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Author Topic:   Are mutations truly random or are they guided?
Taq
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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?


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 Message 119 by Dr Adequate, posted 03-04-2010 4:49 PM Dr Adequate has not yet responded

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 Message 122 by Peepul, posted 03-05-2010 10:55 AM Taq has not yet responded

  
Peepul
Member (Idle past 3092 days)
Posts: 206
Joined: 03-13-2009


Message 122 of 134 (549256)
03-05-2010 10:55 AM
Reply to: Message 121 by Taq
03-05-2010 10:12 AM


Re: Help! my thread has been hyjacked
quote:
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.

I don't think we understand the cell as well as you think we do. Look at how much we are discovering (and still have to discover) about the genome, and how surprising some of those things are. I think there's plenty of room for new discoveries about gene regulation - and it's possible some of those have an impact on the mutation rate, or more probably on the repair rate.

Now of course the cell cannot direct mutations in any intentional way. So the answer to the question 'are mutations guided?' is undoubtedly no.

Edited by Peepul, : No reason given.


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Taq
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Posts: 7672
Joined: 03-06-2009
Member Rating: 2.5


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.


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RAZD
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Posts: 19754
From: the other end of the sidewalk
Joined: 03-14-2004
Member Rating: 5.0


Message 124 of 134 (549326)
03-05-2010 8:18 PM
Reply to: Message 123 by Taq
03-05-2010 11:24 AM


Skin cells in the process of dying are shed continuously
Hi Taq, just a small additional point, one I'm sure you are aware of.

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.

You shed skin cells at a fairly rapid rate, such that in ~four weeks you have a completely new skin. Skin cells reproduce in lower layers by cell division (just like bacteria) and then migrate to the surface, dying in the process before being shed in a continuous process. There is no mechanism for anything in these outer skin layers to move back into the body.

http://en.wikipedia.org/wiki/Skin_cell#Epidermis

quote:
The epidermis contains no blood vessels, and cells in the deepest layers are nourished by diffusion from blood capillaries extending to the upper layers of the dermis. The main type of cells which make up the epidermis are Merkel cells, keratinocytes, with melanocytes and Langerhans cells also present. The epidermis can be further subdivided into the following strata (beginning with the outermost layer): corneum, lucidum (only in palms of hands and bottoms of feet), granulosum, spinosum, basale. Cells are formed through mitosis at the basale layer. The daughter cells (see cell division) move up the strata changing shape and composition as they die due to isolation from their blood source. The cytoplasm is released and the protein keratin is inserted. They eventually reach the corneum and slough off (desquamation). This process is called keratinization and takes place within about 27 days.

Tanning results from the release of melanin into the surrounding skin cells from the melanocytes in response to sunlight.

http://en.wikipedia.org/wiki/Sun_tanning

quote:
Firstly, the UVA-radiation generates oxidative stress, which in turn oxidises pre-existing melanin. This leads to rapid darkening of already existing melanin. Secondly, there is an increased production of melanin (melanogenesis).[1] It is a reaction of the body to photodamage from UVB.[2] Melanogenesis leads to delayed tanning. It first becomes visible about 72 hours after exposure.[1] The tan that is created by an increased melanogenesis lasts much longer than the one that is caused by oxidation of existing melanin.

Darkening of the skin is caused by an increased release of the pigment melanin into the skin's cells after exposure to ultraviolet radiation. Melanin is produced by cells called melanocytes and protects the body from direct and indirect DNA damage absorbing an excess of solar radiation, which can otherwise be harmful.


Both the melanocytes and surrounding cells are part of the process of continual skin shedding. Any mutations that occur in the skin cell then are lost when the cells are shed, rather than being incorporated back into the organism.

Enjoy.


we are limited in our ability to understand
by our ability to understand
Rebel American Zen Deist
... to learn ... to think ... to live ... to laugh ...
to share.


• • • Join the effort to solve medical problems, AIDS/HIV, Cancer and more with Team EvC! (click) • • •

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Coyote
Member (Idle past 180 days)
Posts: 6117
Joined: 01-12-2008


Message 125 of 134 (549328)
03-05-2010 9:12 PM
Reply to: Message 124 by RAZD
03-05-2010 8:18 PM


Re: Skin cells in the process of dying are shed continuously
Good points, RAZD, but not every population has the ability to tan.

These differences are due to one or more mutations somewhere along the line during the migration from Africa to northern Europe.

The populations at the extremes, Africa and Scandinavia, do not tan. Those groups in the middle do. To me that suggests multiple mutations.


Religious belief does not constitute scientific evidence, nor does it convey scientific knowledge.
This message is a reply to:
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Replies to this message:
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RAZD
Member
Posts: 19754
From: the other end of the sidewalk
Joined: 03-14-2004
Member Rating: 5.0


Message 126 of 134 (549332)
03-05-2010 9:51 PM
Reply to: Message 125 by Coyote
03-05-2010 9:12 PM


Re: Skin cells in the process of dying are shed continuously
Hi Coyote,

... but not every population has the ability to tan.

These differences are due to one or more mutations somewhere along the line during the migration from Africa to northern Europe.

The populations at the extremes, Africa and Scandinavia, do not tan. Those groups in the middle do. To me that suggests multiple mutations.

Like any trait, there are variations within the population, and in areas where tanning is beneficial the ability to tan can be selected over the tendency to burn, while in areas where tanning is not beneficial, loss of the ability to tan is not selected against and can come to predominate in the population.

This would show up in the skin cells via different patterns of cell distribution that occur during growth.

http://en.wikipedia.org/wiki/Epidermis_%28skin%29#Skin_color

quote:
The amount and distribution of melanin pigment in the epidermis is the main reason for variation in skin color in modern Homo sapiens. Melanin is found in the small melanosomes, particles formed in melanocytes from where they are transferred to the surrounding keratinocytes. The size, number, and arrangement of the melansomes varies between racial groups, but while the number of melanocytes can vary between different body regions, their numbers remain the same in individual body regions in all human beings. In white and oriental skin the melansomes are packed in "aggregates", but in black skin they are larger and distributed more evenly. The number of melansomes in the keratinocytes increases with UV radiation exposure, whilst their distribution remain largely unaffected. [6]

The distribution pattern is genetic.

Under exposure stress from UV the body reacts by processing more skin stem cells into melanocytes, and thus to produce more melanin in the (soon to be shed) skin. This is why you get deeper tan during the summer, while in the winter the process reverses.

The distribution doesn't change, so genetically you are limited by the distribution characteristic of your ethnic ecological genotype.

And you can cycle between deep summer tan and winter white without affecting your genetic makeup or even the ability to tan faster the next year.

Now if mutations were directed, or responsive to environmental factors, one would expect that there would be a noticeable improvement during a lifetime. One would expect the mutation rate to increase while experiencing the UV stress in the skin, and selection within the organism for increased protection provided by cell that lasted longer.

If mutations were random, then you would have no such effect, the pattern of tanning would be fixed in each individual.

Enjoy.

Edited by RAZD, : topic considerations


we are limited in our ability to understand
by our ability to understand
Rebel American Zen Deist
... to learn ... to think ... to live ... to laugh ...
to share.


• • • Join the effort to solve medical problems, AIDS/HIV, Cancer and more with Team EvC! (click) • • •

This message is a reply to:
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Coyote
Member (Idle past 180 days)
Posts: 6117
Joined: 01-12-2008


Message 127 of 134 (549341)
03-05-2010 11:10 PM
Reply to: Message 126 by RAZD
03-05-2010 9:51 PM


Re: Skin cells in the process of dying are shed continuously
We are apparently talking past one another.

Tanning ability is genetic, due to mutations.

On the trek northward from Africa the need for Vitamin D resulted in selection pressure for lighter colored skin. Very dark skin passes little UV.

In the general Mediterranean area selection pressure favored the summer/winter differences we call tanning.

In the far north selection pressure favored much lighter skin as the sun provided much less UV for the production of Vitamin D.

In the far north people were unable to live until artificial sources of Vitamin D were discovered. The skin simply could not get light enough to provide a sufficient supply.

These traits are passed on within their respective populations.

They are genetic, due to mutations.


Religious belief does not constitute scientific evidence, nor does it convey scientific knowledge.
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Taq
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Posts: 7672
Joined: 03-06-2009
Member Rating: 2.5


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.


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Hyroglyphx
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Posts: 5622
From: Austin, TX
Joined: 05-03-2006


Message 129 of 134 (549688)
03-09-2010 9:10 PM
Reply to: Message 1 by herebedragons
02-27-2010 11:46 PM


What I am suggesting is that random mutations may not be the all powerful driving force of evolution that they have been thought to be. Instead, it makes more sense that mutations, (and therefore adaptation) are directed by the cell and by cellular processes.

I don't think any reputable evolutionists assert that mutations is the driving force in evolution. It certainly plays a large role, but not the only one.

Genetic drift, isolation, etc play equally important roles which can be demonstrated.


"Political correctness is tyranny with manners." -- Charlton Heston
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herebedragons
Member
Posts: 1493
From: Michigan
Joined: 11-22-2009


Message 130 of 134 (550042)
03-12-2010 9:18 AM


sorry for the delay in responding
Hi all.

Just a quick note to say that I have not abandoned this thread. I still have some things to discuss, I have just been very busy lately. I am taking a Sociology couse online and because I got enrolled a bit late, I am playing catch up. I will respond to the issue as soon as I can find the time, hopefully within the week.

Thanks for the patience

Edited by herebedragons, : No reason given.


  
pandion
Member (Idle past 1075 days)
Posts: 166
From: Houston
Joined: 04-06-2009


Message 131 of 134 (550124)
03-12-2010 8:05 PM
Reply to: Message 129 by Hyroglyphx
03-09-2010 9:10 PM


There are several mechanisms of evolution that are generally recognized by evolutionary biologists. Some, of course, act to increase genetic diversity while others act to reduce it.

+ mutation
+ gene flow
+ movable elements
+ recombination
- natural selection
- genetic drift
- biased variation
- non-random mating (including sexual selection)


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kalimero
Member (Idle past 519 days)
Posts: 251
From: Israel
Joined: 04-08-2006


Message 132 of 134 (550987)
03-20-2010 4:41 AM


Guided mutations
Sorry for the general post, but I just wanted to say that there is such a thing as cell-guided mutations. This is a process in antibody diversification known as somatic hypermutation, produced by an enzyme called Activation-induced cytodine deaminase. This is to say that it is not out of the question that cells may regulate the mutational rate of (very) specific regions of DNA. Of course, this is the result of adaptation.
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Wounded King
Member (Idle past 2169 days)
Posts: 4149
From: Edinburgh, Scotland
Joined: 04-09-2003


Message 133 of 134 (550992)
03-20-2010 5:44 AM
Reply to: Message 132 by kalimero
03-20-2010 4:41 AM


Re: Guided mutations
This is true but as you suggest the existence of somatic hypermutation in immune cells no more shows a role for guided mutation causing evolution than the epigenetic changes which lead to lineage differentiation in development show a role for Lamarckian mechanisms in evolution.

It is also important to bear in mind that while somatic hypermutation is restricted to specific regions the actual mutations and rearrangements themselves are still essentially random, especially with regard to the immunological challenges they are going to face. Somatic hypermutation is not targeted in such a way as to respond to a specific immunological challenge, it depends on the generation of vast amounts of random variation followed by selection to find suitable antibodies.

It is definitely worth noting though that where such a guided mechanism exists it has been identified and characterised, unlike the cryptic mechanisms of guidance so many ID supporters postulate.

TTFN,

WK

Edited by Wounded King, : No reason given.


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kalimero
Member (Idle past 519 days)
Posts: 251
From: Israel
Joined: 04-08-2006


Message 134 of 134 (550994)
03-20-2010 6:06 AM
Reply to: Message 133 by Wounded King
03-20-2010 5:44 AM


Re: Guided mutations
This is true but as you suggest the existence of somatic hypermutation in immune cells no more shows a role for guided mutation causing evolution than the epigenetic changes which lead to lineage differentiation in development show a role for Lamarckian mechanisms in evolution.

Your absolutely right about that.

It is also important to bear in mind that while somatic hypermutation is restricted to specific regions the actual mutations and rearrangements themselves are still essentially random, especially with regard to the immunological challenges they are going to face. Somatic hypermutation is not targeted in such a way as to respond to a specific immunological challenge, it depends on the generation of vast amounts of random variation followed by selection to find suitable antibodies.

It's non-random in three ways:

  1. The mutations are local (which you mentioned).
  2. The mutations are limited to certain nucleotides more than others; as the name of the enzyme suggests - cytodine deaminase.
  3. The mutations occur in specific (WRCY) motifs.

It is definitely worth noting though that where such a guided mechanism exists it has been identified and characterised, unlike the cryptic mechanisms of guidance so many ID supporters postulate.

Deliberately cryptic...
As opposed to the kind of cryptic ideas that scientists form, e.g. "dark matter".

Edited by kalimero, : Apparently there is no underlining in this forum, LOL.


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