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Author Topic:   Wright et al. on the Process of Mutation
Taq
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Posts: 8482
Joined: 03-06-2009


Message 49 of 296 (628557)
08-10-2011 12:05 PM
Reply to: Message 46 by John Jones
08-09-2011 6:53 PM


I argued aginst the use of the term fitness.

It would seem that you are arguing over semantics. No matter what word you use there is still the observation that specific alleles increase the chances of an organism producing more offspring than others in a given environment.

As the OP appeared to select biological/chemical facts by using the framework of fitness, then it threatened his enterprise with a tautology. (Fitness can't be a quality "of" a life-form, or "of" X; if fitness is the presence of X. All we end up saying is that fitness is the name of X. )

You are forgetting the observations that they made. They observed that mutants who carried a mutation in the leuB- gene that resulted in an enzyme capable of de novo leucine production produced more offspring than those without the mutation in an environment that lacked extracellular leucine. This is an observation, not a tautology.

Edited by Taq, : No reason given.


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Taq
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Posts: 8482
Joined: 03-06-2009


Message 51 of 296 (631565)
09-01-2011 7:18 PM
Reply to: Message 50 by shadow71
09-01-2011 6:59 PM


If specific alles increase the chances of an organism producing more offspring than others in a given enviroment, and these alles production are more than those w/o the mutation, this sound alot like mutations for fitness, that are not "random" as per Darwin.
Am I wrong in this observation?

As Wolfgang Pauli once put it, you aren't even wrong.

What does "these alleles production are more than those w/o the mutaiton" mean? What "production" are we looking at? Production of mutants? Production of mRNA? Production of protein? Production of offspring? What exactly?

The facts of the matter is that your supposed "genetic engineering systems" can only produce 2 bacteria per BILLION that carry a mutation that is beneficial in the given environment. How do you explain such a low mutation rate? Shouldn't an engineered system produce 500 million per billion beneficial mutations (i.e. 50%)? Why only 2?

Edited by Taq, : No reason given.


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Taq
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Posts: 8482
Joined: 03-06-2009


(1)
Message 56 of 296 (632287)
09-06-2011 8:37 PM
Reply to: Message 52 by shadow71
09-01-2011 7:55 PM


Maybe because those are the beneficial mutations necessary for the system. Engineering systems are designed to be specific and not wasteful.

In this case, it is wasteful. 1,999,999,998 bacteria do not get the mutation they need while only 2 do. Those other bacteria are also acquiring mutations in genes that do not need them. I would hazard a guess that there are more examples of mutations which result in death than there are beneficial mutations.

It is wasteful, by every measure. You would actually have a better chance of winning the random Powerball lottery than a bacteria has for getting the mutation it needs.


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Taq
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Posts: 8482
Joined: 03-06-2009


Message 58 of 296 (632735)
09-09-2011 6:22 PM
Reply to: Message 57 by zi ko
09-09-2011 3:32 PM


Re: beneficial mutations
I don't think your conclusion is right.The 1,999,999,998 bacteria is the right number for an environment that the organism has lived for long time and maybe will live for long time still. and again the 2 is the right number as nature history proves.No waste at all.Nature knows well what is doing.

The number should actually be 999,999,998. I don't know why I put the 1 in front. I got 2 and 1 billion confused I guess. However, the point stands that the authors only measured 2 leuB- reversions per billion bacteria in an environment lacking leucine. That is the observation. Therefore, the other 999,999,998 bacteria did not get the mutation they needed. You actually have a better chance of winning the Powerball lottery than these bacteria do of winning the leuB- reversion lottery.

So how can this be an engineered response when 99.9999998% of the bacteria fail to produce the correct mutation? Why does this engineered response have a 99.9999998% failure rate?

Edited by Taq, : No reason given.


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 Message 61 by zi ko, posted 09-10-2011 1:32 AM Taq has responded

  
Taq
Member
Posts: 8482
Joined: 03-06-2009


Message 60 of 296 (632747)
09-09-2011 7:51 PM
Reply to: Message 59 by Panda
09-09-2011 6:37 PM


Re: beneficial mutations
Wouldn't that be a worse design decision than putting spare-tyres in only 0.0000002% of cars?

Or worse than an airbag that only deploys in 0.0000002% of accidents?


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Taq
Member
Posts: 8482
Joined: 03-06-2009


Message 64 of 296 (633086)
09-12-2011 11:02 AM
Reply to: Message 61 by zi ko
09-10-2011 1:32 AM


Re: beneficial mutations
i think you miss my point. 999,9999,998 of bacteria had got the mutation they needed according to organism's knowledge of the environment's virieties and instability.

No, they hadn't. When grown in the absence of leucine only 2 out of every billion bacteria survived. They didn't have the mutation they needed.

Also there is the possibility that organism in succeeded generations will produce more of the "apropriate" mutations if it sees it usefull.

For the bacteria without the needed mutation there were no successive generations. They stopped growing and were incapable of reproducing.


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Taq
Member
Posts: 8482
Joined: 03-06-2009


(1)
Message 66 of 296 (633119)
09-12-2011 3:28 PM
Reply to: Message 65 by shadow71
09-12-2011 2:59 PM


Re: I'm not so sure
taken in conjunction with her paper discussed on this tread where she finds metabolic activities specifically targeting the leu operon . . .

This is false. The increased mutation rate is specific to single stranded DNA (ssDNA), not the leuB gene. The authors went on to show that they could change the mutation rate of leuB by using a lac promoter and IPTG, both of which are unrelated to leucine.

this I take to mean that there are in fact targeted directed responses to specific condidtions that trigger benefical mutations.

You got the target wrong. The target in this case is ssDNA. This process will increase the mutation rate in all actively transcribed genes, including those that do not need any mutations whatsoever. In fact, this process will also create deleterious mutations in genes that are not leuB.

Even then, you still can not explain why a targetted system only hits its target once very 500 million tries. That doesn't sound like a targetted system to me. You might as well claim that the Powerball lottery is targetted towards a specific person after that person wins.


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Taq
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Posts: 8482
Joined: 03-06-2009


Message 69 of 296 (633263)
09-13-2011 10:58 AM
Reply to: Message 68 by zi ko
09-13-2011 10:25 AM


Re: beneficial mutations
In real nature there are organisms in the fringes of an event that are affected some how.

Yes, they are affected by random mutations (with respect to fitness) and selective pressures.

I think you should provide the number of deleterious and indifferent mutations, so to be able to estimate any probability rate of beneficial mutations. Don't you think so?

It is the same rate as the leuB gene for genes that are actively transcribed. Gyrase is a good example. It is a "housekeeping" gene that is transcribed throughout the bacterium's lifetime. If there is a point mutation that would result in dysfuncitonal gyrase then that mutation has the same chance of occuring as the mutation that produces the leuB- reversion. That is what this study demonstrated. The author's did a great job of showing that the increased leuB- reversion rate was due to leuB- upregulation, so any gene that is upregulated will see the same effects.

Edited by Taq, : No reason given.


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Taq
Member
Posts: 8482
Joined: 03-06-2009


Message 71 of 296 (633276)
09-13-2011 12:33 PM
Reply to: Message 67 by zi ko
09-13-2011 10:09 AM


Re: beneficial mutations
You seem at first look right , but only in the perspectives of narrow lab conditions.

So Shapiro et al. use narrow lab conditions and you and shadow cite their work as supporting guided mutations. When a closer look at those studies does not support your view you abandon those studies. Sounds a bit hypocritical to me.

Nature works on broad scale,with great varieties and areas of more or less affinity of an event,where organisms "see" and understand the changes happening around.There are according to Shapiro decision making loci even in one cell organisms.

You are using a sleight of hand. We are talking about mutations, not the ability of organisms to change their DNA expression patterns in response to the environment. As the Wright paper demonstrated, the bacteria did not sense a mutation in leuB and a lack of leucine in the environment as part of a decision making process to mutate leuB and only leuB. Rather, all actively transcribed genes (e.g. gyrase) will experience an increased rate of mutation at any given time regardless of the effect of those mutations.

The 999,999,999,998 was again the right number for an an experience of same kind of environmet over millions of years.

That makes zero sense. That number is a direct reflection of the random mutation rate in those bacteria, including those out in the wild.

But you don't mention at all how many were the none beneficial mmutations in that particular event. that i think would be very helpful to to estimate any probability rate.

It will be the same as the rate of leuB- reversion for all genes that are transcribed at the same levels as leuB-. That is what Wright et al. demonstrated in this paper. They even replaced the wild type leuB promoter with a lac promoter. They then used IPTG to upregulate leuB. They observed the same phenomenon as with the native leuB promoter. Therefore, the effect is tied to transcription, not an ability to directly sense leucine in the environment and guide mutations specifically to the leuB gene.


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Replies to this message:
 Message 72 by shadow71, posted 09-13-2011 4:41 PM Taq has responded
 Message 74 by zi ko, posted 09-16-2011 3:44 PM Taq has responded

  
Taq
Member
Posts: 8482
Joined: 03-06-2009


Message 73 of 296 (633338)
09-13-2011 4:51 PM
Reply to: Message 72 by shadow71
09-13-2011 4:41 PM


Re: beneficial mutations
Do you agree that this specificity is not compatable with Neo-Darwinism as it was expressed up until the 1960s?

No, I do not. These findings fit quite well with the random mutations described by the Lederberg's, Luria, and Delbruck. These mutations are random with respect to fitness. As I discussed, this mechanism also produces neutral and detrimental mutations through the same mechanism. In fact, this elevated mutation rate is occuring in housekeeping genes even in the presence of leucine when the bacteria does not need any mutations whatsoever.


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Taq
Member
Posts: 8482
Joined: 03-06-2009


Message 80 of 296 (634339)
09-20-2011 7:21 PM
Reply to: Message 78 by shadow71
09-18-2011 7:08 PM


Re: beneficial mutations
My question is does directionality favoring more actively transcribed genomic regions where more revelant genes may be more likely transcribed concur with the Neo-Darwinism of the late 1960s?

Yes, it does. Randomness, as it was defined, was compared to fitness. This study shows the same thing. The mutation rate in the leuB gene is the same whether or not the bacteria need a mutation in that gene.

What would not comport with the definition from the 60's is a mechanism that sensed a specific environmental condition and specifically mutated a specific gene for a desired outcome. That is clearly not what we are seeing here.


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Taq
Member
Posts: 8482
Joined: 03-06-2009


Message 81 of 296 (634341)
09-20-2011 7:27 PM
Reply to: Message 74 by zi ko
09-16-2011 3:44 PM


Re: beneficial mutations
So you accept organisms are able to change their DNA expression patterns in responce to the environment.

Of course. What does this have to do with mutation?

But where this interaction stops?

It stops short of guiding mutations.

If you accept that there is a mechanism for this, why this mechanism function does not reach to the point to involve inherited changes in genome?

Because the mechanisms that turn genes on and off do not change the DNA sequence. They change the binding of RNA polymerase to the upstream portion of the gene. There is nothing in this process that copies DNA into new DNA or changes the base sequence of DNA.

I am talking only about nature,s own intelligence, that paves the way to random mutations regarding fitness, but not at all random regarding to life percervence.

You are talking about things you have no evidence for.

Note that nature intelligence, so evident around us , man's brain the outmost examble,can equally be a result of evolution, with no supernatural involvement if you wish. It is a matter of belief choice.

Or we can get rid of beliefs altogether and follow the evidence. So what evidence can I follow that will show me how mutations are not random with respect to fitness. Would you agree that this evidence is not found in this Wright et al. paper?


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Taq
Member
Posts: 8482
Joined: 03-06-2009


Message 88 of 296 (634416)
09-21-2011 11:29 AM


Reiteration
It is probably worth my time to reiterate my stance on the definition of random mutations and how it relates to the study in question. From my opening post:

quote:
Just to get it out of the way, I define random mutations as changes in the DNA sequence that are blind to the needs of the organism. IOW, mutations are random with respect to fitness. I am not saying that mutation rates are constant through time, nor am I saying that each base has an equal chance of being substituted, inserted, or deleted. With respect to the paper, I will attempt to demonstrate that the same mechanisms that produce reversions in leuB- organisms will also cause deleterious mutations in very important and vital genes as well as mutations which do not change the fitness of offspring.

IOW, the processes that create mutations are blind to the impact these mutations will have on fitness. Specifically for this study, the mechanism under question increases the mutation rate in all genes that are upregulated. This was confirmed by Wright et al. by replacing the wild type promoter of leuB with an IPTG inducible promoter (derived from the lac promoter if memory serves) that is independent of leucine concentrations in the environment. These mutations will run the gambit from lethal to strongly beneficial. For example, lethal mutations in vital housekeeping genes like DNA gyrase will be increased due to this mechanism.

Edited by Taq, : No reason given.


  
Taq
Member
Posts: 8482
Joined: 03-06-2009


Message 91 of 296 (634522)
09-22-2011 11:28 AM
Reply to: Message 89 by zi ko
09-21-2011 9:51 PM


Re: beneficial mutations
Guiding had been completed by all preceded paving work.

Why does this paving work only work 1 time out of every 500 million divisions?

The only difference between me and you is that I accept nature's intelligence, which i see all over around, while you accept randomness as the cause of mystery of life and evolution as well without any evidence. We are both just believers.

No belief is necessary. I have shown through objective evidence that mutations are random. "Nature's intelligence" is nothing more than a metaphor you use. It is not an objective measure of anything as your posts have shown.

You are right . Mutations are random, but only to fitness, not to life perseverance.

Please show us how you determined this with reference to the results in the Wright et al. paper.


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Taq
Member
Posts: 8482
Joined: 03-06-2009


Message 96 of 296 (634689)
09-23-2011 12:05 PM
Reply to: Message 94 by shadow71
09-22-2011 4:19 PM


Re: Do you agree that this specificity is not compatable with NeoRe: beneficial mutations
Just trying to establish if Wright's paper does in fact comply with the Darwinian theory up to the modern synthesis,

IMHO, I have established that the findings in the paper are random with respect to fitness. Therefore, it is consistent with the Modern Synthesis. The authors found that there is no specificity for beneficial mutations in leuB, nor is there specificity for the leuB gene in general. Even more, the rate at which the leuB- reversions occur (1 in every 500 million divisions) rules out a deterministic process that produces specific mutations in leuB.

If you disagree with this assessment then I would be more than happy to further discuss the results found in the paper.

or if in fact Wright is of the opinion that her findings in the paper are not compatable with Darwinian theory up to the modern synthesis.

The problem here is that Wright et al. cite work done by Weismann in 1893, well before the Modern Synthesis was complete. The author's opinion of what the Modern Synthesis is or isn't seems to differ from the general opinion of most scientists.


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