It looks like you're using an Ad Blocker.
Please white-list or disable AboveTopSecret.com in your ad-blocking tool.
Thank you.
Some features of ATS will be disabled while you continue to use an ad-blocker.
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.
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 don�t 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.
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.
2. Junk DNA- the supposed left over from Eons of evolution ain�t junk but useful DNA
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 isn�t enough time in Earth�s history to make it work.
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?�
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.
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.
...but radiation is not the only source of mutation.
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.))
As far as I know, our genome isn't completely mapped out and we're not sure of the function of everything.
Not if you think the world is only 6,000 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.
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.
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 doesn�t 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 that�s 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. That�s 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.
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.
Originally posted by AlexKennedy
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.
Originally posted by BlackJackal
If so, one should be able to construct gene phylogenies which should exhibit a nested pattern. I would very much like to see this evidence.
Um... you want to see genetic phylogenies?
How about here, here, here, (here's a related one), here, here, here, here, here, or here?
And that's just for starters, of course. If you're really interested in Phylogenetics, why not pick up a first-year Genetics textbook and read it?
Originally posted by BlackJackal
Its not that easy I want you to show me the genetic phylogene for the one or few cells that started out on earth and how they evolved into what you see today. The problem is that you can't because neither can scientists.
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.
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.
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.
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.
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.
Why does this damage occur? Why does it have to be switched off?
Why can't an expressed copy mutate randomly and eventually take on a new or related function?
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.
So what is your point, it does occur throughout the genome, how is this problem. Seems like it feeds the process to me?
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.
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.
Nope. In laymans terms in a larger genome there are more oppurtunities to hit upon the same function starting from different genes.
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.
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.