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Author Topic:   Are mutations truly random or are they guided?
Taq
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Posts: 9972
Joined: 03-06-2009
Member Rating: 5.5


Message 121 of 134 (549254)
03-05-2010 10:12 AM
Reply to: Message 119 by Dr Adequate
03-04-2010 4:49 PM


Re: Help! my thread has been hyjacked
Point #1 : the mechanisms that you envisage do not exist. Yes, the cell is complicated, but scientists have given us a fairly good idea of what each bit of it does. We know what the ribosome does, we know what tRNA does, we know what aminoacyl tRNA synthetase does. Yes, the biological mechanisms are complicated, but biologists understand them. There is no mysterious mechanism left over which might do the thing that you envisage some cellular mechanism doing.
In addition, we understand the molecular mechanisms that produce mutations be they from outside sources (radiation, chemical mutagens) or the inherent properties of the enzymes involved in replication and DNA repair.
On top of that, these mechanisms are just as likely to produce maladaptions as they are positive adaptions.
To sum it up in a single sentence:
How can mutations be guided when they are produced by mechanisms that are uninformed by fitness, can produce reduced fitness, and are rarely beneficial with respect to a specific environmental challenge?

This message is a reply to:
 Message 119 by Dr Adequate, posted 03-04-2010 4:49 PM Dr Adequate has not replied

Replies to this message:
 Message 122 by Peepul, posted 03-05-2010 10:55 AM Taq has not replied

  
Taq
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Posts: 9972
Joined: 03-06-2009
Member Rating: 5.5


Message 123 of 134 (549259)
03-05-2010 11:24 AM


Reply to Bolder-dash
This is a reply to B-d's post in the Report discussion problems here: No.2 thread, post #286.
Taq: You are confusing phenotype plasticity with evolution. They are not the same thing. Evolution does not occur to one individual during it's lifetime. Evolution occurs at the level of the population over generations.
B-d: Actually it only occurs through individuals. Individuals get the mutation (according to you) and they either pass it on or they don't. You are confusing the issue by trying to count a population as a thing. A population is an idea.
I guess B-d has never heard of a thing called "Population Genetics". A population is a group of interbreeding individuals. It is an objective, real thing that can be verified by gene flow.
Tanning and pulmonary/vascular reconstruction are not due to mutations. A person does not acquire a mutation upon exposure to sunlight that then results in higher melanin production. And even if this occurred in somatic melanocytes it would NOT be inheritable. Tanning is an induced phenotype that does not require a single mutation. This process can not explain why humans are different from chimps. Those differences are due to differences in DNA. The theory of evolution attempts to explain why those differences in DNA exist.
A study looking at bacteria does nothing to meet the criteria of creating a new form.
As I have already shown, B-d's criteria is nothing more than a word game. If he can call the parent species and the daughter species by the same name then it isn't a "new creature". B-d's argument is based on semantics, and nothing else.
In reality, what we do have is organisms that have never existed before. The bacteria at the end of these experiments have genomes that exist nowhere else, and nowhere in history.
If you believe that all information obtained from looking at a bacteria can apply to all of the living world, then I guess you think it would take 200,000 generations of an animal species to develop something as simple as a resistance to an illness.
Let's use humans and chimps as an example, since you don't seem to like bacteria. We can get a pretty good estimate of the human mutation rate by looking at modern human populations. We can also compare human and chimp psuedogenes to get an idea of the mutation rate needed to produce the DNA differences seen in these sections of DNA. Also, 200,000 generations is about right for the number of generations between humans and our common ancestor with chimps (200,000 generations with a 20 year generation time is 4 million years which is just a skosh short of the proposed 5-7 million years since common ancestry). So what do we see? We observe that the observed human mutation rate is consistent with the mutation rate needed to produce the DNA differences seen between humans and chimps.
quote:
Hum Mutat. 2003 Jan;21(1):12-27.
Direct estimates of human per nucleotide mutation rates at 20 loci causing Mendelian diseases.
Kondrashov AS.
National Center for Biotechnology Information, NIH, Bethesda, Maryland 20892, USA. Kondrashov@ncbi.nlm.nih.gov
I estimate per nucleotide rates of spontaneous mutations of different kinds in humans directly from the data on per locus mutation rates and on sequences of de novo nonsense nucleotide substitutions, deletions, insertions, and complex events at eight loci causing autosomal dominant diseases and 12 loci causing X-linked diseases. The results are in good agreement with indirect estimates, obtained by comparison of orthologous human and chimpanzee pseudogenes. The average direct estimate of the combined rate of all mutations is 1.8x10(-8) per nucleotide per generation, and the coefficient of variation of this rate across the 20 loci is 0.53. Single nucleotide substitutions are approximately 25 times more common than all other mutations, deletions are approximately three times more common than insertions, complex mutations are very rare, and CpG context increases substitution rates by an order of magnitude. There is only a moderate tendency for loci with high per locus mutation rates to also have higher per nucleotide substitution rates, and per nucleotide rates of deletions and insertions are statistically independent on the per locus mutation rate. Rates of different kinds of mutations are strongly correlated across loci. Mutational hot spots with per nucleotide rates above 5x10(-7) make only a minor contribution to human mutation. In the next decade, direct measurements will produce a rather precise, quantitative description of human spontaneous mutation at the DNA level. Published 2002 Wiley-Liss, Inc.
So there you go. The observed random mutation rate is consistent with the DNA divergence seen in animals.
Of course you don't claim this when its inconvenient to claim this-you throw it out and take it away when it suits your argument. Hiding from the need to explain things through random mutations doesn't make the problem disappear-you can't close your eyes and ignore it like hide and go seek.
B-d is flailing away at a strawman. We are arguing that random mutation COMBINED WITH NATURAL SELECTION is responsible for the biodiversity we see in modern species and in the fossil record. You don't get to remove a mechanism from the process and claim it is still the same process.
If evolution were a process existing in all populations, why is it so hard to find evidences of these populations-split by their mutated and unmutated brothers, yet still possessing all the same features other than ONE new adaptive advantage that is creating new information?
It is not hard to find that evidence. The DNA differences between humans and chimps are those mutations. If we include the gorilla genome (gorillas branched off before humans and chimps split) we can also infer the DNA sequence of the common ancestor of humans and chimps allowing us to find candidate mutations that conferred an advantage in each lineage. How can this be done? Quite simple, actually. DNA bases that are the same in both humans and gorillas but different in chimps are candidates for advantageous mutations in the chimp lineage. DNA bases that are the same in both chimps and gorillas but different in humans are candidates for advantageous mutations in humans.
The point of the discussion is to provide evidence that random mutations are causing life forms to be created.
Random mutations do not create life forms. Biological reproduction does.
Those life forms can be entirely new creatures,
Not according to evolution they can't. Evolution proposes that biological reproduction produces offspring that are modified versions versions of their parents. Evolution doesn't produce new creatures. It produces modified creatures. Evolution doesn't produce gills all in one swoop. It modifies existing structures. Bird wings are modified dinosaur arms. The mammalian middle ear is made up of modified reptillian jaw bones. The list goes on and on of modified features, not new ones.
So what you are asking for is evidence that should not exist if evolution is true. You want disproof of evolution before you will accept it as true. You are completely backwards.
No, you know that some drug resistance mutations COULD possibly be random.
No, it IS random with respect to fitness. It is OBSERVED to be so. In the Lederberg plate replica experiment the mutations which confer antibiotic resistance occur in the ABSENCE of antibiotics. The same for mutations which confer phage resistance in the Luria-Delbruck fluctuation experiment. Exposure to both antibiotics and phage do not increase the rate of these mutations above background mutation rates. This is not a defensive reaction either, since this only occurs in one in every several million bacteria. These types of resistance are arrived at by blind luck.
Most of these mutations are deleterious anyway, and disappear rapidly when the pressure is gone.
Ahh yes, the environment fallacy. Are polar bears maladapted because they die quickly when you place them in a desert? All adaptation is described with respect to the environment. You don't get to call something disadvantageous because it does not serve the organism well when you put them into a different environment. If these mutations are disadvantageous in the environment in which they evolved then the organisms without the mutation should make up the majority of the population. This isn't what we see.

Replies to this message:
 Message 124 by RAZD, posted 03-05-2010 8:18 PM Taq has not replied

  
Taq
Member
Posts: 9972
Joined: 03-06-2009
Member Rating: 5.5


Message 128 of 134 (549630)
03-09-2010 11:17 AM
Reply to: Message 127 by Coyote
03-05-2010 11:10 PM


Re: Skin cells in the process of dying are shed continuously
Tanning ability is genetic, due to mutations.
Correct. However, the process of tanning is not. The important contrast here is evolution vs. phenotype plasticity. Going back to the experiments I discussed earlier (plate replica and fluctuation assay) one can differentiate between the two. In the plate replica experiment, if resistance is due to phenotype plsticity then the resistant colonies would not be from the same spot on the master plate. In the Luria-Delbruck fluctuation experiment, if phage resistance was due to phenotype plasticity then the number of resistant clones would be about the same for each parallel culture. This is not what we find. In the plate replica experiment the resistant colonies are clonal. That is, they come from the same spot on the master plate. In the fluctuation experiment the variation in the number of resistant clones in each parallel culture is due to a mutation occuring in a random generation prior to challenge (if the mutation occurs in an early generation there are many resistant clones, and fewer if the mutation occurs in a later generation).
Adaptation within a single generation across the entire population is not evolution. The process of tanning is not evolution. That is why it is important to define evolution with reference to allele frequencies. It differentiates evolution from phenotype plasticity. If evolution is simply defined as adaptation to the environment without reference to heriable traits or mutation/alleles then phenotype plasticity would be part of evolution. However, mutations which confer the ability to tan and spread through a population over generations is evolution.

This message is a reply to:
 Message 127 by Coyote, posted 03-05-2010 11:10 PM Coyote has not replied

  
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