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Author | Topic: Delineation in terminology: mutations | |||||||||||||||||||||||||||||||||
Itinerant Lurker Member (Idle past 2677 days) Posts: 67 Joined: |
I'm currently in a discussion with someone claiming that mutations are,
quote: He's even, apparently, written a paper on the subject and really, REALLY likes to talk about it. The full text is available here.
ABSTRACT WITHIN the last few decades, awareness has developed in the world of genetics having to do with the nature of genetic change. According to classical thought, DNA damaging events and mutations occur randomly throughout the genome of organisms purely by accident. However, a growing body of evidence demonstrates that some genetic change occurs in non-replication, non-random events. The literature gives evidence of two distinct categories of genetic change addressed by the single term mutation. These two categories consist of (1) replication-dependent, random chance genetic changes, and (2) non-random chance genetic adaptive change that originate as non-replication dependent changes. Logically, failure to distinguish between these two processes by separate terminology may have caused problems in understanding genetic systems. This paper aims to examine and make delineation between these two phenomena, so further research can proceed with improved knowledge and understanding of genomic processes, which require clear differentiation. Reasonable misunderstanding of many issues concerning heritability, variation, adaptation, and especially mutation, appear as potentially misleading factors without such demarcation. This has the potential of directly affecting cancer research, as well as other pertinent medical fields dealing with genetic diseases.
My view is that he's trying to define his way out of admitting that random mutations account for beneficial variation, and that his claim that mutations occur non-randomly in regards to fitness is unsupported by the copious sources he very much enjoys citing. Anyway, I thought I'd re-post the paper here for those with a more technical knowledge as fodder for discussion. Edited by Itinerant Lurker, : No reason given.
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AdminModulous Administrator Posts: 897 Joined: |
Rule 6: Avoid lengthy cut-n-pastes. Introduce the point in your own words and provide a link to your source as a reference. If your source is not on-line you may contact the Site Administrator to have it made available on-line.
Maybe just post the abstract or part of the conclusion, and give an overview in your own words - with bonus points for including your own opinion.
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Itinerant Lurker Member (Idle past 2677 days) Posts: 67 Joined: |
Apologies. Better?
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AdminModulous Administrator Posts: 897 Joined: |
Thread copied here from the Delineation in terminology: mutations thread in the Proposed New Topics forum.
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RAZD Member (Idle past 1426 days) Posts: 20714 From: the other end of the sidewalk Joined: |
The full text is available here. ah, so it isn't published in a peer review journal.
and really, REALLY likes to talk about it perhaps you could invite him here to expand on his "paper" ... 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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Dr Adequate Member (Idle past 306 days) Posts: 16113 Joined: |
". . .any and all adaptive change you can point to. NONE of them originate from a true mutational event (random chance, replication-dependent copy errors), they all originate from genomic mechanisms reacting to the outside environment." Well, that raises a few questions. For example, if there is some mechanism to (for example) repair the his operon, as in the Ames test, why doesn't it take place in all the bacteria that find themselves short of histidine and having a broken his operon --- why, instead, does it take place at such low rates as to be consistent with this event being caused by chance? (We might ask similar questions about, for example, Lenski's bacteria. If the evolution of citrate-eating bacteria is induced by a mechanism for doing so, then why did only one of the strains evolve it?) Why is the rate of repair raised by the presence of mutagens, which are also known to increase the rate of harmful mutations as well? What the heck is the mechanism? In the case of the Ames test, the mechanism must somehow "know" what the [i]his[/h] operon ought to look like. This information is stored once on the genome in the his operon, but when the operon is broken, it isn't there any more. Where, then, is the backup copy stored? And it's not just repairing broken genomes that this mechanism can do. It can adapt organisms to a wide range of conditions not found in nature. So in the case of the Lenski experiments, there must have been this mechanism sitting in E. coli, unused, waiting to spring into action when Lenski created the artificial environment in which the adaptation would be useful. What mechanism caused this adaptation, and where in the cells was the information stored as to what the genome should look like in the case that some scientist introduced the bacteria to the appropriate environment? --- As for his proposal to alter the English language, I think it would be confusing and inconvenient. Edited by Dr Adequate, : No reason given.
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Taq Member Posts: 10038 Joined: Member Rating: 5.3 |
From the abstract:
"According to classical thought, DNA damaging events and mutations occur randomly throughout the genome of organisms purely by accident. However, a growing body of evidence demonstrates that some genetic change occurs in non-replication, non-random events." That raises two flags right away. From the very start, the randomness of mutations has always referred to fitness, not to the region of the genome. In fact, we discovered that mutations were random before we discovered DNA. When we say that mutations are random we mean that the processes that produce mutations are blind to the needs of the organism. The second red flag is the use of non-random events. This is a bit like saying that the lottery is non-random because it takes place on non-random days.
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sfs Member (Idle past 2555 days) Posts: 464 From: Cambridge, MA USA Joined: |
Quite a lot of mutation has nothing to do with replication -- that's been known for a long time. UV light causes pyrimidine dimers to form in DNA, transcription makes double-stranded breaks (which often are repaired incorrectly) more likely, and methylated cytosines spontaneously deaminate.
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NoNukes Inactive Member |
My view is that he's trying to define his way out of admitting that random mutations account for beneficial variation, I don't think there is a problem with definition. This looks like simple denial. Assuming even that the issues observed in single celled organisms can be given the interpretation he gives them, the mechanisms that work in a single celled critter simply cannot be translated to animals for extremely obvious reasons. However it is very difficult to get advocates to dwell on those issues. We've had very similar discussions in threads started by "shadow71'. Edited by NoNukes, : No reason given.Under a government which imprisons any unjustly, the true place for a just man is also in prison. Thoreau: Civil Disobedience (1846) I believe that a scientist looking at nonscientific problems is just as dumb as the next guy.Richard P. Feynman If there is no struggle, there is no progress. Those who profess to favor freedom, and deprecate agitation, are men who want crops without plowing up the ground, they want rain without thunder and lightning. Frederick Douglass
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