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Author Topic:   Will mutations become less freqent?
RAZD
Member (Idle past 1405 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 10 of 25 (334141)
07-21-2006 10:06 PM
Reply to: Message 6 by Elliot
07-19-2006 11:56 AM


I was still theorising in a stable environment, which is entirely possible.
You would need to eliminate seasons, all climate variations, all tecktonic effects and all predator-prey relationships.
Also have you never heard of convergent evolution? If the dinosaurs had a steady environment then they would have less need for mutations.
I'm not sure you understand convergent evolution or you are not conveying what you are meaning here. It has nothing to do with the rate of mutation, and the organisms would still need to evolve to converge.
Are you thinking that all life would end up as essentially one (1) type of plant (all plants converged), one (1) type of herbivore (all herbivores and some omnivores converged) and one (1) type of carnivore (all carnivores and remaining omnivores converged)?
Even with that scenario you would have the ongoing "arms-race" between the eaten (to not be eaten) and the eater (to eat).
Welcome to the fray.
Enjoy.

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This message is a reply to:
 Message 6 by Elliot, posted 07-19-2006 11:56 AM Elliot has replied

Replies to this message:
 Message 11 by Elliot, posted 07-22-2006 4:40 AM RAZD has not replied

  
RAZD
Member (Idle past 1405 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 15 of 25 (334469)
07-23-2006 8:33 AM
Reply to: Message 14 by Elliot
07-22-2006 11:43 AM


Stable environment do exist.
I disagreed, and have posted why. You chose to minimize the effects, but by doing this you are ignoring the need for variations involved.
At best there are environments that oscillate around a median, but even then those oscillations cause adaptations and variations to be selected. These may be no more significant than the change in beak size of the Galapagos Finches studied by Grant and Grant
Just a moment...
But these are still changes and they are still selection responses to variations in the environment. They still have the repository of accumulated genetic {genome} plus new beneficial (to current "micro?" environment) and the accumulation of {previously neutral} mutations that may or may not be beneficial in the changes-- those that are get selected for (larger beaks in dry periods, small beaks in wet periods) those that aren't get de-selected (small beaks in dry periods, large beaks in wet periods). The population on a whole appears unchanged, but they have oscillated between different forms -- forms that were available due to the level of mutations the population had in reserve due to mutations.
If the DNA had selected for such a low level of mutation that {large\small} beaks would not exist in the population the species would have become extinct even though the environment was "stable" ... (by your definition when you excluded the variations I mentioned).
Take an example of two people with bank accounts, they each earn $100 a week and spend $100 a week, they both have their earning automatically deposited in a bank account and use debit cards to spend with. One has no buffer, the account is empty just before the next deposit, and the other has $1000 in buffer: which will be able to survive economic oscillations in their costs that force them to exceed spending $100 in one week?
Take some fossils for example, some species which we have fossils for that still exist, their skeletal structure remains similar, these are millions of years apart, and as they have little need to change, they don't.
The fact that we have species alive today that are related to ancient species does not mean they are unchanged.
Crocodiles
Sharks
Coelacanths
and the like
Are all different species today than the ones alive millions of years ago. Size and other morphological changes have occurred as well as divergence from those ancient forms.
Further, their ancestors survived (1) ice ages and (2) the K-T extinction event caused by the Yucatan meteor strike 65 million years ago (as have the ancestors of all life today) -- so they can not be said to have lived in stable environments.
And if their current form is working just fine, then the risk of a bad mutation would outweigh the benefits of a good one, so the DNA process (rightly said - IF it can be improved) would be more accurate.
There is a logical error here. As pointed out, most mutations are harmful, and they are handled by the current selection just fine. If the current method of dealing with bad mutations is working just fine, then the risk of bad mutation to the species as a whole is virtually non-existent.
It is not harmful mutations that cause extinction, rather it is lack of adaptation that causes extinction, and every time selection is for a slight adaptation to best fit the current environment, then there is selection for sufficient mutations to provide the diversity.
The logical conclusion is that if the rate of mutation has evolved (or rather the susceptibility to mutation) that then this occurred a long time ago, long before dinosaurs evolved, before the P-T extinction event.
There does seem to be evidence that some sections of DNA are more susceptible to mutations than other, and there is evidence that bacteria can change their rates of mutation, increasing it when they are environmentally stressed, and both of these lines of evidence would indicate that the minimum level of mutation needed for the ongoing survival of life in general (not just of species) has evolved ... and already reached an equilibrium with the need for variations.
Enjoy.

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This message is a reply to:
 Message 14 by Elliot, posted 07-22-2006 11:43 AM Elliot has not replied

Replies to this message:
 Message 16 by Discreet Label, posted 07-23-2006 5:47 PM RAZD has replied

  
RAZD
Member (Idle past 1405 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 17 of 25 (335875)
07-27-2006 9:48 PM
Reply to: Message 16 by Discreet Label
07-23-2006 5:47 PM


So big question that arose out of that why aren't we dead?
I would say either the model that predicts cell death in this scenario is faulty or you are missing some element in it (not necessarily your fault - your source may have missed it before passing it on to you).
From what little I understand about biology, and what has been described, is that double strand breaks, a single one is enough to kill a cell. At this point it is pretty much believed that double strand breaks occur at a rate of 10-60 times per cell...
The technical answer would need to come from a molecular biologist (bradcap1, WK, etc), but a google on {double strand DNA breaks} brings up these as the first two "hits" (note "DSB" means double strand break):
Mating Type Switch Donor Preference
Sensing and repairing DNA double-strand breaks | Carcinogenesis | Oxford Academic
The first fairly "layman friendly"
A number of models have been put forth over the years to explain how DNA recombination occurs. The basis of these models lies in what has been learned of recombination from yeast and other fungi. Fungi have been studied intensively because they possess certain properties such as the ability to yield four viable meiotic products (spores) that can be assayed and analyzed. For example, a mutation that is heterozygous will give rise to two mutant spores and two wild type spores, a 2+:2- pattern that is considered to be classically Mendelian. The appearance of non-Mendelian patterns such as 1+:3- (a "gene conversion") or the presence of "sectored" colonies (colonies with a divided phenotype) gave rise to a series of models to explain these events.
and the second more technical:
The DNA double-strand break (DSB) is the principle cytotoxic lesion for ionizing radiation and radio-mimetic chemicals but can also be caused by mechanical stress on chromosomes or when a replicative DNA polymerase encounters a DNA single-strand break or other type of DNA lesion. DSBs also occur as intermediates in various biological events, such as V(D)J recombination in developing lymphoid cells. Inaccurate repair or lack of repair of a DSB can lead to mutations or to larger-scale genomic instability through the generation of dicentric or acentric chromosomal fragments. Such genome changes may have tumourigenic potential.
The second also says:
DSBs are potent inducers of mutations and of cell death. In metazoa, just one DSB can kill a cell if it leads to the inactivation of an essential gene or, more commonly, triggers apoptosis (5).
So I would say that is part of the answer to your question -- where the DSB occurs makes a difference.
I don't know where this actually fits into the whole mutation limitations.
The question is whether this (and other kinds) of mutation can be prevented or restricted by some genetic shield process.
I don't see that happening to any great(er) degree -- the current mechanism (natural selection) removes the individual organisms where DSB's do cause (cell) death -- particularly in unicellular life, metazoa, so additional protection is not necessary.
Where the process is NOT lethal, the question then is whether or not it can be prevented. The chemical bond cannot be made any stronger or weaker, so the only way to reduce it being interrupted is to form either some kind of shield or to develop some kind of additional repair mechanism that is faultless -- both things evolution is notoriously incapable of (and we don't need to discuss the implications of this for "design" do we?)
After all it is the current repair mechanism that puts the strands together with the cross-over eh? And as long as the organism functions and passes on those genes to the next generation then the repair is "successful" so there is no need to modify the repair mechanism if it succeeds.
Can the rates of mutation change? Yes, it has been observed. I believe (quick scan of second paper) it is through changing the way the repair mechanisms react and respond.
Can mutation be eliminated? Yes, but I believe total extinction would be part of that "ultimate solution" as it would leave life with no safety position.
The problem is that life is not invested in just one or two species and that different species have different rates of mutations -- the selection of species is also part of the mechanism for selection of the mutation rate that suits the need for diversity in the global population -- in my humble (but sometimes arrogant) opinion anyway.
Enjoy.

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This message is a reply to:
 Message 16 by Discreet Label, posted 07-23-2006 5:47 PM Discreet Label has replied

Replies to this message:
 Message 18 by Discreet Label, posted 07-27-2006 10:29 PM RAZD has not replied

  
RAZD
Member (Idle past 1405 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 21 of 25 (335978)
07-28-2006 7:34 AM
Reply to: Message 20 by Wounded King
07-28-2006 6:20 AM


... most of our DNA seems to serve at best a structural function ...
One of the observations I have gleaned from the {Human Proteome Folding} project on the World Grid work,
World Community Grid - Research - Human Proteome Folding - Phase 2,
is that it is important what parts of the proteins are exposed to be active or able to be active -- the rest is "structure" to ensure the proper parts are exposed in the final folded molecule.
... and is far less likely to be perturbed by the insertion of a few non-template nucleotides, certainly less so than by having a persistent DSB.
Presumably DNA would have similar {structure} issues.
Common view (laypeople) is that there is one strand of DNA in each nucleus (mental picture of long twisting double chain of colored balls with toothpicks between ...) - but this view conflicts with the 22 (human) chromosomes we (laypeople) also "know" about (mental picture of 22 odd shaped lumps, of which one looks oddly like an "X" and another type looks oddly like a "Y" ... ).
Now it seems that DNA is rather randomly broken into smaller segments and reformed as\when necessary (when duplication is needed?), so the whole system may be much more dynamic than is commonly envisaged.
In a coding region or a crtical regulatory region then such insertions certainly could be detrimental, ...
When duplication is needed -- but may it also be necessary to {open up - access the 'internal' folded structure} the DNA for other functions? And then have some mechanism to recombine it?

Join the effort to unravel {AIDSHIV} with Team EvC! (click)

we are limited in our ability to understand
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RebelAAmericanOZen[Deist
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This message is a reply to:
 Message 20 by Wounded King, posted 07-28-2006 6:20 AM Wounded King has replied

Replies to this message:
 Message 22 by Wounded King, posted 07-28-2006 8:46 AM RAZD has replied

  
RAZD
Member (Idle past 1405 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 23 of 25 (336171)
07-28-2006 7:07 PM
Reply to: Message 22 by Wounded King
07-28-2006 8:46 AM


... and further modifications of the organisation of nucleosomes themselves can produce tighter packing of DNA into what is known as heterochromatin. Therefore even if DNA undergoes a DSB the two 'fragments' are not floating dissociated from one another but still joined together by the larger superstructure of the chromosome.
Thanks, yeah the common mis-impression of free-floating DNA strands in a liquid "egg yolk" nucleus is more due to "popular news" than reality eh? And what is even less understood popularly (if even thought about) is the structure of the chromosomes.
So the DNA is pretty much held in place by other molecules within the chromosome, molecules that are also responsible for the overall shape of the chromosome?
Would not segments on the outside be more vulnerable to damage? And breaks on the outside areas would be less tied down close to each other? (is this (one reason) why some segments are more prone to mutations than others?)
Overall sounds like a mechanism to minimize random recombinations and to stabilize the genetic structure.
Some Topoisomerases actually produce double stranded breaks in order to untangle chromosomes.
I would guess that these are the more common DSB's that were mentioned above, and would (by 'choice') be non-lethal to the cell.
Dna must normally be opened up from its compacted heterochromatic state if a gene is to be transcribed prior to protein synthesis. There is a constant dynamic restructuring of chromatin as and when certain genes are no longer required. Much of the regulation of this is provided by modifications to the histone proteins, specifically methylation and acetylation of the histones.
Pretty dynamic. And a sequence of such operations ends up with cell specialization via chemical communication with adjacent cells to determine which sequence to open when?
Thanks.

Join the effort to unravel {AIDSHIV} with Team EvC! (click)

we are limited in our ability to understand
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RebelAAmericanOZen[Deist
... to learn ... to think ... to live ... to laugh ...
to share.

This message is a reply to:
 Message 22 by Wounded King, posted 07-28-2006 8:46 AM Wounded King has not replied

  
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