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Author Topic:   Evolution Theory Issue - Great Debate -mindspawn and RAZD only
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 38 of 65 (689914)
02-06-2013 11:32 AM
Reply to: Message 37 by RAZD
02-05-2013 5:34 PM


Re: time wasted, and revisiting mutations again
Fitness is determined by selection mechanism, for a genetic change to improve fitness it must be expressed in the phenotype, and it must be tested by selection to show a benefit for the individual/s with the genetic change.
If it does not involve novel traits/functions/features then it can't increase fitness (at best it would be neutral), so this process must involve novel traits/functions/features to affect fitness to meet your criteria.
No problem with this.
The word "complexity" has no real meaning to me, to say that something is "more complex" does not provide any predictive quality regarding fitness or evolution. At most it is an emergent facet that is 99% in the eye of the beholder. You have defined it to be additional coding genes, but you don't use it that way, and it has connotations that distract from the debate. Nor can you predict when such duplications occur.
I may have used it in its wider sense once or twice, but generally I have been pretty consistent in my use of the word complexity.
What I have said is that we do not know what the original life form DNA was like -- and that makes any concept about what was or was not included untestable.
Could it have had long strands? yes
Could it have had short strands? yes
We don't know.
But I would be surprised if genes that evolved recently would have been around, or that any genes that have survived from that time remain unchanged
Ok so you are admitting that its likely that evolution would involve additional coding genes over time? Great! Or is this still a strawman? I'm not sure? Anyway let's use that as a basis for further discussion and get on with it.
That you don't understand that these are still mutations is part of your problem in understanding selection in specific and evolution in general.
I'm no expert in genetics, only recently learning this stuff, but what you are saying about allele combinations being mutations is frankly, very wrong, and we should have concluded on that basic point many many posts ago:
Mutation - Wikipedia
In genetics, a mutation is a change of the nucleotide sequence of the genome of an organism, virus, or extrachromosomal genetic element.
(if the nucleotide sequence is identical to one of the alleles of a parent, there is no mutation)
Genetic Variation Definition, Causes, and Examples
Genetic variation occurs mainly through DNA mutation , gene flow (movement of genes from one population to another) and sexual reproduction.
(you see that, mutation OR sexual reproduction cause variation)
Genetic variation - Understanding Evolution
Without genetic variation, some of the basic mechanisms of evolutionary change cannot operate.
There are three primary sources of genetic variation, which we will learn more about:
Mutations are changes in the DNA. A single mutation can have a large effect, but in many cases, evolutionary change is based on the accumulation of many mutations.
Gene flow is any movement of genes from one population to another and is an important source of genetic variation.
Sex can introduce new gene combinations into a population. This genetic shuffling is another important source of genetic variation
(you see that, mutation OR genetic shuffling cause variation. Gene combinations is not seen as mutation)
Natural Selection - Understanding Evolution
If you have variation, differential reproduction, and heredity, you will have evolution by natural selection as an outcome. It is as simple as that
Simple as that! Variation can occur through mutation or new gene combinations, either will lead to evolution. You do NOT need mutation to get evolution.
Could we kindly conclude on the word "mutation", that its a different process to new gene combinations inherited from the alleles of the two parents? Mutations are changes within nucloetide sequences. The new sequences are not found in the alleles of either parent.
Please read the following carefully for signs of allele combinations being mutations
Mutation - Wikipedia

This message is a reply to:
 Message 37 by RAZD, posted 02-05-2013 5:34 PM RAZD has replied

Replies to this message:
 Message 39 by RAZD, posted 02-07-2013 12:22 PM mindspawn has replied

  
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 40 of 65 (690010)
02-07-2013 2:09 PM
Reply to: Message 39 by RAZD
02-07-2013 12:22 PM


Re: ... revisiting mutations genetic change once again
Again, I suggest that we use "variation" or "variety" as this is much more applicable to the issue at hand: adding a new variety of coding gene that improves fitness in the breeding population.
This is much more concise and precise in terms of conveying the meaning intended without confusion, yes?
Your only objection to the use of the word "complexity" was that its subjective, difficult to measure. I introduced the thought that if an organism gains one coding gene this could be a measurable form of increased complexity. I therefore felt I have successfully dealt with the objection to using the word complexity, and haven't seen any points from you to the contrary. Until you deal with this, you are bringing up unnecessary additional topics. Anyway I'm willing to compromise, let's just not use the word complexity and I will try not to use alternative words like intricacy. Drop "complexity" from your list. However "variation" is not an adequate substitute, it conveys a completely different meaning to "complexity" and should be used for its own meaning.
They are still mutations in my book, but if you want we can use the term "genetic change" as proposed in Message 37:
In "your book"? Try reading up on basic genetics. If you want us to struggle through this topic without using words that everyone else agrees on, go for it, let us drop the use of the word "mutation".
If you will not compromise on what everyone else agrees with, makes this whole discussion pretty pointless though, because if you will not agree to easy consensus issues when you are obviously wrong, how will you ever agree to more controversial points? Its all a bit pointless really if you cannot have a win-win discussion based on truth.
Again, this is more concise and precise in terms of conveying the meaning intended without confusion, yes?
I don't agree one bit, and have never come across anyone else who misunderstands the word "mutation". It is one of the most used words in genetic literature, but if you RAZD would prefer not to use the word "mutation", let us do it your way.
By the way, please answer this, do you think that it is a reasonable assumption that the earliest organisms had relatively few coding genes compared to modern organisms?

This message is a reply to:
 Message 39 by RAZD, posted 02-07-2013 12:22 PM RAZD has replied

Replies to this message:
 Message 42 by RAZD, posted 02-07-2013 6:33 PM mindspawn has replied

  
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 43 of 65 (690032)
02-08-2013 1:45 AM
Reply to: Message 42 by RAZD
02-07-2013 6:33 PM


Re: ... revisiting mutations genetic change once again
By the way, please answer this, do you think that it is a reasonable assumption that the earliest organisms had relatively few coding genes compared to modern organisms?
I see you ignored this question, please answer it, it is core to this debate.

This message is a reply to:
 Message 42 by RAZD, posted 02-07-2013 6:33 PM RAZD has replied

Replies to this message:
 Message 45 by RAZD, posted 02-09-2013 11:54 AM mindspawn has replied
 Message 47 by RAZD, posted 02-09-2013 8:26 PM mindspawn has replied

  
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 44 of 65 (690100)
02-09-2013 2:30 AM
Reply to: Message 41 by RAZD
02-07-2013 5:18 PM


Re: mutation vs selection and the causes of novelty
When you make up numbers and do not justify them with any objective evidence you can get whatever result you want. IE - if only 3 genes contribute to trait "A" and there are 2 alleles of one, 3 of another and 6 of the third then there are only 36 possible combinations, which is fairly limited (imho) and it is also highly likely that all those variations already exist within a normal breeding population and are subject to immediate selection should the ecology change.
Traits that are highly conserved typically have few alleles, and traits undergoing strong selection typically have few alleles (as less fit ones are eliminated).
Everything you say here makes sense. Its just that my example is more related to reality than your example: let's get educated by the Magic School Bus : MOST traits are affected by many genes:
The Magic School Bus: From Genes To Traits: How Genotype Affects Phenotype
Due to such dramatic effects of small mutations, it was believed at the time that each gene codes for a particular trait. Today, it is possible to measure miniscule effects of multiple genes and it is well understood that the "one gene/one trait" paradigm is largely incorrect. Most traits are affected by many genes, and most genes are involved in the development of multiple traits.
And generally there are more than 6 alleles per locus across a population, so the numbers that I put forward are a lot more realistic than your "36" combinations per position. In fact, my numbers were conservative.
Actually it's objective fact that racing animal speeds have not increased significantly for some time -- you can look up the times and graph them.
The other side of sexual gene mixing is that breeders don't always get the "desirable" traits/functions/features in the offspring, because the trait mixing is random. Thus breeding winning males with winning female does not alway produce winning offspring
Its ironic that you keep using this single example to prove your point, when in message 27 you made it clear that you believe that cherry picking and confirmation bias are not sufficient evidence for making a good point. Let's just agree to disagree on this point unless you have better evidence than cherry picking or confirmation bias.
I would be extremely surprised to find that you would not need to change any of the gene sequences to get from the genome of one Kangaroo species to another, to say nothing of getting to the Tasmanian Devil genome.
(I was referring to the Tasmanian wolf - it had many kangaroo-like qualities, and its predator's jaw is comparatively weak for a predator)
We are not going to conclude this argument based on cherry picking or what would surprise you. Already I have posted evidence , and even your horse example proves that traits can be emphasized through variation and selection. Put a population together that is selected for a specific trait, and there's a chance that one of those will have a unique combination of genes that emphasizes the trait more than seen in the original population. This emphasis of traits is both logical and observed, even if its observed to taper off quite rapidly near its peak as you pointed out (bell curve).
Could we kindly drop this discussion, with either consensus of the "bell curve" of the observation of traits through selective breeding (or natural selection in nature) , or alternatively just agree to disagree until most mammals are sequenced which will conclude the argument in my eyes.
... and yet, curiously, even if your claim is true, evolution will continue to be true for the development of novel traits/functions/features, so no it is not really a challenge to the theory, per se, so at most it would need a slight adjustment for an additional mechanism to account for novel coding genes. Theories are approximations of reality and these approximations improve with each adjustment. For instance Newton's law of gravity is an approximation of how gravity works, Einsteins relativity improves the accuracy of that approximation and defaults to Newton's law in specific cases (such as we normally experience here on earth).
Its not a challenge to your theory, which includes the possibility that genes were already there from the start, which is the creationist position as well. The introduction of new additional novel coding genes would be essential to most evolutionists projection of evolutionary processes from first-life.
I agree with other processes of evolution, but not the theory of evolution's claim to explain the existence of modern life forms (that do have many coding genes)
okay let's use "coding gene duplication" seeing as that is your last definition.
Evolutionists claim its not just through duplication that novel coding genes come about, I used the words "gains one coding gene" recently, and feel that's a better definition of complexity. An organism gains complexity if it gains a coding gene.
Change in the composition of hereditary traits occurs through genetic change/s.
Changes in the frequency of their distribution occurs through selection and genetic drift.
Note that genetic drift occurs when individuals die by stochastic events (volcanoes, earthquakes, falling trees, etc) unrelated to fitness. Like selection it only operates to remove traits from breeding populations, and thus also does not result in the development of new traits
I understand what you are saying about selection, yes it can only work on the existing traits, and only variation can emphasize a trait. So we have consensus on selection.
In my defense I believe selection certainly does contribute to new traits because it causes a trait to be emphasized thoughout a population, and therefore there will be a wider variation of that trait in each subsequent generation in which the population having that trait grows. (there is more chance of variation in a large population than in a small population)
I don't see any point in using a term where there is disagreement on the meaning, as that is a sure path to confusion.
So let's use "genetic change/s" to be clear. One can also use specific subcategories if greater clarity is needed.
We can't really replace words, especially since we have no consensus of what the original word means. (that doesn't make any sense)
But we can use the phrase "genetic change" (doesn't this mean genetic variation?). Anyway let's use the term if you like. So to clarify, you are including variation through sexual reproduction (new gene combinations in the offspring) when you use the phrase "genetic change"?
Edited by mindspawn, : No reason given.
Edited by mindspawn, : clarification

This message is a reply to:
 Message 41 by RAZD, posted 02-07-2013 5:18 PM RAZD has replied

Replies to this message:
 Message 46 by RAZD, posted 02-09-2013 2:56 PM mindspawn has replied

  
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 48 of 65 (690184)
02-10-2013 5:07 AM
Reply to: Message 45 by RAZD
02-09-2013 11:54 AM


Re: getting ready to move on?
Power out last night just as ready to post this. Temp power now. Foot of snow outside. Fun.
lol, I don't envy you. We don't get snow here , way too cold for me.
Curiously, I believe (opinion) that it is possible that many of the original coding genes have been lost or changed, and that the number of original genes is therefore rather irrelevant.
Sorry, you have said this before, thanks for answering again.
That new coding genes are produced is not a major conundrum for the theory of evolution, as this would occur through the basic process of evolution from generation to generation:
This is an assumption.
I've included some words here that we have not discussed yet - stochastic, gamete, zygote, for instance - but I don't anticipate any (mis)understanding problems with these words.
If you agree with this (still somewhat simplistic picture) we can move on to examples of this process.
Like I have said before, I agree with most processes of evolution. But not processes that involve the adding of coding genes. So some applications of those processes are merely theoretical in my eyes but don't work in the real world. I have no issues with the terminology.
Edited by mindspawn, : No reason given.

This message is a reply to:
 Message 45 by RAZD, posted 02-09-2013 11:54 AM RAZD has seen this message but not replied

  
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 49 of 65 (690185)
02-10-2013 5:50 AM
Reply to: Message 46 by RAZD
02-09-2013 2:56 PM


Re: regroup
It's not cherry picking when all the evidence points in the same direction ... unless you can show a case where speed keeps increasing without limit -- and without genetic change -- as you claim
I believe the horses have not been given enough time for one, and secondly the entire population has not been bred for speed. If all horses were bred only for speed, and most of the population was changed (as occurs in nature when a new trait becomes dominant throughout a population via selective pressure) then you can apply the horse example.
But why keep arguing this point, I agree that the most significant changes occur rapidly , as per your "skew curve distribution", this makes sense. Even if we keep to that view, my point is made, variation through new gene combinations leads to new traits. (speed in horses). New gene combinations are one of the main sources of variation.
Organisms are compromises of traits to fit ecologies, and you can't continually modify one trait/function/feature without affecting others. Look at the cheetah for instance compared to the leopard: it is very fast, but it does not have much endurance and its bones are fragile by comparison. It also has a much less varied genome than the leopard.
This is my point you are making for me, the organism will adapt through new gene combinations until reaching the best balance for the new environment. Offspring are a new combination of the genes of a parent, and this is one process of evolution that can emphasize favorable allele combinations until they are fixed into a population.
Do you want to discuss evidence for this or equivocate on what you mean?
Let's discuss the evidence.
Edited by mindspawn, : No reason given.

This message is a reply to:
 Message 46 by RAZD, posted 02-09-2013 2:56 PM RAZD has seen this message but not replied

  
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 50 of 65 (690186)
02-10-2013 6:48 AM
Reply to: Message 47 by RAZD
02-09-2013 8:26 PM


Re: coding gene duplication, increased fitness, examples
Here we see a documented duplicated protein coding gene, one that provided beneficial use of new food source and increased fitness. QED. Let the denial and equivocation commence
E-coli:
The citT is normally silent, being re-activated via duplication. The duplication event did not create an extra coding gene, just re-acti
vated an old silent gene that was already common in the population.
.. and when we have a trait that was "already there" (as in the Chlorella) the response is immediate after the selection pressure is applied.
Chlorella:
Did the chlorella example involve extra coding genes? This example of yours seems to be referring to multi-cellular life.
Polyploid and tetraploid organisms are common. This rarely does add fitness because there is a certain genetic hardiness that comes from having "backup" chromosomes, the organism becomes less susceptible to damaging mutations. However as is consistently observed, if the duplicates are coding, then the organism loses fitness, it is the non-coding duplications of polyploidy and tetraploidy that sometimes add fitness. So these are not examples of additional coding genes.
As Many Exceptions As Rules: Haploid, Diploid, And Those You Should Avoid
This still leaves the question as to how this species overcomes the problems in embryonic and fetal development attributed to tetraploidy. The unbalanced gene function in tetraploid cells has some how been overcome in fetal vizcacha rats. A study in 2008 showed that X-inactivation does indeed silence all but one copy of the X chromosome in the T. barrerae.
Wholesale duplication of chromosomes, not just genes. Novel traits/functions/features derived. A new species formed as a result. Fitness is observed by survival of the new species.
Evolution has no problem duplicating parts of gene sequences, whole gene sequences, whole chromosomes, and whole genomes and then utilizing those duplicated sequences etc in new ways by genetic changes to the otherwise redundant sequences.
I'm looking for additional coding genes, not silent copies.

This message is a reply to:
 Message 47 by RAZD, posted 02-09-2013 8:26 PM RAZD has replied

Replies to this message:
 Message 51 by RAZD, posted 02-10-2013 3:11 PM mindspawn has replied

  
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 52 of 65 (690251)
02-11-2013 6:24 AM
Reply to: Message 51 by RAZD
02-10-2013 3:11 PM


Re: coding gene duplication, increased fitness, examples
That's too bad. I've got a lovely view outside my windows.
It's 40F today ... inside 22F outside. Not too bad, like winter camping. We have gas so can cook, and an extension chord from neighbor's generator to run sump pump and wifi -- the important things. Typing with gloves on is ... interesting.
Power back on now, heat is working, the gloves are off ... .
Great! Yes the snowy landscapes make great viewing.
New variations are caused by new genetic sequences that result in new traits/functions/features. Again this is a stochastic process and it is not caused by selection
I thought we have already agreed on selection. I also agree with what you are saying here regarding new features and new genetic sequences.
The citT is unable to process citrate in an aerobic environment, it is there for using citrate in an anaerobic environment. Thus it is not "re-activated" as you claim.
This is like a fish breathing air or a human breathing water.
The duplication itself does not "activate" the citT gene in the aerobic environment, it is the two previous mutations that enable this to happen.
This is like a fish getting air lungs before being placed in air or a human getting gills before being placed in water.
The CitT gene is known to be responsible for the Cit+ phenotype:
The Escherichia coli Citrate Carrier CitT: a Member of a Novel Eubacterial Transporter Family Related to the 2-Oxoglutarate/Malate Translocator from Spinach Chloroplasts - PMC
Restriction analysis of plasmid DNA isolated from several Cit+ clones showed that all contained pUC19 with the 1.5-kb HindIII/BamHI insert carrying citT. One of the pUC19-citT plasmids was transformed again into E. coli DH5α and plated on Simmons’ citrate agar. In this case, all transformants were able to utilize citrate, confirming that citT is responsible for the Cit+ phenotype
As shown above, the trait already existed in the CitT gene, however this gene was normally silent in the population of your example: "This duplication immediately conferred the Cit+ trait by creating a new regulatory module in which the normally silent citT gene is placed under the control of a promoter for an adjacent gene called rnk. The new promoter activates expression of the citrate transporter when oxygen is present, and thereby enabling aerobic growth on citrate"
The gene was normally silent, needing a promoter, when it was duplicated, this established a new but weak promoter for the gene which was then activated in aerobic environments. This whole description is about a citrate transporter gene normally silent that was then activated. The promoter sequence for the gene seems to have undergone a change, but NOT the gene itself. They do not discuss the other gene which appears to remain silent, and seems to be inverted which would disable it. I see this study as more about promoters than contributing towards any evidence of the evolution of coding genes.
And "rarely" still means that occasionally it is beneficial, and that is all that is required. Evolution is not always a "lived happily ever after" story.
Yes, non-coding duplications are occasionally beneficial. This does not contribute towards this thread which is about additional beneficial coding genes.
The point of the Chlorella example was to show you what "re-activation" of "an old silent gene that was already common in the population" looks like in the real world.
It happens virtually instantaneously, within one or two generations, and doesn't take 30 years and thousands of generations.
Furthermore, we KNOW that this was NOT a case of "re-activation" of "an old silent gene that was already common in the population" because it did NOT occur in the OTHER E. coli populations without the mutations. Only in the populations where the sequence was modified through three mutation events were they capable of processing citrate in an aerobic environment, a new ecological niche for them, and a beneficial source of new energy.
I'm a little confused here. Are you referring to E.coli or chlorella? The E. coli example was about the silent gene, the chlorella example was referring to the ability of chlorella cells to join together into multi-cellular organisms. My question related to whether the chlorella example was relevant to our coding gene discussion, your answer seems to relate to E. coli. Can you explain the relevance of the Chlorella example please (the single cell green algae which adapts under predatory pressure).
And yet, curiously, we still see cases where the organisms are fit, they survive, they breed.
What this shows is that gene duplication occurs at many levels and is not a necessarily rare event, nor is it necessarily lethal. This is especially true in the plant kingdom.
You mention beneficial duplication, a process I believe in. You seem to be missing the word "coding" when you present your evidence. I said the following and fail to see why your reply does not mention coding regions:
"However as is consistently observed, if the duplicates are coding, then the organism loses fitness."
I don't know how you have managed to miss the word "coding" in all my posts so far. When we defined what a coding gene is, we actually defined what a gene was, instead of delving into the word "coding". This is possibly my mistake as I always assumed that everyone who discusses these things already knows what a coding gene is, and assumed you noticed that I had deliberately used the phrase "coding gene" rather than just "gene" in most of my posts. I now see that this important definition has been left out.
You get genes that code for proteins (they produce proteins) and you get pseudogenes that are dysfunctional. These pseudogenes are often described as "disabled" or lacking "expression"
Pseudogenes are dysfunctional relatives of genes that have lost their protein-coding ability or are otherwise no longer expressed in the cell.[1] Pseudogenes often result from the accumulation of multiple mutations within a gene whose product is not required for the survival of the organism.
Although some do not have introns or promoters (these pseudogenes are copied from mRNA and incorporated into the chromosome and are called processed pseudogenes),[2] most have some gene-like features (such as promoters, CpG islands, and splice sites), they are nonetheless considered nonfunctional, due to their lack of protein-coding ability resulting from various genetic disablements (premature stop codons, frameshifts, or a lack of transcription) or their inability to encode RNA (such as with rRNA pseudogenes). The term was coined in 1977 by Jacq et al.[3]
I am aware that pseudogenes sometimes add fitness, but my focus is on protein-coding genes because these have shown to have a high degree of functionality in the genome and are more easily counted and defined.
You're moving the goalposts.
Not at all. You have shown an unusual lack of interest in the word "coding" that I have been consistently using throughout the thread. Hopefully this is now sorted out, a coding gene is one that codes for proteins. Pseudogenes, silent genes, disabled genes are non-coding. Any evidence you put forward that the re-enabling or creating of pseudogenes adds to fitness is irrelevant to this discussion.
In post 13 I emphasized that we were referring to coding genes, definitely no moving the goalposts:
These have got be ADDITIONAL. Not a mutated gene. NEW ADDITIONAL NOVEL genes. I have to be very careful with the wording here, because you can even have new non-coding sequences that add to an organisms fitness, and I am not referring to non-coding sequences either
Proof of additional coding genes that are beneficial would help your case, that is what I have been asking for all the time. I have already agreed that non-coding regions add fitness (post 13), and I have also agreed with the process of re-activating of a de-activated gene adding fitness in my post 21:
All the other processes we agree on (point mutations, disabling of a gene, subsequent enabling of a gene, deletions, duplications).
Even in post 1, you quoted me twice asking for proof of additional CODING genes, so this requirement has always been there from the start of this thread and there has been no moving of goalposts, maybe you have misunderstood my position.
Edited by mindspawn, : No reason given.
Edited by mindspawn, : No reason given.
Edited by mindspawn, : No reason given.
Edited by mindspawn, : No reason given.

This message is a reply to:
 Message 51 by RAZD, posted 02-10-2013 3:11 PM RAZD has replied

Replies to this message:
 Message 55 by RAZD, posted 02-16-2013 6:23 PM mindspawn has replied

  
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 53 of 65 (690812)
02-16-2013 10:35 AM


Hi RAZD, while discussing these additional coding genes with you, I am aware that for you in particular the need to prove the process of additional coding genes could be a strawman argument, because of your acceptance of the possibility that organisms could have started out with many coding genes, which is very similar to the creationist position. Due to this its possible you have seen less of a need to prove this process and are less committed than other evolutionists to prove the position, your focus being on other evolutionary processes that I also do believe in.
Other evolutionists acknowledge the increases in complexity , including coding genes over time as essential building blocks in explaining the majority of organisms in current existence. I therefore am going ahead to deal with their evidence as per the peanut gallery, feel free to object if you feel its inappropriate in this thread.

Replies to this message:
 Message 54 by RAZD, posted 02-16-2013 11:57 AM mindspawn has replied

  
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 56 of 65 (690924)
02-18-2013 4:07 AM
Reply to: Message 54 by RAZD
02-16-2013 11:57 AM


Re: new topic perhaps
You misunderstand me, badly.
If you go back and read the early posts I believe\hope\trust you will find that while I basically disagree with you, I have probably cut you more slack than other members of the forum would, that I have looked at it with a more open minded approach, while still remaining skeptical.
I find your manners pretty good, I find your comprehension of my position a little lacking, you are too focussed on my actual wording to have a real good understanding and debate on the core issues at stake.
Feel free to start a thread on that -- as that allows people to respond to you -- the peanut gallery is not for debate with participants of the Great Debates. Some will be more than happy to discuss your hypotheticals on an open thread.
Fair enough.

This message is a reply to:
 Message 54 by RAZD, posted 02-16-2013 11:57 AM RAZD has replied

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mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 57 of 65 (690925)
02-18-2013 4:24 AM
Reply to: Message 55 by RAZD
02-16-2013 6:23 PM


Re: coding gene duplication, increased fitness, examples
Sorry for the delay in response -- I've been busy with kitchen mods and have been too tired to do this topic justice. It takes me hours of concentrated effort to review and put together what I feel is a proper response to your questions/arguments, and I hope you appreciate that this isn't an "off the cuff" reaction.
I do appreciate that, no problem.
The gene was "silent" in aerobic environments\ecologies because it is used in anaerobic environments\ecologies. As I noted in my analogy previously, this is like you being underwater where your use of lungs is "silent" because you cannot use the oxygen in the water.
Aerobic and anaerobic metabolisms are as fundamentally different as fish breathing air and humans breathing water.
I feel I did acknowledge that and said basically the same thing in my posts. I see you are not one to back down on a point, but you are really wasting your time with this particular example and showing that you are missing my whole point.
You asked for it to be a coding gene: you got that.
You example fails to show that the duplicated gene was coding. In fact your article seems to indicate that the duplicated gene was inverted, which would disable it. I already said this. Maybe you like to blur the point with excessive posts, but please just move onto the next study, your current one is all about a duplication event that activated a promoter, but you fail to give any evidence that the duplicated gene itself was protein-coding. The normally silent gene was activated, this is no additional gene, but is a silent gene that activated using a new promoter sequence. In the end, we have a gene that was always there, being activated, and another gene being duplicated but non-coding. No additional coding genes.
Edited by mindspawn, : No reason given.
Edited by mindspawn, : No reason given.
Edited by mindspawn, : No reason given.

This message is a reply to:
 Message 55 by RAZD, posted 02-16-2013 6:23 PM RAZD has replied

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 Message 59 by RAZD, posted 02-18-2013 9:07 PM mindspawn has replied

  
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 60 of 65 (691012)
02-19-2013 4:48 AM
Reply to: Message 59 by RAZD
02-18-2013 9:07 PM


Re: Denial and equivocation are not rebuttal arguments.
Let me see if I get this right then: you want a coding gene duplication that suddenly becomes a completely new coding gene that never existed before ... is that correct?
Suddenly or slowly, yes , I am asking for an explanation for how the number of coding genes can increase in number in an organism.

This message is a reply to:
 Message 59 by RAZD, posted 02-18-2013 9:07 PM RAZD has replied

Replies to this message:
 Message 61 by RAZD, posted 02-19-2013 9:01 PM mindspawn has replied

  
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 62 of 65 (691074)
02-20-2013 7:35 AM
Reply to: Message 61 by RAZD
02-19-2013 9:01 PM


Re: Denial and equivocation are not rebuttal arguments.
You can have a duplication of a coding gene, with additional modification in the genome such that the duplicated gene performs a function that the single copy does not perform. Example: the cit+ behavior in E.coli to metabolize citrate in an aerobic environment due to two mutations and the duplication of the citT coding gene.
True
Why does it take two copies for this to work -- if it was a cryptic\hidden\silent gene activated by the mutations, then why doesn't it work with one copy? I would suspect that the transport protein being coded may be folded a different way, affecting how it functions, due to the proximity with each other, as the folding of a protein is as important (if not more so) as the molecular sequence.
You are not understanding the study. It was the new positioning of the duplicated sequence that allowed an aerobic promoter of ANOTHER gene to start working on the Cit gene. Can you see that? The duplication activated a different promoter when normally the gene was silent.
So instead of one silent gene, you had a duplication event, followed by one gene being activated in aerobic conditions and becoming Cit+ using another adjacent gene's promoter, the rnk gene (Quote: This duplication immediately conferred the Cit+ trait by creating a new regulatory module in which the normally silent citT gene is placed under the control of a promoter for an adjacent gene called rnk.)
First, "already there" -- when you start with a duplication -- your requirement -- you necessarily start with genetic sequences that were "already there" (cryptic\hidden\silent) and thus your criticism that the gene was "already there" is really a bogus dodge, a ruse you use to convince yourself that this is not new novel behavior\function.
The question is not whether those sequences were there, but whether the genetic coding behavior was modified and a function was being performed that was not present in the previous generation for it to be novel:
Would you agree that a novel gene\feature\function\trait would be one that did not exist in a previous generation?
yes, but remember I am not merely discussing novel genes. ...
Over 30,000 previous generations did not perform the cit+ behavior in aerobic conditions, ergo this qualifies as novel behavior according to the agreed definition.
Second, "duplicated gene was inverted" -- it isn't in this case, but why should this matter? I know you said "which would disable it" but this is not always the case. If you think about it there should be no difference to coding from promoter to terminator, as how would the molecular construction of the protein know?
I'm not disputing the novel function, the only dispute that I have had with your example, is that it did not add a coding gene, it merely activated an inactive gene. Thus the net number of active genes decreased by one (silent gene) and then increased by one (activated gene) reaching the original number with no net gain. One of the two duplicates remained silent. The fact that it added a novel function whilst being re-activated is in your favour, but it just isn't an additional gene, its a changed gene, which I have already acknowledged.
Since then I have another problem with your example, although these mutated e.coli gain temporary fitness in laboratory conditions, they lose fitness in the natural processes of osmosis found in nature. ie the mutation is damaging.
Your example would be better if it didn't revolve around silent genes.

This message is a reply to:
 Message 61 by RAZD, posted 02-19-2013 9:01 PM RAZD has replied

Replies to this message:
 Message 63 by RAZD, posted 02-24-2013 12:17 PM mindspawn has replied

  
mindspawn
Member (Idle past 2660 days)
Posts: 1015
Joined: 10-22-2012


Message 64 of 65 (691702)
02-24-2013 1:38 PM
Reply to: Message 63 by RAZD
02-24-2013 12:17 PM


Re: Denial and equivocation are not rebuttal arguments.
One is right after the other -- head to tail -- and not in a different location.
So why is the effect only seen once the duplication has occurred -- why doesn't that same promoter act on the single copy?
Is it because of the promoter or because of the coding gene? Or does a coding gene activating with a different promoter then produce a different (folded or altered) protein?
As far as I can see its the same protein produced, its own promoter did not activate the protein production. The new promoter activated the gene to produce proteins. Its affect is only seen after the duplication event, because the event involved more than just the duplication of that particular gene. Somehow the gene came under the influence of another gene's promoter. the studt does not give details how this occurred.
RAZD I want to explain my position so there is no confusion. My position is based on the assumption that the first prokaryote type organism had about 1000 coding genes as observed in modern prokaryotes. The figure "1000" isn't as important as the concept that most organisms have increased in number of coding genes over time, whatever the starting number was. This assumption does appear to be a strawman argument for you, because you have indicated its possible for the first organism to have had many coding genes, but it seems to be a discussion we are continuing with.
In essence I want to see how a 1000 coding gene organism can become a 1001 coding gene organism. Or a 21000 coding gene organism can become a 21001 coding gene organism. Now evolutionary theory does not require consistent additions, any organism can evolve decreases as well as increases in protein coding genes depending on what would improve fitness at that time. Thus a 1000 gene organism can become 999 genes. Then go back to 1000 genes. This still does not explain how evolution can claim additional coding genes over time.
This is why I believe your example is not good enough, to illustrate this , let's assume that region of the genome had ten genes:
CCCCCCCCCC (ten coding genes)
Then due to a lack of promotion, the one gene goes silent:
CCCCCSCCCC (9 coding genes and one silent gene)
Then there is a mutation event in which the silent gene is duplicated:
CCCCCSSCCCC (9 coding genes, two silent genes)
However we know this isn't exactly what happened because the one copy was activated due to an adjacent promoter from another gene now affecting it:
CCCCCSCCCCC (10 coding genes, one silent gene)
The net result is that the organism has returned to 10 coding genes, its original state before that original gene went silent. One of these genes has a changed promoter , it still produces proteins for nitrates, but is activated in different circumstances than before, so the organism has undergone a novel change, but has not increased in the number of novel genes. The great test is when the original silent gene also activates maybe under another set of environmental conditions, will the doubled protein production destroy the E.Coli? We do not know if the double up will kill it, because there has been NO increase in protein coding genes, there were ten, then nine, then ten in that region. Eleven coding genes could kill it, because a duplicated gene when both copies code for proteins often kills an organism. Or even a loss of fitness could occur, which seems to be the case anyway, because this organism lost its ability to survive during osmosis which always occurs in nature.
So your example is unrelated to the gain of additional coding genes over time, a process acknowledged as fundamental to most evolutionists.
ps , I'm really curious how they determined that the initial 12 populations of E.Coli were identical, this seems like a very strong statement for 1988 when full genome sequencing of E.Coli only occurred in 1997? Any lack of uniformity back then would change the entire interpretation of the evidence.
Edited by mindspawn, : No reason given.
Edited by mindspawn, : No reason given.

This message is a reply to:
 Message 63 by RAZD, posted 02-24-2013 12:17 PM RAZD has replied

Replies to this message:
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