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.
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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.