located here
www.abovetopsecret.com... )

As for genes being shifted around you are undouptedly referring to Spontaneous Mispairing. This occurs when nucleotide bases spontaneously shift to different isomers (or different conformations). This occurs without any mutagen being present. These isomers form different kinds of hydrogen bonds than do the normal conformations. During the replication of the DNA strand, the polymerase selects a different nucleotide to pair with and isonmer than the one it would have otherwise selected. These spontaneous errors occur in fewer than one in a billion nucleotides per generation.

These forms of mutations only result in loss of DNA material and information. There are two main kinds

1. Slipped Mispairing- When Chromosomes pair, sequences may sometimes misalign, looping out a portion of one strand. Usually such misaligned pairing is only transistory , and the strands revert quickly back to the normal arrangement. However if the DNA is unable to repair itself it simply cuts out the looped strand in an attempt to correct it. This results in a deletion of several hundred nucleotides from one of the strands. Many of the deletions created this way start or stop in the middle of a codon. When they occur they lead to the creation of a genetic message that is out of synchrony with the normal reading pattern, leading to devastating results for the orgainism

2. Frameshift Mispairing- Lets say you have the sentence THE FAT CAT ATE THE RAT. Now by mutation you lose the letter F, the DNA in an attempt to fix itself shifts everything together and the result is THE ATC ATA TET HER AT which is meaningless.

The most important thing to know about spontaneous mutations is that they occur very rarely. They result from transient changes in the conformation of nucleotides and also from the accidental mispairing of nonidentical but similar sequences.

So how can this form of mutation help evolution?

...but radiation is not the only source of mutation.


No its not you also have spontaneous (covered above), Transposition, Chemical, Homologue Pairing, and mispairing of repeated sequences. All of these will mutate yes but the larger the genome the less likely that a mutation of any kind will occur in the target gene and not in a needed gene.

A personal one, then: I'm immune to smallpox (no one else in my family is, however (we know this from vaccination scars, and my lack of them was explained to me by doctors... I'm immune, naturally.))


The reason why you are immune and your parents are not is not because of a mutation but because you inherited a recessive trait from your parents. There is also no guarantee that you will pass on this trait to your offspring because you will have to meet a lady that also has that trait since it is recessive and if she has an expressive recessive gene like you do then your child will also but if she has one dominant and one recessive it is possible that your child will not have the immunity.

You can calculate whether or not your child will inherit that trait through the hardy Weinberg equilibrium.

You being immune to smallpox is not a mutation but just the passing of traits


As far as I know, our genome isn't completely mapped out and we're not sure of the function of everything.


Not completely but new research is definitely cutting the junk DNA down as we go.

Not if you think the world is only 6,000 years old.


I am currently working on a mathematical response to this but I assumed the world was 4.5 billion years old.

As far as I know, it doesn't. It works, or you're ill and frail, or it's not useful (tails on humans), or you're dead.


If it did not work everyday you would die.

Read all about it here

www.nih.gov...



[Edited on 2-6-2004 by BlackJackal]



reply posted on 4-6-2004 @ 04:40 PM by BlackJackal
Alright this is for Amantine and Byrd

This supports your arguments found within this thread about Junk DNA just take a look.

www.newscientist.com...

It is not often that the audience at a scientific meeting gasps in amazement during a talk. But that is what happened recently when researchers revealed that they had deleted huge chunks of the genome of mice without it making any discernable difference to the animals.

The result is totally unexpected because the deleted sequences included so-called "conserved regions" thought to have important functions.

All DNA tends to acquire random mutations, but if these occur in a region that has an important function, individuals will not survive. Key sequences should thus remain virtually unchanged, even between species. So by comparing the genomes of different species and looking for regions that are conserved, geneticists hope to pick out those that have an important function.



You can call me alot of things but you can't call me unfair.


[Edited on 4-6-2004 by BlackJackal]


reply posted on 25-6-2004 @ 01:55 PM by BlackJackal
First thing first Gene duplication does produce new genetic information but not new functional genes.

Secondly, since when is gene duplication rarely lethal? Have a look at a few links

Partial COL1A2 gene duplication produces features of osteogenesis imperfecta and Ehlers-Danlos syndrome type VII

SMN gene duplication and the emergence of the SMN2 gene occurred in distinct hominids: SMN2 is unique to Homo sapiens

Downs Syndrome

Thalassemias

Charcot-Marie-Tooth Disease Fact Sheet

Lastly in order for gene duplication to work in the first place the genes have to somehow be turned off while they mutate. I have explained this quite thoroughly already so I will just reiterate it here.

The problem with Gene duplication is that yes it represents an increase in DNA material but not new functional genes. Evolution needs new and improved genes to function and this is not a viable answer for several reasons.

The idea behind Gene Duplication is that a gene in an organism gets an extra copy of itself during cell division, reproduction, etc. The main idea is that one gene will carry on day to day operations as usual while the second doesnt do anything and is free to mutate with a get out of natural selection free card (this way the Gene is not disgarded). After a while the gene mutates into something that is useful is somehow turned on and thus fine tuned by natural selection at that time. Well thats the theory.

So lets review what has to happen to make this a reality

1. The Gene has to be copied by some copying event which is not a science by any stretch of the imagination, still just chance.
2. The copied gene has to be switched off somehow to prevent damage to the organism.
3. Randomly mutate to something that gives the organism a new function.
4. Somehow become switched on to be fine tuned by natural selection.

Now another problem with gene duplication is that the mutation does not just occur in the target gene it occurs throughout the entire genome. Point mutations in the target gene are extremely rare representing around 1 part in 30,000 and the larger the genome the more remote the possibilities. The reason why is because as you increase genome size the mutation rate goes down because of the increased chance of catastrophic errors. In laymans terms this means the larger the genome the longer you have to wait for a mutation to occur in the copied gene much less a beneficial mutation. Even the 4.5 billion years is not enough time to account for this form of particle to man explanation. Thats plenty of time you may ask but no its not it may start out quickly with a smaill genome but after you reach the genome of an amoeba the time between helpful mutations increases exponentially.



reply posted on 25-6-2004 @ 03:21 PM by AlexKennedy
Originally posted by BlackJackal
Lastly in order for gene duplication to work in the first place the genes have to somehow be turned off while they mutate. I have explained this quite thoroughly already so I will just reiterate it here.


The only problem with what you just said is that it is completely untrue.

First of all "switching" genes on and off is not like a light switch. Just about any gene which encodes an ribosome binding site and has a Methionine codon will be translated at SOME rate, unless there are specific inhibitory factors also encoded. The issue is the AMOUNT of transcription and translation that actually occurs. In many cases of gene duplication, the second copy of the gene is inserted right after the first. This means that the binding site for the original transcription machienry will work just fine to transcribe both copies of the gene. The ribosome binding site on the mRNA which is thus produced will also work just fine to translate both copies of the gene (I know what you're thinking : "what if there's a rho-dependant terminator after the first copy of the gene?" Well, there is still a significant chance the second copy of the gene will be inserted before the terminator... I believe that this is not a problem if the terminator is rho-independant, but perhaps someone who remembers more clearly could answer for me-- I could check the textbooks, but I'm lazy ).

Since most regulation within mammalian cells occurs at the level of the enzyme itself (yes, this is a gross oversimplification, but tough), it doesn't really matter HOW MANY copies of the enzyme are produced. Beside that, however, the same regulatory mechanisms that will prevent a single copy of a gene from being over-transcribed or over-translated will also prevent two copies from doing the same thing.

BlackJackal, you seem to be purposely avoiding understanding the nature by which enzymes are "produced" from genetic information. I would encourage you to think deeply about what you are saying, and possibly put some study into the concept of the central dogma, rather than just spouting off about genetics.


reply posted on 25-6-2004 @ 04:45 PM by Crysstaafur
Although I am not an expert with low level biological activities, I am an expert with logic structures (I am a programmer).
So I am going to approach this from a different angle that behaves simularly to information manipulation in genes(ie mutations).
A value does not necessarily have to have an additional digit to represent a higher value unless we are dealing with base 1, which would be pointless.
I would be inclined to think that a mutation that advances macro-evolution could very well be a single gene rearranged chemically, though it is highly probable in the event that an additional gene is added to a grouping that significant change can happen, likewise with the subtraction of a gene as well, let alone a sub with an adjacent modification of a near gene to compensate.
Could two small subsystems of genes cause a large effect in a small amount of time, yes. If you take two scaler values of opposing axis, and
get there dot product does the end result have a value larger than either of the previous scalers, yes. could it be possible for molecules from a nearby strand of Dna(as in right next to..) were to change for x reason, could the loose chemical bond with an existing strand parallel to the mutated strand?(genuine question)
I am simply pointing out that simple items working together can go either way, either a complex end result relative to the previous form, or remain simple, and that sometimes a symbolically complex structure may become simpler, but become structurally more complex. In short, perhap the terms of complex and simple as they are used are atm are subjective and may be a monkey wrench in the gearworks of this debate.


[edit on 25-6-2004 by Crysstaafur]


reply posted on 25-6-2004 @ 11:03 PM by AlexKennedy
Originally posted by BlackJackal
No the fact is that if evolution has occured you should be able to backtrace to the first cells but it hasn't happened.


That's BS, and you know it's BS. What you want is for me to be able to magically tell you what the genetic sequence was from a cell formed millions of years ago which is no longer in existence. It's not possible. There are gene families, and I've shown that they exist (look at some of the links above). What you want is for me to show you what proto-genes were like, and only God has that information.

Anyway, I'm not writing any of this for your benefit. It's quite apparent to me that you cannot be convinced of evolution's reality. That's fine, have whatever incorrect beliefs you want. Hopefully, other people who are on the fence on the issue will make note of several points:

i) you apparently don't know even basic genetics, since talk of duplicating genes and the actual mechanisms of transcription and translation floor you.

ii) you dogmatically re-assert the same points (e.g. the canard that an increase in genetic information is impossible) despite their having been thoroughly disproven (I gave two separate accounts, one very simple and one a little more complex to explain the phenomenon, but you wouldn't listen).

iii) when you are finally backed into a corner, you ask for impossible-to-provide evidence to convince you.

I wouldn't be surprised if you weren't just parroting back anti-evolution arguments that you read somewhere, considering your lack of understanding in re the basic genetic processes. But as I've said before, I know I'm not going to convince you. If anyone else is interested in asking me answerable questions, just let me know.


reply posted on 27-6-2004 @ 11:34 PM by BlackJackal
Alright it appears that I have made a few statements in this thread that seem to be a little off base. Allan Force, a renowned geneticst in the area of gene duplication, replied to my assertations as follows:

The problem with Gene duplication is that yes it represents an increase in DNA material but not new functional genes. Evolution needs new and improved genes to function and this is not a viable answer for several reasons.

The main idea is that one gene will carry on day to day operations as usual while the second doesnt do anything and is free to mutate with a get out of natural selection free card (this way the Gene is not disgarded).


Mutations hit both copies and one them may become inactive due to degenerative mutations.
However, beneficial mutations may also occur following slightly deleterious or neutral mutations which may confer a new function.

The arctic fish AFGP proteins probably needed two mutations to produce an incipient AFGP activity. See Chris Chen's work on AFGPs.



After a while the gene mutates into something that is useful is somehow turned on and thus fine tuned by natural selection at that time. Well thats the theory.



Well there isn't THE THEORY, there are in fact many models for neofunctionalization. One of these models says a duplicate needs to be turned off, and then mutations accumulate, and this followed by the gene turning back on and evolving a new function, but this is only one model.



So lets review what has to happen to make this a reality

1. The Gene has to be copied by some copying event which is not a science by any stretch of the imagination, still just chance.

Several papers (M Lynch papers and W. Li papers) have estimated the rate of gene duplication as about 1 duplication per gene per million years from actually counting the number of gene duplicates in fully sequenced genomes of multiple organisms.


2. The copied gene has to be switched off somehow to prevent damage to the organism.

Why does this damage occur? Why does it have to be switched off?


3. Randomly mutate to something that gives the organism a new function.

Why can't an expressed copy mutate randomly and eventually take on a new or related function?


4. Somehow become switched on to be fine tuned by natural selection.

Epigenetic silencing might aid this type of mechanism assuming it has to happen. (See Riggs and Rhodin, 2003

But I don't see why a copy has to be turned off?
Please explain the evidence that says it has to be shutoff.



Now another problem with gene duplication is that the mutation does not just occur in the target gene it occurs throughout the entire genome.

So what is your point, it does occur throughout the genome, how is this problem. Seems like it feeds the process to me?



Point mutations in the target gene are extremely rare representing around 1 part in 30,000 and the larger the genome the more remote the possibilities.

Again where do you get this stuff from. What does 1 part in 30000 mean?

The nt mutation rate in a coding region of an animal is somewhere in the neighborhood of .00000001-.000000001.

Take a gene of 300 amino acids, that is
900 coding nucleotides of which some fraction, ~1/3, don't change the amino acid
are effectively neutral. So we have 600nt * .00000001 = .000006 mutations per allele per generation. There are 2*N alleles in a population.

N expected mutations per generation
1000 0.012
10000 0.12
100000 1.2
1000000 12

Now you can estimate the number of coding region mutations for your deisred number of generations.
For example, in 1000 generations in a population size of 100000, the number of mutations which are expected to occur are between 1200-120.

Sorry your math and assessment is just plain wrong here.



The reason why is because as you increase genome size the mutation rate goes down because of the increased chance of catastrophic errors.

Really? Actually this is completely inaccurate
statement.

The rate of gene duplication per gene is actually nearly equivalent in yeast and the nematode c. elegans (.02 per gene per million years, see Lynch papers and Li papers again.) but the genome size is vastly different.


In laymans terms this means the larger the genome the longer you have to wait for a mutation to occur in the copied gene much less a beneficial mutation.

Nope. In laymans terms in a larger genome there are more oppurtunities to hit upon the same function starting from different genes.


Thats plenty of time you may ask but no its not it may start out quickly with a smaill genome but after you reach the genome of an amoeba the time between helpful mutations increases exponentially.

Again, wherever you got this from is simply wrong.
The duplication rate does not decrease with increasing genome size. In fact it may increase due to various factors including whole genome duplication events which are very frequent in plants and also have occurred in fishes and amphibians.

-------------------------------------------------------------------

After this exchange I asked him if Gene duplication was a viable method for evolution and I gave him my sources he responded with the following statement.

Basically what I am saying is most of the assumptions apparently made on those sites are wrong. We have cases of genes evolving new functions and cases of duplicate genes evolving new functions, what we wish we had are more examples.

Yes, in general evolution is likely to happen through gene duplication, but the story is more complex than that. Please see my page for papers that might clear things up.


Many people will not beleive this but I am not out to try and sell a dogma I am out to discover the truth. If the truth means that I am wrong then so be it, I have no qualms about that. I want to know the truth and sometimes that takes questioning the norm.

I just wanted everyone to have this information and for everyone to know that I am very objective when it comes to this subject.
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