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Author Topic:   Evolution Theory Issue - Great Debate -mindspawn and RAZD only
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 30 of 65 (689526)
01-31-2013 7:14 PM
Reply to: Message 29 by mindspawn
01-31-2013 2:53 AM


mutation vs selection
I took a lot of time to create an acronym, instead of politely asking me not to use that acronym, this is your response, to call my acronym blahblah? Nice one RAZD!
Understood, I spend a lot of time on my replies, and presenting information, and a lot of it seem to be ignored (or hopefully accepted without comment ). When you ignore parts of my posts, that is me talking past you - it all goes blahdeblahblahblah to you.
However, making up an acronym before you have established a need for it can interfere with communication and I would be prefer the longer sentence (less potential for confusion). The blahblah actually referred more to the definition of the acronym, btw, using terms that we haven't really addressed at this point. Your acronym seemed to me to be setting up a strawman that doesn't accurately portray how evolution necessarily works when novel features are developed.
I understand your sentiments, for the sake of argument, let us define complexity as additional coding genes. ...
What is a "coding gene" versus a "non-coding gene" and how do we tell them apart?
What I have in this regard is:
PHSchool.com Retirement–Prentice Hall–Savvas Learning Company
quote:
Concept 4: Basic Structure of a Protein-Coding Gene
A protein-coding gene consists of a promoter followed by the coding sequence for the protein and then a terminator.
The promoter is a base-pair sequence that specifies where transcription begins.
The coding sequence is a base-pair sequence that includes coding information for the polypeptide chain specified by the gene.
The terminator is a sequence that specifies the end of the mRNA transcript.
... If one organism has one more coding gene than another with an otherwise identical chromosomal organization, this is added complexity.
Okay, so then the walkingsticks presumably lost complexity when they lost wings and gained complexity when they gained wings?
Message 12: For instance we can look at the evolutionary history of walking sticks:
See Figure 1 from Nature 421, 264 - 267 (16 January 2003); doi:10.1038/nature01313 (reproduced below)
Walkingstick insects originally started out as winged insects (blue at start and top row). That diversified.
And some lost wings (red). And diversified.
And some regained wings (blue again). And diversified.
And one lost wings again (Lapaphus parakensis, below, red again).
And this doesn't even address the ones where one sex (usually male) has wings and the other sex doesn't (the red includes these, so it is hard to determine from this graphic how many times the female sex gained and lost wings independent of the winged males).
  • Is one with wings "more complex" than one without wings?
  • Is one without wings "more complex" than one with wings?
  • Is one with wingless females and winged males "more complex"?
Does the relative apparent differences in complexity predict which form is more fit for the ecology?
Where do the female wingless male winged walkingsticks fit into this paradigm - half complexity between winged and wingless?
Are all winged species equally complex?
Are all non-winged species equally complex?
... If one organism has one more coding gene than another with an otherwise identical chromosomal organization, this is added complexity.
And we compare the number of "coding genes" between A. dubia and H. sapiens ...
Message 12: A Sample of Species and Genome Size (in base pairs)
Amoeba dubia
670,000,000,000
Homo sapiens
2,900,000,000
... which is more complex?
And I need to have your consensus that most organisms have increased in coding genes from the original organism. Do you think its possible that the original organism started with as many coding genes as a human? YES or NO
As I don't know what the original organism started with, I can't really say. What I can say is that the process of evolution has resulted in occasional gain in the number of genes (coding or otherwise) and occasional loss in the number of genes (coding or otherwise), and that both cases could result in novel traits\functions\features in the phenotypes within a breeding population.
I agree with the confirmation bias and the cherry picking, but what I did was give SOME support for my position. I am not claiming a concluded principle, neither do I claim that the lack of support for your position is a concluded principle. It merely weakens the theory of evolution's ability to explain all life-forms to the status of an hypothesis, if you have no evidence for organisms gaining novel coding genes that increase fitness.
In your opinion. We know that mutations of all types can be either deleterious, neutral or beneficial, so citing only deleterious instances does not weaken the knowledge that mutations can be either deleterious, neutral or beneficial. Citing instances of black swans in one location does not weaken the position that white swans are also known in other locations.
True, completely agree with this. New species and new traits can develop slowly , generation to generation, ... This is macro-evolution at work through minor changes, generation to generation.
Indeed. As was observed in the Pelycodus fossil record (at the top of the diagram the population divides into two daughter populations, thus showing a speciation event).
And as is observed with the Greenish Warbler populations that show minor changes as you go from one end of the ring species to the other, but reaching the point where two population overlap but do not interbreed because these minor differences are sufficient to block breeding. The features\functions\traits in one population are different from the features\functions\traits in the other population.
... without the requirement of an additional new novel coding gene, or a definite duplication mutation ...
And here we run into trouble with this concept of yours regarding "coding genes" ... why is it necessary to only consider "coding genes" when looking for novel genes\features\functions\traits?
Is not the new trait a novel one?
The phrase "genetic sequence" seems ambiguous to me, so I can't answer that for sure. ...
A point mutation does not always change the sequences within a gene.
Let's not equivocate between gene and genetic sequence.
Assume a genetic sequence (whether it is a whole gene or not, or several genes is not important yet),
say ... AAGTCCGTAAGGG ... (where the ... indicate that the sequence continues to each side of the section in question),
Can you add or delete a molecule at any point in this sequence without changing the sequence?
... If the sequence changes, that does seem like a mutation, ...
Indeed, whether it is a point mutation or a complete gene duplication, any change to the overall genetic sequence is a mutation, and one that did not exist in the genome before the mutation, yes?
... but if allele frequencies change, that is not a mutation. ...
Correct, that is selection or drift.
... Thus the genetic make-up of the population can change over time through non-mutational processes.
Not quite clear here. Changing the frequency of alleles does not change the genetic make-up of the breeding population, loss of alleles through selection or drift changes the genetic make-up of the breeding population, but this does not add new genes\features\functions\traits.
Selection, drift, etc do not develop new genes\features\functions\traits - that only occurs through mutations.
Not every mutation results in new genes\features\functions\traits as some are not in hereditary sections of DNA (mutations within skin cells are not hereditary for example), some mutations are deleterious, some are neutral and some are beneficial, but they may not add up to novel features\functions\traits until additional generations of added mutations have occurred.
Whether a mutation improves fitness means that the mutation is expressed in the phenotype so selection can occur, and that selection operates on the whole individual, not necessarily one specific genetic sequence.
I disagree that selection mechanisms do not cause novel traits; through selection the allele frequency that enhances that feature/trait can be emphasized in the population of the very next generation. Continuous selection can cause a new feature/trait/function to dominate in a population (without the need for novel genes).
But that novel trait was not developed by selection, rather selection operated on its existence in the population to make it dominant. What made it novel was the genetic mutation/s that resulted in the selectable trait.
So now we add "coding gene" to our list of terms -- can we drop "intricacy" if you want to use complexity?
  1. evolution (process) - yes
  2. theory (scientific) - yes
  3. hypothesis (scientific) - yes
  4. the theory of evolution - yes
  5. novel genes\features\functions\traits - yes
  6. complexity - ... maybe ... (see 'n')
  7. speciation (divergent) - yes
  8. fitness - yes
  9. god hypothesis - (dropped for now)
  10. hidden gene hypothesis - (dropped for now)
  11. micro-evolution (= 'a' above) - (drop?)
  12. macro-evolution - (drop?)
  13. intricacy (= complexity) - (drop?)
  14. coding gene - needs to be defined
Enjoy
Edited by RAZD, : .
Edited by RAZD, : clrty
Edited by RAZD, : link

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.


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This message is a reply to:
 Message 29 by mindspawn, posted 01-31-2013 2:53 AM mindspawn has replied

Replies to this message:
 Message 31 by mindspawn, posted 02-01-2013 3:01 AM RAZD has replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


(1)
Message 32 of 65 (689636)
02-01-2013 11:01 PM
Reply to: Message 31 by mindspawn
02-01-2013 3:01 AM


mutation vs selection and novelty
I will take this as a badly communicated "YES" to my question. You truly seem to believe its possible rather than impossible that the very first organism had as many coding genes as some modern organisms like humans. I don't want to mock, but that is truly ridiculous. Utter nonsense. If your answer is "NO" then just say it. I have never heard of such an utter copout to the matter of complexity.
Then you are intentionally misunderstanding what I am saying.
When it is impossible to know what the first organism was like, then all you have are guesses -- you do NOT have yes or no answers with any validity.
Nor is it necessary to fixate on the possible first life to discuss novel traits/features/functions and the genetic basis for them: we can see that novel traits evolve.
What you have asserted here is the argument from incredulity, a logical fallacy. Not an evidence based conclusion.
If I ignore anything its because its repeats of detail that I thought we have already discussed and concluded and agreed, ...
This is fine, I have a tendency to overstate things to ensure we are talking about the same thing, and I do tend to be pedantic in this regard.
... or possibly introducing new minor side issues when we already have too many side issues to deal with.
Side issues can be a problem, so yes please try to keep me focused on the topic.
As far as introducing a strawman, I see that part of this discussion is to show you that evolution requires this process of gaining new novel coding genes. So it appears to be a strawman but the process is essential to evolution. ...
Curiously, I don't have a problem with evolution processes developing or losing novel traits/features/functions and the genetic basis for them via mutations and selection.
What I have some concern is with your apparent fixation on one particular mechanism to be the only way to get this result. That is the strawman issue.
... The alternative , that the first lifeform contained as many novel coding genes as the most extensive existing today is ridiculously laughable. ...
What I am saying is that discussion of the first life is unnecessary to the discussion of the evolution of novel traits/features/functions and the genetic basis for them.
We can focus on the evolution of life since the development of eukaryotes from prokaryotes for instance, as much more is known about life at that point in time, and we are still going from single cell life to multicellular life forms. Or we can focus on life since the formation of multicellular life forms. Or we can focus on later developments. There is no particular point where we absolutely need to start in discussing the formation of novel traits/features/functions and the genetic basis for them.
Is the blue-green algae alive now the same as the blue-green algae alive then? It has undergone billions of years of evolution, yes? Is it more "complex" (have more coding genes)? Is a sponge more complex than single cell life?
... Thus the thought that there could have been many coding sequences simultaneously appearing in the first organism is hilarious, and so a novel coding gene gaining process is inevitable to evolution.
More argument from incredulity. They don't all have to be in a single organism, there could have been many variations that developed life. RNA life is one theory in this regard, and may be the only remnant left from pre-DNA life forms. There could well have been others.
We also see that the formation of eukaryotes seems to be from combining two life forms into one, with the absorbed one becoming the mitochondria or chloroplasts in the cells. We also see horizontal gene transfer between single cell bacterial forms, and can logically deduce that this is not new at this level of development. One whole "coding gene" could be transfered from one bacteria to another, thus improving the fitness of the second without it needing to evolve it independently. There is evidence of this in resistance to anti-biotics in modern times.
The important thing in science is to recognize when we do not know, and be frank about it. We can hypothesize and conjecture what the hypothesis would mean, but we still don't know.
Yes, this type of complexity gain I agree with, the complexity gain that I feel we are missing evidence for is when an additional NOVEL coding gene is gained in an organism. Regaining lost complexity is observable, gaining new complexity I feel needs more evidence.
I agree with you that complexity is difficult to measure in most circumstances, a grey area. ...
I would say that the difficulty is ubiquitous, in part due to the fact that it is mostly a subjective opinion rather than an empirically developed conclusion. The evidence of the walking-sticks for instance does not tell you which ones have more "coding genes" and thus it is just assumed that the winged forms have more than the wingless ones. This is confirmation bias and opinion.
... Where it is clear that there has been gained complexity, is when there is a new, additional novel coding gene in an organism. ...
In your opinion. Are blind cave fish fit for their environment? Do they have a trait/function/feature that did not exist in ancestral populations? They are blind. Do they become blind by adding coding genetic sequences? Do they become blind by modifying an existing coding genetic sequences? Does that modification exist in the ancestral population?
... This added complexity is essential to evolution even if appearing like a strawman argument, it is not actually one. As explained above, the alternative is laughable that the first organism had as many of these genes as modern ones.
The addition of novel traits/features/functions and the genetic basis for them is necessary as part of the explanation for the diversity of life as we know it. Whether this is only due to single coding gene duplications is questionable.
To compare homo sapiens to amoeba dubia is missing the point that each of them evolved according to evolutionary theory. They therefore have more novel coding genes than they had before. ...
Excellent. Their genetic sequences have evolved independently since their last common ancestor, each adding and losing sequences in that process. We can use that information to form nested hierarchies based on their - and other organisms - hereditary history, comparing shared - homologous - genetic sequences, paralogous genetic sequences, ohnologous genetic sequences, ... and evolutionary modifications to them since a last common ancestor.
Well you are very welcome to cite your examples or evidence that duplications can create novel coding genes that are beneficial. That is all I ask for. With one view having evidence, and the other view without evidence, the argument definitely favors the view with some evidence.
There is plenty of evidence available for the formation of novel traits/features/functions and the genetic basis for them, and we will get to them once we understand each other on basic genetics and evolutionary processes.
Let's not equivocate between gene and genetic sequence.
Assume a genetic sequence (whether it is a whole gene or not, or several genes is not important yet),
say ... AAGTCCGTAAGGG ... (where the ... indicate that the sequence continues to each side of the section in question),
Can you add or delete a molecule at any point in this sequence without changing the sequence?
No, ...
Good. Those mutations change the sequence. Can you add or delete a section of molecules at any point in this sequence without changing the sequence?
... but you can change a molecule, and therefore have a mutation with no change in sequence.
So if I change a G to an A, say,
... AAGTCCGTAAGGG ...
to
... AAGTCCATAAGGG ...
-- it is the exact same sequence?
Indeed, whether it is a point mutation or a complete gene duplication, any change to the overall genetic sequence is a mutation, and one that did not exist in the genome before the mutation, yes?
This is true.
Excellent.
You should be clear here, because I have explained it. When you have many many trillions of possible allele combinations, the amount of new traits already contained in the genetic code is huge. ...
But the number for each trait is fairly limited. Alleles for eye color do not add speed for running.
... Unlimited. ...
Sadly (for you), very false.
... When you change a set of alleles into a new set of combinations never seen on earth before, its impossible to say there will never be a new trait expressed within that unique combination of alleles. ...
Change by mutation/s?
Change by mixing eye color alleles with skin color alleles with running alleles in different ways?
There are only a set number of alleles in a breeding population at any one time for any specific trait, and that limits the number of combinations within a (sexual) species to any two (parent) alleles from those in the mix. If there are 6 alleles for hair color, for example, then there are 21 pairs that can be combined in an offspring:
11 12 13 14 15 16 22 23 24 25 26 33 34 35 36 44 45 46 55 56 66
Selection cannot add any more possible variations, all it can do is select those that are best fit for survival\reproduction.
... When you change a set of alleles into a new set of combinations never seen on earth before, its impossible to say there will never be a new trait expressed within that unique combination of alleles. ...
The probability of one of these combinations not being in the general population at any generation of several hundred breeding pairs is really quite small.
... I find your insistence on traits being caused only by mutations illogical. ...
Unfortunately (for you), opinion has been demonstrated to be amazingly ineffective at altering reality in any noticeable way.
... You could fill the planet earth shoulder to shoulder with unique humans, over a trillion earths in this universe, over a trillion universes, and not even get close to the number of different allele combinations possible in humans. I don't say that figure lightly, it really is true. ...
All living humans are unique because of the mix of alleles for different traits/function/features AND because each human has new mutations (several per person) that are not from either of their parents, and yet there is still a small, limited number of combinations for hair color for selection to affect. Selection cannot cause a new hair color, mutation can.
... There is no logic behind your insistence that not one of those unique humans would have a new trait. ...
Argument from incredulity again, sorry: your insistence on omitting mutations is illogical because they have been observed to happen in individuals in each generation.
... At ten alleles per position, and 20000 gene locations, we have 10^20000 unique allele combinations. ie 20 000 zeros . A trillion x trillion x trillion doesn't even cover the first 100 zeros. ...
But still only 10 for hair color -- without mutation.
... Given enough environmental pressures humans could develop down an evolutionary path that causes humans to be vastly different to today, without the need for any mutation.
With 1 to 10 hair colors -- without mutation.
For example, the trait for ability to handle hotter temperatures is expressed in the allele frequncies in flies. There is a regular relationship between certain alleles and latitude:
Population genetics of the metabolically related Adh, Gpdh and Tpi polymorphisms in Drosophila melanogaster I. Geographic variation in Gpdh and Tpi allele frequencies in different continents | SpringerLink
And a small set of alleles that affect this trait\feature\function (... 21? ... coincidence?)
Not necessarily. By interbreeding those with the trait, you can emphasize the trait beyond anything seen in the original population. ...
You make it more common in the population. Red hair does not become redder, blond hair does not become blonder -- without new mutations.
... This is a well known breeding technique and is not associated with mutations. Its possible that nature can do the same. Lets say a leopard population finds itself isolated in desert conditions with few trees due to increased aridity in a certain region. Only the fastest survive. The fastest breed with the fastest in the next generation, the others being too weak to be good breeding partners. You can end up with a new breed of smaller desert leopards (like cheetahs) that can run faster than any individual in the original population. The trait for speed has been emphasized. There are no theoretical limits to these kinds of processes, unless you would like to introduce a limiting factor? ...
It is still selection of available alleles, not new, and the traits/functions/features are those of the existing genetics, not new.
Curiously, horse breeders and greyhound dog breeders cannot make their breeds faster by rebreedind the same previous generation alleles.
If what you said was true then new speed records should be set every year. This is not the case. The speed is limited by the fitness of the existing alleles being selected, and without new mutations to enable increased speed the limit for those existing alleles is reached fairly quickly when selection is strong -- as in breeding situations.
The new allele combinations would possibly express the traits for speed and for lung capacity and for the ability to drop temperature of the overheated animal, and it would take many generations for the best possible combinations of these alleles to express themselves and settle into a new allele frequency within the new population.
And obviously horse and dog racing breeders are complete morons.
What selection can accomplish:
speed ability of individuals in population before new selection pressure:
       xxx
xxxxx
xxxxxxx
xxxxxxxxxxx
xxxxxxxxxxxxxxxxx
ie a bell-curve
This would include alleles for muscles, breathing and heat dissipation, because selection operates on the whole phenotype.
speed ability of individuals in population after a few generations of strong selection:
              xxx
xxxxx
xxxxxxx
xxxxxxxxxxx
xxxxxxxxxxxxxxx
ie a skew curve.
The average speed of the population increases but the maximum speed of the fastest one doesn't.
Now if selection pressure is very strong a lot of the average, mediocre and below individuals will perish before reproduction, thus reducing the number of alleles available for breeding.
ie IF there were 6 alleles for muscles, only the 2 or 3 fastest would survive selection in the first few generations. Same for all alleles that provide fitness under strong selection.
In addition, if alleles for improved lung capacity, say, were not already joined with alleles for muscles within the population, the individuals with the best lung capacity could perish before getting combined with muscles.
Yes we can drop intricacy, why not keep micro-evolution and macro-evolution, I thought we agreed on your definitions, I'm not sure why you are dropping them when we have agreement? Unless you anticipate no need for those terms in our discussion which is fine by me. Up to you.
Thats correct, more technically, the gene starts at the start codon.
Excellent.
I have no need to use either micro- or macro- and find that using macro- generally contributes to confusion.
  1. evolution (process) - yes
  2. theory (scientific) - yes
  3. hypothesis (scientific) - yes
  4. the theory of evolution - yes
  5. novel genes\features\functions\traits - yes
  6. complexity - ... maybe ...
  7. speciation (divergent) - yes
  8. fitness - yes
  9. god hypothesis - (dropped for now)
  10. hidden gene hypothesis - (dropped for now)
  11. micro-evolution (= 'a' above) - (dropped for now)
  12. macro-evolution - (dropped for now)
  13. intricacy (= complexity) - (dropped for now)
  14. coding gene - yes
Note that I am keeping "complexity" in the "maybe" state, as I don't think it really provides a measure of what you seem to be meaning when you use the term, and I don't see that your requirement for coding gene duplication is required for new traits/functions/features to evolve. I'd rather use "increase in coding genes" than "complexity" as there is less chance of confusion on the part of readers in what you mean.
Enjoy
Edited by RAZD, : clrty

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:
 Message 31 by mindspawn, posted 02-01-2013 3:01 AM mindspawn has replied

Replies to this message:
 Message 33 by mindspawn, posted 02-02-2013 2:52 PM RAZD has replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


(1)
Message 34 of 65 (689714)
02-03-2013 5:00 PM
Reply to: Message 33 by mindspawn
02-02-2013 2:52 PM


mutation vs selection and the causes of novelty
I'm not intentionally misunderstanding what you are saying. I asked you to admit its impossible for nature to create the first organism with 20000 coding genes. By your inability to admit that it is impossible you are implying that it is actually possible. You emphasize this view by repeating that we do not know what the first organism is like. without actually saying it, you have left open the possibility that its possible. This is incredulous.
And I find your fascination with first life bewildering in the extreme.
We don't know. It doesn't get simpler than that.
The first life we have any record of is the blue-green algae at some 3.5 billion years ago, iirc, and even then we cannot tell how similar it is to blue-green algae today, other than leaving mats of strands of cells and making stromatolites. We do not know if it has coding genes that life today does not have, and we do not know if it has the same coding genes as modern blue-green algae.
Cyanobacteria - Wikipedia
quote:
Scientific classification
Domain: Bacteria
Phylum: Cyanobacteria
I would be extremely surprised if those ancient blue-green algae would be classified in one of the species living today.
We have no record of earlier life, and thus any speculation is just that: speculation, not hypothesis, not educated guess, but pure speculation.
You don't test theories with speculations.
We don't know what first life involved, and speculation here gets into the side topic of "what is life" and where you draw an arbitrary line between speculation about chemical processes and evolutionary life.
You refer to an argument from incredulity. Well if you have no evidence that any organism can be created from nothing, even a simple organism, its not a valid hypothesis. How would one test to see if its possible for the first life-form to have many many more coding genes than observed in a prokaryote fossil?
I don't know that it can, I don't know that it can't, and I don't know how many variations on a theme of replication may have been involved such that many near-life systems could come together in a variety of ways.
Further I consider it absolutely pointless and away from the topic at hand to pursue.
A hypothesis (plural hypotheses) is a proposed explanation for a phenomenon. For a hypothesis to be a scientific hypothesis, the scientific method requires that one can test it. Scientists generally base scientific hypotheses on previous observations that cannot satisfactorily be explained with the available scientific theories
All true, the problem is that we do not know enough at this time to do more than speculate, and one person's speculation is as (in)valid as any other person's speculation.
Those prokaryote fossils look like today's prokaryotes, your proposed hypothesis that they could have had a lot more coding genes is an absolutely ridiculous speculation, ...
Can you falsify the speculation that early life had coding genes that are no longer in the population?
... and you are using this proposal to avoid facing the fact that many evolutionists WILL admit:
Most of today's life-forms have more coding genes than the oldest observed fossil life-forms most likely had, ...
But now you are no longer talking about first life. The "oldest observed fossil life-forms" is an entirely different discussion point from first life, as it is an already evolved fully functional life form.
And again, we do not have DNA evidence so there is no way to tell for sure whether or not
  • all coding genes in all cells of the "oldest observed fossil life-forms" are present in current life forms, or
  • all cells of the "oldest observed fossil life-forms" all had exactly the same mix of coding genes ...
And I would be extremely surprised to find that either of these were the case. If I am going to speculate it would be that things we see in life today occurred in the past: that some coding genes are lost (via selection and drift etc), some coding genes are gained (via mutation), and that individuals in a breeding population have different mixes of coding genes, such that the number of genes in the population is greater than the number of genes in any one individual, and that we just do not know what coding genes were or were not in the population of the "oldest observed fossil life-forms" - capice?
... and therefore a process that involves gains in novel coding genes has to be part of evolutionary theory for it to stand. This is no strawman argument, it is essential to evolution.
And again, it is completely and totally unnecessary to speculate about early life to reach this conclusion.
If you refuse to admit this , then we have nothing further to discuss, this thread is about the lack of evolutionary processes to explain additional novel coding genes.
And this is why it is a straw man argument.
If you want agreement that novel gene sequences, and the expression of them in the novel traits\functions\features that result, are necessary to explain the diversity of life as we know it then there is absolutely no argument there at all.
However, the argument that novel gene sequences are necessary to explain novel traits/functions/features can be made from any point in the natural history of life on earth where novel traits/functions/features have been observed:
  • the transition from prokaryote to eukaryote
  • the transition from single cell life to colony/multi-cellular life
  • the transition from colony/multi-cellular life to division-of-labor-multi-cellular life
    ...
  • the transition from fish fin to tetrapod foot and leg
    ...
  • the transition from reptilian jaw and ear to mammalian jaw and ear
    ...
  • the transition from one variety of greenish warble to another where interbreeding does not occur
  • etc etc etc
Are you a creationist? If your argument against increased complexity is that abiogenesis created many complex organisms and there has been losses of complexity since, this is very close to creationism. You then don't have to justify increased complexity, because you are also believer in miracles. The spontaneous creation of complex life containing many thousands of novel coding genes is in the realm of miracles and fantasy, welcome to the supernatural club!
Is this supposed to scare me or something? The argument from consequences is another logical fallacy ...
I am a Deist. I do not fantasize that "complexity" means anything of value in evolutionary biology. I do not fantasize about things I don't know. I do not fantasize that speculation about the first life is the only basis for logical discussion of the evolution of novel traits.
I agree that what you are saying is generally observed, but there could be a few alleles in a separate population that could again accelerate a trait once bred in. ...
And selection would then be limited to what they can provide, however they would not be novel traits for the imported individuals from that separate population, as they would already have evolved there, and you end up with the same questions for that population.
... I also agree with the bell curve, the reality is a slowdown in improvements over time as the new allele frequencies are settling. Regardless, allele combinations are infinite ...
Wrong. There are a finite number of alleles for any one trait in an existing population. Without mutations adding new alleles there is necessarily a finite number of combinations. Even if every individual in a breeding population had different alleles from the others there is a limit to the number of alleles due to there being a fixed number of individuals in that population.
What we see is a process of mutation adding alleles and selection reducing alleles, and that the number of alleles for any trait is fairly limited.
... and can affect traits. You seem to feel that the number of genes per trait (eg eyes) are limited, ...
In any one breeding population, without mutation adding new alleles. Amusingly this is what the objective empirical evidence in all the research papers on the numbers of alleles for traits in populations show.
... but there are some genes that are more relevant to chemical balances, size of organs, hormones, digestion of specific foods that can help that organ. So the number of varied genomic regions affecting a trait could be numerous, not isolated to the obvious region in the genome.
And different combinations of those different traits/functions/features occur through the mutations involved in reproduction, not through selection. The genetic sequences of the offspring are different from those of either parent due to gene mixing (in sexual reproduction). Selection does not cause this.
Curiously, the breeders for the fastest horses and dogs appear to be totally incompetent at being able to search these out and gather them into new winning breeds, even though they have been trying for thousands of years of intense breeding to get even a 1% increase.
I believe an organism like a Tasmanian wolf can be evolved from a kangaroo without the need for mutation. Its just a few adjustments to teeth, digestion, limbs, all the variety contained within existing alleles, and possible under strong environmental pressure for a predator. Who is right and wrong on this particular issue can only be decided when there is more genome sequencing of animals, if completely differing species are found to have nearly matching genomes, I will be right. Until then we are both speculating without evidence.
No, you will still be wrong, because you apparently don't understand the difference between mutation and selection. Rearranging genetic sequences is mutation, adjustments to "teeth, digestion, limbs, (etc)" would be mutation. You would need many mutations to the genetic sequences to get a Tasmanian Devil from a Kangaroo ... in fact you would need mutations to get from one species of Kangaroo to another species of Kangaroo.
New combinations of alleles for different traits in offspring (ie muscles from one parent and hair color from the other parent) is due to the mutations that occur during the sexual reproduction processes, not selection.
Depends on how you define "sequence", maybe, maybe not, let's go with your definition, is this really relevant?
Yes:
Any change to the genetic sequence is a mutation by definition. Some are deleterious, some are neutral and some are beneficial.
Mutation - Wikipedia
quote:
In genetics, a mutation is a change of the nucleotide sequence of the genome of an organism, ...
Any change in the genetic sequence is a mutation, every change in the genetic sequence is a mutation, and when the total sequence in an offspring is not the sequence in a parent ... it is due to mutation/s.
I have been pretty clear in my agreement on most evolutionary processes. I have absolutely no idea why you are saying that I have a "requirement for coding gene duplication is required for new traits/functions/features to evolve". I have been repeatedly and clearly saying the opposite, and this is central to my argument.
No you haven't been clear, obviously, if I have it wrong. This is why we need consistent terminology and understanding.
For the record I will explain it again:
A) I do not believe coding gene duplication is required for new traits/functions/features to evolve.
They evolve through many other observable processes, devolving, deletions, changed allele frequencies, gene disabling.
ie through new mutations, ... and also through gene duplicating mutations ...
... They evolve through many other observable processes, devolving, deletions, changed allele frequencies, gene disabling.
Wrong. Selection does not cause new traits/functions/features ... it selects new traits/functions/features when provided by new mutations.
Selection is incapable of changing the genetic sequences.
B) I believe gains in novel coding genes are absolutely essential to the theory of evolution ...
This is your straw man again. It is not absolutely essential, because the only thing evolution needs is the appearance of novel traits/features/functions in the phenotypes of a breeding population so that selection operates on those new traits/features/functions in addition to the previously existing ones to find those that are best fit for the ecological challenges and opportunities that each organism faces.
Selection does not operate at the genetic level, but on the combined expressions of the genotype in the phenotype.
... as an explanation for the observation of most modern organisms that have many novel coding genes. I believe these gains need some evidence. (The alternative that organisms started out with many novel coding genes is so akin to creationism, we would be on the same side: the spontaneous and miraculous appearance of organisms with many novel coding genes)
Selection mechanisms and any change to the frequency of alleles within a population by other means (drift etc) do not create novel traits/functions/features.
It does not matter what you believe. What matters is what the objective empirical evidence shows. What the evidence shows is that evolution occurs via mutation and selection:
Mutation occurs in the genotype (upper left box), selection occurs on the phenotype (lower right box).
Do you AGREE or DISAGREE that:
Any change in the genetic sequence is a mutation, every change in the genetic sequence is a mutation, and when the total sequence in an offspring is not the sequence in a parent ... it is due to mutation/s.
  1. evolution (process) - yes
  2. theory (scientific) - yes
  3. hypothesis (scientific) - yes
  4. the theory of evolution - yes
  5. novel genes\features\functions\traits - yes
  6. complexity - ... maybe ...
  7. speciation (divergent) - yes
  8. fitness - yes
  9. god hypothesis - (dropped for now)
  10. hidden gene hypothesis - (dropped for now)
  11. micro-evolution (= 'a' above) - (dropped for now)
  12. macro-evolution - (dropped for now)
  13. intricacy (= complexity) - (dropped for now)
  14. coding gene - yes
  15. mutation - ... (new)
A proper discussion of novel traits/features/functions cannot be made without understanding the difference between mutation and selection and the different effects of mutation and selection on the breeding population/s.
Enjoy
Edited by RAZD, : link cyano
Edited by RAZD, : roo
Edited by RAZD, : clrty,

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This message is a reply to:
 Message 33 by mindspawn, posted 02-02-2013 2:52 PM mindspawn has replied

Replies to this message:
 Message 35 by mindspawn, posted 02-04-2013 2:17 AM RAZD has replied
 Message 36 by mindspawn, posted 02-04-2013 5:55 AM RAZD has replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


(1)
Message 37 of 65 (689888)
02-05-2013 5:34 PM
Reply to: Message 35 by mindspawn
02-04-2013 2:17 AM


time wasted, and revisiting mutations again
First off, would you agree that this is an accurate quote of your position:
quote:
Message 1:
mindspawn has stated a concern that:
"... recent DNA sequencing is not providing enough support for the hypothesis of evolution. (ie increased DNA complexity of new and uniquely functional active coding genes within an organism is not observed to add fitness)."
and
"I have been looking ... for some evidence that a gene can duplicate, and then produce a novel function in the duplicated coding gene that adds fitness. Haven't seen it yet, this basic process of evolution remains unproven. Without it we would just have bacteria on earth, mutating and evolving into alternative forms but never gaining in complexity."

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.
I've stricken out comments that I feel are not appropriate for debate (incendiary or trolling comments) or that don't contribute to the debate (get off into side topics) and comments where you are making assumptions about my positions that are incorrect and irrelevant.
The fact that you are a deist and also like me believe its possible that DNA started out with long strands of many thousands of novel coding genes, means we are actually in near complete agreement. I believe in stasis or reduced novel coding genes over time, you believe in reduced or increased novel coding genes over time, the increases not being central to your view.
You would be wrong.
Frankly I don't see you as a true evolutionist, if evolutionists are now admitting that the full genome size could have been there from the start, this is the creationist view too. From an empirical view, neither of us was there to see how the DNA strand came into being, I believe it was created supernaturally, you through abiogenesis?
I believe we don't know. We don't have enough evidence to know.
Looking at the experimental results for abiogenesis, it appears that early life may have included a number of different nucleotide replicating molecules, of which RNA and DNA are the survivors. The first DNA may have been single stranded. I would be surprised if the first coding genes were not rather haphazard and inefficient compared to modern evolved (and refined by evolution) genes. It may have taken several steps to make some proteins for instance. There is also the possibility that repetition was used to provide both redundancy and increased production from less efficient production systems, and this would naturally lead to long strands of DNA, but length does not equate to having more variety in coding genes. Selection at that time could be rather simplistic and not affect things like overly long nucleotide strands. I would also be surprised if many of the original coding genes survived billions of years of evolution intact and in their original configuration and be unchanged today.
But this is speculation, opinion, and certainly not a basis for testing the theory of evolution.
I personally think any informed neutral party would be more aware than you of the complexity involved in sequencing a set of codons in such an order as to not damage an organism, and to do this repeatedly over 3 billion or more base pairs is impossible without an intelligent designer or a believable process. The slow process of evolution from simplicity to complexity is far more believable than your proposed possible sudden complexity view of evolution.
Words used in pseudoscience appear to have meaning, but on closer inspection are not defined in a way that is useful.
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.
A much more useful term would be variety. Variation has usefulness for evolution, and it can be readily determined. You cannot tell from looking at this diagram which species is more "complex" than the others without making assumptions:
But anyone can look at that diagram and see that the walking sticks evolved from one common ancestor population to 39 different species, that each wing loss or wing gain event adds variation to the amount of variation then existing, and increases the total diversity. The species with wingless females and winged males is another additional variation adding diversity.
We can also predict that variations will occur via mutations in breeding populations, and that they can then be subject to selection when expressed in the phenotype.
We can also look at that diagram and see that the two Embioptera species Oligotoma nigra and Teratembia n.sp retain the most ancestral traits, and would be classified as having plesiomorphic traits, while the species Lopaphus parakensis has the most apomorphic, or derived, traits. These terms are used in cladistics as descriptors for the branches of a nested hierarchy (such as is shown with the walking sticks).
Variation within a breeding population also predicts greater likelihood that some will survive changing ecological conditions.
I believe observers would be extremely amused to see evolutionist's convergence with creationists on this sudden appearance of complexity, and it reminds me of the creationist's catastrophic view on the fossil record, and how mainstream science has adapted from uniformitarianism to include some catastrophism as predicted by creationism.
Which just shows that you do not understand what uniformitarianism means in geology in specific and science in general. This is a typical misunderstanding\misrepresentation of creationism and creationists. But are you trying to GishGallop on the topic now?
I don't need to , its an untestable and ridiculous concept that early life had complex genomes, and this is not even a valid hypothesis that should enter into the arena of respected scientific debate. Why debate ridiculous concepts that are untestable? That is why only accepted hypotheses and theories are subjected to falsification, they have to first reach that status of being a hypothesis.
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.
This may be true for asexual organisms but not true for sexual organisms. ...
It is true for all organisms.
... The offspring in sexual organisms are a combination of the alleles in both parents. ...
Which did not occur in either parent, and are thus mutations, by definition, as was noted in Message 34:
quote:
Any change to the genetic sequence is a mutation by definition. Some are deleterious, some are neutral and some are beneficial.
Mutation - Wikipedia
quote:
In genetics, a mutation is a change of the nucleotide sequence of the genome of an organism, ...
Any change in the genetic sequence is a mutation, every change in the genetic sequence is a mutation, and when the total sequence in an offspring is not the sequence in a parent ... it is due to mutation/s.
If you want we can use the term "genetic change" instead of mutation. The scale of the change is irrelevant to the fact that any change in the total genetic sequence is defined as a mutation. Polyploidy is a mutation.
... Thus the sequences in the offspring differ to each parent every time even if there are no mutations involved. The offspring shows different combinations of genes to the parent.
That you don't understand that these are still mutations is part of your problem in understanding selection in specific and evolution in general.
If you want agreement that novel gene sequences, and the expression of them in the novel traits\functions\features that result, are necessary to explain the diversity of life as we know it then there is absolutely no argument there at all.
Ok this is significant, ...
Which is why the obsessive fascination with speculating about the first life forms in irrelevant to the discussion of novel traits\features\functions, and has waste way too much of our time already.
... have to rush off, will deal with this in my next post.
And I too.
Enjoy

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This message is a reply to:
 Message 35 by mindspawn, posted 02-04-2013 2:17 AM mindspawn has replied

Replies to this message:
 Message 38 by mindspawn, posted 02-06-2013 11:32 AM RAZD has replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 39 of 65 (689996)
02-07-2013 12:22 PM
Reply to: Message 38 by mindspawn
02-06-2013 11:32 AM


... revisiting mutations genetic change once again
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.
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?
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 nucleotide sequences. The new sequences are not found in the alleles of either parent.
They are still mutations in my book, but if you want we can use the term "genetic change" as proposed in Message 37:
If you want we can use the term "genetic change" instead of mutation. The scale of the change is irrelevant to the fact that any change in the total genetic sequence is defined as a mutation. Polyploidy is a mutation. It also becomes a tautology that genetic change is genetic change.
There are advantages to using "genetic change" in terms of general understanding. Mutation carries a lot of baggage/misunderstanding/connotations (organisms mutating into something else is a common lay person misunderstanding -- see Lack of random environments Message 1 for example), and "genetic change" avoids this.
Again, this is more concise and precise in terms of conveying the meaning intended without confusion, yes?
Now in the diagram above we have genetic change in the upper left (formation of new individuals), and selection (of individual fitness) in the bottom right.
Selection still does not contribute to making novel traits/features/functions ... it only selects traits/features/functions that allow the organisms to survive and reproduce. Those variations in traits/features/functions have to already be in the population to be subject to selection, and new traits/features/functions are caused by genetic change/s.
  1. evolution (process) - yes
  2. theory (scientific) - yes
  3. hypothesis (scientific) - yes
  4. the theory of evolution - yes
  5. novel genes\features\functions\traits - yes
  6. complexity - ... use "variation" instead
  7. speciation (divergent) - yes
  8. fitness - yes
  9. god hypothesis - (dropped for now)
  10. hidden gene hypothesis - (dropped for now)
  11. micro-evolution (= 'a' above) - (dropped for now)
  12. macro-evolution - (dropped for now)
  13. intricacy (= complexity) - (dropped for now)
  14. coding gene - yes
  15. mutation - ... use "genetic change" instead
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.
Next issue after resolving use of "genetic change" and understanding that selection does not contribute to making novel traits/features/functions ... it only selects novel traits/features/functions when they allow the organisms to survive and reproduce.
Enjoy.
Edited by RAZD, : link

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This message is a reply to:
 Message 38 by mindspawn, posted 02-06-2013 11:32 AM mindspawn has replied

Replies to this message:
 Message 40 by mindspawn, posted 02-07-2013 2:09 PM RAZD has replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 41 of 65 (690018)
02-07-2013 5:18 PM
Reply to: Message 36 by mindspawn
02-04-2013 5:55 AM


Re: mutation vs selection and the causes of novelty
If only 20 genes of 20000 genes in an organism affect a trait, and each gene average ten alleles, the number of allele combinations is 100 000 000 000 000 000 000. Fairly limited?? No
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).
Let's agree to disagree unless you have proof rather than opinion based on observations of selective breeding of horses for speed. ...
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.
... I believe in the next few years one of us will be proved wrong. Let's watch genome sequencing of marsupials in Australia. I don't mind being wrong here, but I'm sure I'm right, just by the sheer number of combinations possible.
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.
Good, but I am referring to gains in novel coding genes, not just changes. (Increased no. of novel coding genes). Its funny that the peanut gallery has picked up on this, agrees that increased numbers of novel coding genes are essential to evolution, and are already posting evidence for the evolutionist position on this. ...
Which should tell you that you're position is likely untenable ... once we have sorted through the terminology to see why selection does not add novel features/functions/traits, but acts on the phenotypes of existing organisms to determine fitness within a specific ecology.
... I may never get there in this thread, being bogged down into a mire of semantic distractions (feel the frustration!) ...
And yet you clearly have not understood how selection works, and this is due to "semantic distractions" that still need to be ironed out.
... But just remember if you ever get around to posting your evidence for gene-adding processes, ...
For which there is evidence, as noted in the Peanut Gallery, the question is whether or not you will accept this evidence for what it shows, and critical to this acceptance is understanding the meanings of the words through the agreement of the terminology used.
... its the theory of evolution that is being challenged. ...
... 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).
Enjoy.

we are limited in our ability to understand
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This message is a reply to:
 Message 36 by mindspawn, posted 02-04-2013 5:55 AM mindspawn has replied

Replies to this message:
 Message 44 by mindspawn, posted 02-09-2013 2:30 AM RAZD has replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 42 of 65 (690024)
02-07-2013 6:33 PM
Reply to: Message 40 by mindspawn
02-07-2013 2:09 PM


Re: ... revisiting mutations genetic change once again
... 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. ...
okay let's use "coding gene duplication" seeing as that is your last definition.
... but if you RAZD would prefer not to use the word "mutation", let us do it your way. ...
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.
  1. evolution (process) - yes
  2. theory (scientific) - yes
  3. hypothesis (scientific) - yes
  4. the theory of evolution - yes
  5. novel genes\features\functions\traits - yes
  6. complexity - ... use "coding gene duplication" instead
  7. speciation (divergent) - yes
  8. fitness - yes
  9. god hypothesis - (dropped for now)
  10. hidden gene hypothesis - (dropped for now)
  11. micro-evolution (= 'a' above) - (dropped for now)
  12. macro-evolution - (dropped for now)
  13. intricacy (= complexity) - (dropped for now)
  14. coding gene - yes
  15. mutation - ... use "genetic change" instead
Remember that we agreed that the process of evolution was defined in Message 1 as:
quote:
For this thread I would propose using this definition for the process of evolution:
The process of evolution involves changes in the composition of hereditary traits, and changes to the frequency of their distributions within breeding populations from generation to generation, in response to ecological challenges and opportunities.

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
Enjoy.
Edited by RAZD, : recap

we are limited in our ability to understand
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This message is a reply to:
 Message 40 by mindspawn, posted 02-07-2013 2:09 PM mindspawn has replied

Replies to this message:
 Message 43 by mindspawn, posted 02-08-2013 1:45 AM RAZD has replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 45 of 65 (690126)
02-09-2013 11:54 AM
Reply to: Message 43 by mindspawn
02-08-2013 1:45 AM


getting ready to move on?
Power out last night just as ready to post this. Temp power now. Foot of snow outside. Fun.
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.
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.
And no it isn't the core of the debate, the core of the debate is whether or not coding genes have been duplicated and then added fitness to the breeding population.
Again, I believe that gene coding duplication has occurred throughout the evolutionary history of life on earth, because it is reasonable to believe that something that occurs in the present occurred in the past as well (this, btw, is the true interpretation of "uniformitarianism" -- that the laws of nature that apply today also applied in the past ... and there is plenty of evidence that this is so).
And I repeat what I stated in Message 37:
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.
And I also expect (opinion) the biology was different in the early years, where different coding genes could be developed in different organisms before being brought together via horizontal transfer later on. We know horizontal transfer occurs todaty. Horizontal gene transfer is like sex for single cell life.
What we do know is that the ecology was considerably different even when the blue-green algae were building stromatolites 3.5 billion years ago, due to the lower levels of oxygen in the atmosphere if nothing else.
Thus I would expect that a number of genes that were suitable for that early ecology to have been replaced or modified to fit the different ecologies we see today.
... do you think that it is a reasonable assumption that the earliest organisms had relatively few coding genes compared to modern organisms?
Let me put it this way: I believe (opinion) that few of the coding genes present in organisms alive today were extant in the earliest life forms known.
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:
We can expand this image verbally, now that we have covered most of the basic terminology, to see if we are on the same page:
Evolution Do Loop for Living Species (ie - not extinct)
  1. A breeding population typically consist of
    1. a variety of mature adults technically capable of breeding, each with a set of hereditary traits/functions/features
      • some have more opportunities to breed and will typically produce more offspring than others
      • some have less opportunities to breed and will typically produce less offspring than others
    2. some individuals that are too old, too young or too disabled to be capable of breeding.
  2. The offspring population typically has a different variety and frequency of hereditary traits/functions/features from the parent population
    1. some existing hereditary traits/functions/features are from parent/s
      • there are more offspring with hereditary traits/functions/features of parent/s that reproduce more (increasing their frequency)
      • there are fewer offspring with hereditary traits/functions/features of parent/s that reproduce less (decreasing their frequency)
      • offspring of sexual species typically have a different mix of dominant\recessive\etc copies of genes than either parent, getting one copy from each parent (changing the frequency of expressed genes)
      • offspring of asexual species typically have the same mix of dominant\recessive\etc copies of genes as their parent, however each copy can be subject to random genetic change/s
    2. some hereditary traits/functions/features that are modified from parent/s copies by random genetic change/s.
  3. Breeding/reproduction produces added variation/s due to random genetic change/s during the reproductive process
    1. random genetic change may be due to small modifications, duplicating, adding, moving, or deleting bits of the genetic sequence/s
    2. random genetic change may be due to large modifications, duplicating, adding, moving, or deleting whole sections of the genetic sequence/s
    3. random genetic change may affect whole genes, duplicating, adding, moving, or deleting whole coding gene sections of the genetic sequence/s
    4. sexual reproduction involves additional random genetic change due to the stochastic way the gametes are formed in each parent, and the stochastic way they are then combined to form the zygotes of offspring.
  4. Some genetic changes do not affect the phenotype (ie are not expressed) and thus are neutral to selection.
  5. Some genetic changes do affect the phenotype and thus may be affected by selection
    1. some increase the survival and/or reproductive success of the organism (and thus are beneficial)
    2. some do not change the survival and/or reproductive success of the organism (and thus are neutral)
    3. some decrease the survival and/or reproductive success of the organism (and thus are deleterious)
    4. some are lethal.
  6. Selection removes the least fit individuals and thus tends to remove the least fit hereditary traits/functions/features and the genetic sequences that produce them, thereby reducing the frequency of those traits/functions/features in the population.
  7. Sexual selection can asymetrically affect individual reproduction and can increase the frequency of "sexually desirable" hereditary traits/functions/features even when deleterious for survival, or reduce the frequency of "sexually undesirable" hereditary traits/functions/features even when beneficial for survival.
  8. Drift can remove an individual or a group of individuals via stochastic accident (falling trees, earthquakes, tornadoes, etc) and thus may randomly remove hereditary traits/functions/features and the genetic sequences that produce them without regard to fitness.
  9. Sexual drift can occur in sexual species when a particular gene of the parent happens to be by-passed in reproduction due to the stochastic nature of gamete production and combination in the zygotes, a gene (beneficial, neutral or deleterious) can be randomly omitted\forgotten in the mating process (a 50:50 possibility in each mating).
  10. Of the offspring that survive to breed/reproduce
    1. individuals with beneficial hereditary traits/functions/features typically breed more than
    2. individuals with neutral hereditary traits/functions/features, which typically breed more than
    3. individuals with deleterious hereditary traits/functions/features, which typically breed more than
    4. dead individuals
    5. however, individuals can have mixtures of beneficial, neutral and deleterious hereditary traits/functions/features, so deleterious hereditary traits/functions/features can "piggy-back" on beneficial hereditary traits/functions/features and persist in the breeding population.
  11. All individuals that survive to breed form the breeding population for the next generation, starting over at step 1 ... (please notice the overlap between 10 and 1).
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.
Enjoy

we are limited in our ability to understand
by our ability to understand
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This message is a reply to:
 Message 43 by mindspawn, posted 02-08-2013 1:45 AM mindspawn has replied

Replies to this message:
 Message 48 by mindspawn, posted 02-10-2013 5:07 AM RAZD has seen this message but not replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


(1)
Message 46 of 65 (690144)
02-09-2013 2:56 PM
Reply to: Message 44 by mindspawn
02-09-2013 2:30 AM


regroup
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.
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.
Curiously it has been demonstrated that dogs, horses, pigeons, etc etc etc ... any racing animal -- cannot be bred to go faster without (genetic change) mutations (as you claimed again), as evidenced by all the racing animal breeders intently attempting to gain speed via breeding.
... 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).
The degree that this can happen without genetic change -- as you claimed -- is limited, and the "emphasis" that results is seen in the number of individuals with the trait, not with further development of the trait. Quantity, not quality.
When you start with a specific trait/function/feature for selection you will start with a bell curve distribution:
(from http://drrickyount.com/2011/12/bell-curve-and-curving-grades)
When you select for "A" without adding any new trait/function/feature via genetic change/s (as you claim) you end up with a skew curve distribution:
(ibid)
When the trait is under strong selection you will lose traits that are not combined in the more fit organisms, the number of available traits to combine drops. You still get a skew curve instead of a bell curve, but it will be truncated, like raising the horizontal axis and the breeding population becomes smaller and has less available variation.
Remember that selection removes less fit traits/functions/features from the breeding population, and the stronger the selection the more traits/functions/features are less fit and are removed.
Once all (or almost all) the offspring have all the available traits/functions/features that contribute to the selection fitness paradigm ("A") they can't increase more without new traits/functions/features that occur via genetic change/s.
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.
Fragile bones is also a problem that horse/dog/etc racing animal breeders encounter where we see animals that win one race and then can't run in others because a critical leg bone breaks.
Breeders in general have problems with reduced variation cause by selection then causing physiological and health problems.
An example from natural selection involves run-away sexual selection, where a trait/feature/function is selected as part of mating to the point where it endangers the organism for survival, ie - peacock tail, etc.
This is the kind of thing that points to strong selection for a single trait at the expense of others. You don't get something for nothing.
(I was referring to the Tasmanian wolf - it had many kangaroo-like qualities, and its predator's jaw is comparatively weak for a predator)
It has many marsupial qualities that it shares with all other marsupials, including kangaroos and sugar gliders and marsupial moles.
It does not have a placental mammal jaw because it is a marsupial. It does have a good predator jaw for the ecology it inhabited -- marsupial Australia -- and that is all that matters.
We can't really replace words, especially since we have no consensus of what the original word means. (that doesn't make any sense)
A word can be replaced by it's definition otherwise it doesn't make sense.
If you disagree that mutation means genetic change, that it means something else, while I say it means genetic change, then using "genetic change" gets to the meaning that I intend without the confusing you with the something else you feel mutation means.
Same holds true for using "coding gene duplication" -- your definition for complexity -- because complexity has other issues than coding gene duplication.
The idea is to convey the meaning, not argue about words.
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.
Moving the goal posts?
Of course duplication is not the only means to develop novel coding genes, as existing ones can be modified by genetic change to be novel coding genes. There is evidence of this happening.
There is also evidence of gene duplication and subsequent modification of one or both copies into novel coding genes by genetic change.
Do you want to discuss evidence for this or equivocate on what you mean?
... which includes the possibility that genes were already there from the start, ...
If you are going to use this cop-out, it will be up to you to show that the fully functional coding gene existed but went unused for some inexplicable hypothetical reason. And then provide the reason.
Enjoy.
Edited by RAZD, : clrty

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This message is a reply to:
 Message 44 by mindspawn, posted 02-09-2013 2:30 AM mindspawn has replied

Replies to this message:
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RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 47 of 65 (690169)
02-09-2013 8:26 PM
Reply to: Message 43 by mindspawn
02-08-2013 1:45 AM


coding gene duplication, increased fitness, examples
This is long, because it is full of information and evidence.
E. coli long-term evolution experiment
quote:
The E. coli long-term evolution experiment is an ongoing study in experimental evolution led by Richard Lenski that has been tracking genetic changes in 12 initially identical populations of asexual Escherichia coli bacteria since 24 February 1988.[1] The populations reached the milestone of 50,000 generations in February 2010.
Since the experiment's inception, Lenski and his colleagues have reported a wide array of genetic changes; some evolutionary adaptations have occurred in all 12 populations, while others have only appeared in one or a few populations. One particularly striking adaption was the evolution of a strain of E. coli that was able to use citric acid as a carbon source in an aerobic environment.[2]
In 2012, a team of researchers working under Lenski reported the results of a genomic analysis of the Cit+ trait that shed light on the genetic basis and evolutionary history of the trait.[5] The researchers had sequenced the entire genomes of twenty-nine clones isolated from various time points in the Ara-3 population's history. They used these sequences to reconstruct the phylogenetic history of the population, which showed that the population had diversified into three clades by 20,000 generations. The Cit+ variants had evolved in one of these, which they called Clade 3. Clones that had been found to be potentiated in earlier research were distributed among all three clades, but were over-represented in Clade 3. This led the researchers to conclude that there had been at least two potentiating mutations involved in Cit+ evolution. The researchers also found that all Cit+ clones sequenced had in their genomes a duplication mutation of 2933 base pairs that involved the gene for the citrate transporter protein used in anaerobic growth on citrate, citT. The duplication is tandem, resulting in two copies that are head-to-tail with respect to each other. 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. Movement of this new regulatory module (called the rnk-citT module) into the genome of a potentiated Cit- clone was shown to be sufficient to produce a Cit+ phenotype. However, the initial Cit+ phenotype conferred by the duplication was very weak, and only granted a ~1% fitness benefit. The researchers found that the number of copies of the rnk-citT module had to be increased to strengthen the Cit+ trait sufficiently to permit the bacteria to grow well on the citrate, and that further mutations after the Cit+ bacteria became dominant in the population continued to accumulate that refined and improved growth on citrate. The researchers conclude that the evolution of the Cit+ trait suggests that new traits evolve through three stages: potentiation, in which mutations accumulate over a lineage's history that make a trait accessible, actualization, in which one or more mutation render a new trait manifest, and refinement, in which the trait is improved by further mutations.
(color added for emphasis)
Note that because this is an asexual species there is no confusion between "mutation" and "genetic change" in our understandings.
Message 1: mindspawn has stated a concern that:
"I have been looking ... for some evidence that a gene can duplicate, and then produce a novel function in the duplicated coding gene that adds fitness. Haven't seen it yet,..."
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.

Message 17: So to conclude, any genetic evidence brought forward regarding genes evolving will be compared to the "always was there" hypothesis so we can look at the evidence in an unbiased fashion, which is the essence of the evolution/creation debate. Whether mentioned or unmentioned, the comparison has to be there the whole time.
Which is, of course, a bogus hypothesis, more of a creationist dodge than science ...
So how we know it was not "always there" hiding, waiting for need, ready to pounce on unsuspecting biologists?
Watching multicellularity evolve before our eyes
quote:
Chlorella vulgaris is an asexual, unicellular green alga. It has been observed in the laboratory to maintain unicellularity for thousands of generations. Boraas and his collaborators (1998) kept Chlorella for two decades in this way. Then they decided to add a predator, Ochromonas vallescia, also a unicellular organism. It has a flagellum (a tail with which it can swim about), and it eats Chlorella. This is bad news for the Chlorella population, which thus experiences a shift in selective pressure. While it was previously adapted to maximize growth by uptake of nutrients, with Ochromonas around it is suddenly more advantageous to have some sort of defense, even if that should come at a cost of the rate at which it can reproduce.
While we could imagine other mechanisms of defense, size is an obvious choice. Very soon (about 10 days) after the introduction of the flagellate predator, Chlorella colonies started to form. These initially consisted of aggregates of tens to hundreds on Chlorella cells, adhering to each other. Their sheer size prevented the predator from eating them, and thus the multicellular Chlorella was fitter than the unicellular ones, and as a result the unicellular Chlorella all but disappeared. Multicellularity had evolved right before the lucky scientists'
Recall that Chlorella is better able to utilize the nutrients in the environment when they are single cells. Thus, the colonies of tens to hundreds of cells soon disappeared, replaced by colonies of of only eight cells. This seems to be the optimal size for uptake of nutrients and defense against Ochromonas. When Boraas et al. removed the predator from the environment, Chlorella colonies continued to make multicellular offspring. However, with the selection pressure to be large gone, the unicellular Chlorella took over again.
The significance of this experiment is that it lends support to the hypothesis that a predator-prey arms race could provide the needed environmental change to enable multicellular organisms to evolve. It also is an outstanding example of observed evolution in the laboratory. It can be argued that the unicellular and multicellular Chlorella are different species, and this is then also an example of speciation observed.
Now contrast this Chlorella with the famous E. coli experiment by Blount et al. reported in PNAS this year. In short, after years of culturing E. coli bacteria in the lab, they one day evolved the capacity to metabolize a new nutrient, citrate. Scientists use E. coli's inability to metabolize citrate to distinguish it from other bacteria, so the fact that they suddenly evolved the ability to eat it can also be argued to be an instance of speciation.
However, there is a clear difference from Boraas' experiment, namely that Chlorella evolved almost instantly when the selection pressure changed. It thus responded to the change on the basis of standing genetic variation: different genotypes present in the population. There were already some Chlorella cells that were able to adhere to their daughter cells, but it was unfavorable to do so until the appearance of predators. In Blount's experiment it was always favorable to consume citrate. There was plenty of it, and E. coli was deliberately starved on its usual nutrient. Yet they had to wait 30 years to observe E. coli evolving to eat citrate, because the genetic components enabling them to do so had to evolve first. A yet unknown sequence of necessary mutations was required, and once it appeared, E. coli speciated.
It took 30 years and thousands of generations for E. coli to evolve the Cit+ ability, it required two prior "potentiation" mutations before "actualization" with a third mutation. The mutations were not in documented genetic sequences in previous generations, it was not "already there" ...
... and when we have a trait that was "already there" (as in the Chlorella) the response is immediate after the selection pressure is applied.
Expect more denial and equivocation to follow.
Note that "Blount et al" is Z. D. Blount, C. Z. Borland, R. E. Lenski (2008) -- the E. coli experiment discussed above.
Note too that this is speciation because some evolve cit+ and some don't: two daughter populations with different traits/features/functions living in different ecologies. This is one way speciation can be determined in asexual species (rather than by breeding isolation).

Icing on the cake
polyploidy
quote:
Polyploid cells and organisms are those containing more than two paired (homologous) sets of chromosomes. Most eukaryotic species are diploid, meaning they have two sets of chromosomes one set inherited from each parent. However polyploidy is found in some organisms and is especially common in plants. In addition, polyploidy also occurs in some tissues of animals who are otherwise diploid, such as human muscle tissues.[1] This is known as endopolyploidy. (Monoploid organisms also occur; a monoploid has only one set of chromosomes. These include the vast majority of prokaryotes.)
Polyploidy refers to a numerical change in a whole set of chromosomes. Organisms in which a particular chromosome, or chromosome segment, is under- or overrepresented are said to be aneuploid (from the Greek words meaning "not," "good," and "fold"). Therefore the distinction between aneuploidy and polyploidy is that aneuploidy refers to a numerical change in part of the chromosome set, whereas polyploidy refers to a numerical change in the whole set of chromosomes.[2]
Polyploidy may occur due to abnormal cell division, either during mitosis, or commonly during metaphase I in meiosis.
Polyploidy occurs in some animals, such as goldfish,[3] salmon, and salamanders, but is especially common among ferns and flowering plants (see Hibiscus rosa-sinensis), ...
Plains Viscacha Rat
quote:
The plains viscacha rat or red vizcacha rat (Tympanoctomys barrerae) is a species of rodent in the family Octodontidae. It is monotypic within the genus Tympanoctomys.[3] It is endemic to central western Argentina, where it has a fragmented range.[1] Its natural habitat is desert scrubland, dunes and salt flats, where it eats halophyte plants.[1] It is a solitary, nocturnal rodent that constructs large mounds with complex burrows.[1][4]
This species of rodent is unusual because it is tetraploid (4x = 2n = 102). Scientists think that this species may have arisen when an ancestor (very possibly the mountain vizcacha rat, Octomys mimax, chromosome count 2x = 2n = 56) doubled its chromosome number, presumably by errors in mitosis or meiosis within the animal's reproductive organs.[5] Research has found another closely related species (Pipanacoctomys aureus) which is also tetraploid and appears to be the sister species of T. barrerae.[6]
The species is threatened by destruction of its fragmented and restricted habitat.[1]

Whole-genome duplications in South American desert rodents (Octodontidae)
quote:
The discovery of tetraploidy in the red viscacha rat, Tympanoctomys barrerae (4n = 102) has emphasized the evolutionary role of genome duplication in mammals. The tetraploid status of this species is corroborated here by in situ PCR and Southern blot analysis of a single-copy gene. The species meiotic configuration strongly suggests a hybrid derivation. To investigate the origin of T. barrerae further, the recently described Pipanacoctomys aureus was studied. This 92-chromosome species also has a duplicated genome size, redundant gene copy number and diploid-like meiotic pairing, consistent with an event of allotetraploidization. Phylogenetic analysis of mitochondrial sequences indicates sister-group relationships between these two tetraploid rodents. The new karyotypic data and the phylogenetic relationships suggest the participation of the ancestral lineages of Octomys mimax in the genesis of P. aureus. The high overall DNA similarity and shared band homology revealed by genomic Southern hybridization as well as matching chromosome numbers between O. mimax and the descendant tetraploid species support the notion of introgressive hybridization between these taxa. 2004 The Linnean Society of London, Biological Journal of the Linnean Society, 2004, 82, 443—451.
Molecular cytogenetics and allotetraploidy in the red vizcacha rat, Tympanoctomys barrerae (Rodentia, Octodontidae)
quote:
The theoretical impossibility of polyploidy in mammals was overturned by the discovery of tetraploidy in the red vizcacha rat, Tympanoctomys barrerae (2n = 102). As a consequence of genome duplication, remarkably increased cell dimensions are observed in the spermatozoa and in different somatic cell lines of this species. Locus duplication had been previously demonstrated by in situ PCR and Southern blot analysis of single-copy genes. Here, we corroborate duplication of loci in multiple-copy (major rDNAs) and single-copy (Hoxc8) genes by fluorescence in situ hybridization. We also demonstrate that nucleolar dominance, a large-scale epigenetic silencing phenomenon characteristic of allopolyploids, explains the presence of only one Ag-NOR chromosome pair in T. barrerae. Nucleolar dominance, together with the chromosomal heteromorphism detected in the G-banding pattern and synaptonemal complexes of the species’ diploid-like meiosis, consistently indicates allotetraploidy. Allotetraploidization can coherently explain the peculiarities of gene silencing, cell dimensions, and karyotypic features of T. barrerae that remain unexplained by assuming diploidy and a large genome size attained by the dispersion of repetitive sequences.
Fig. 5. G-bands of T. barrerae's chromosomes arranged in quadruplets. Disomic or trisomic similarity is observed in some quadruplets. Pair 41 is the NOR pair, having a secondary constriction in the long arm. The X chromosomes are among the largest elements, and Y is the only acrocentric in the karyotype.
more at link
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.
Enjoy.
Edited by RAZD, : clrty

we are limited in our ability to understand
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This message is a reply to:
 Message 43 by mindspawn, posted 02-08-2013 1:45 AM mindspawn has replied

Replies to this message:
 Message 50 by mindspawn, posted 02-10-2013 6:48 AM RAZD has replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


(2)
Message 51 of 65 (690200)
02-10-2013 3:11 PM
Reply to: Message 50 by mindspawn
02-10-2013 6:48 AM


Re: coding gene duplication, increased fitness, examples
Message 48
lol, I don't envy you. We don't get snow here , ...
That's too bad. I've got a lovely view outside my windows.
... way too cold for me.
It's 40°F today ... inside 22°F 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 ... .
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.
And as I have said before denial does not change the facts, and opinion does not affect reality.
Message 49
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.
First, there will never be enough time for your scenario, biology does not work that way. You will never breed each horse with all others in a way that only selects for speed. Horses don't have that many offspring, even with artificial insemination used by breeders, and there are other constraints on fitness than pure speed: it's always a compromise.
Second, the horse species is already bred for speed, this is why they have long legs and large lungs and nostrils, why they have pads in their hooves that act as secondary pumps to push blood back up the legs when they run, and why they are selected by breeders for racing. They developed to be the optimized compromise for their ecology. You will not get more development via natural processes, only via artificial breeding (which - imho - has reached it's limit with breeders today, and it will take artificial genetic design to increase further).
Third, in the natural world there are stochastic impediments that block your hypothetical best of all best breeding for offspring. If a horse can only breed with horses within 50 miles, they will never breed directly with ones further away. If two fast horses are more that 50 miles apart they will never interbreed directly, and you would need to rely on gene flow and good luck to combine their genes. The further they are separated the bigger the impediments become. Evolution is local, not mail-order.
Even if you could get two best horses together there is a one in four chance of getting a best of best offspring. And when you get it, the next generation may (likely will) lose it.This is why breeders develop purebreds to increase the possibility of maintaining the desired traits. (Mendelian selection).
The stronger the selection pressure the more unlikely the natural combination becomes, and the more likely that separated populations will occur that will evolve independently without gene flow (speciate).
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). ...
No, it leads to more of the positive selected individuals passing their beneficial traits to the following generations. Greater numbers of "A" individuals is not a new A+ trait.
Selection does not cause new gene combinations to occur, it just reacts to the phenotypes that exist. If "A+" does not already exist in the population it cannot be made to exist by selection. Mating two organisms together does not cause the most useful combinations to occur, what gets passed to the offspring is chance combinations.
... New gene combinations are one of the main sources of variation.
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.
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
I think we are talking past each other here because of the disagreement over the role of sexual combination/s, mutation/s and genetic change/s.
However you cut the mustard though, what you have is random generation of new genetic sequences. A parent does not choose what traits to pass on to its offspring. A mating pair does not choose the best combinations of genes for their offspring.
If there are new randomly generated genetic sequences, and if these affect the phenotype, then they may be subject to selection. Those best suited to surviving and reproducing will pass more of their genes to the next generation, but this will not select for more fit than necessary. Nor will their breeding guarantee that those traits will be passed on.
Let's discuss the evidence.
Indeed.
Message 50
The citT is normally silent, being re-activated via duplication. The duplication event did not create an extra coding gene, just re-activated an old silent gene that was already common in the population.
As I said in Message 47:
... Let the denial and equivocation commence.
Right on cue.
The citT is normally silent, being re-activated via duplication. The duplication event did not create an extra coding gene, just re-activated an old silent gene that was already common in the population.
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.
But more importantly you are equivocating on your original claim:
Message 1: mindspawn has stated a concern that:
"I have been looking ... for some evidence that a gene can duplicate, and then produce a novel function in the duplicated coding gene that adds fitness. Haven't seen it yet,..."
  • You asked for a gene duplication event: you got that.
  • You asked for it to then provide a novel function: you got that.
  • You asked for it to show increased fitness: you got that.
You got what you asked for, the fact that you don't like it doesn't change the fact that you got what you asked for.
Cognitive dissonance occurs when evidence\information from outside your experience\knowledge contradicts the worldview you have build up, and the degree to which the new evidence\information is resisted depends on the strength of your personal beliefs - how much you don't like it - regardless of how factual the new evidence\information is.
.. 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.
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.
As I said in Message 47 QED - quod erat dēmōnstrandum (that which was to be demonstrated).
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. ...
It rarely adds fitness because it adds fitness?
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.
... 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.
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.
I'm looking for additional coding genes, not silent copies.
You're moving the goalposts.
Enjoy.

we are limited in our ability to understand
by our ability to understand
Rebel American Zen Deist
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This message is a reply to:
 Message 50 by mindspawn, posted 02-10-2013 6:48 AM mindspawn has replied

Replies to this message:
 Message 52 by mindspawn, posted 02-11-2013 6:24 AM RAZD has replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 54 of 65 (690818)
02-16-2013 11:57 AM
Reply to: Message 53 by mindspawn
02-16-2013 10:35 AM


new topic perhaps
... 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, ...
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 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.
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.
Enjoy
Edited by RAZD, : clrty
Edited by RAZD, : No reason given.

we are limited in our ability to understand
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This message is a reply to:
 Message 53 by mindspawn, posted 02-16-2013 10:35 AM mindspawn has replied

Replies to this message:
 Message 56 by mindspawn, posted 02-18-2013 4:07 AM RAZD has replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


(1)
Message 55 of 65 (690837)
02-16-2013 6:23 PM
Reply to: Message 52 by mindspawn
02-11-2013 6:24 AM


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'm going to start out by picking some nits:
The CitT gene is known to be responsible for the Cit+ phenotype:
Not quite: the CitT gene is well known to code for the protein responsible for transporting citrate into the cell under anoxic\anaerobic conditions, and it is well known that this does not work in aerobic conditions with "wild" E.coli.
The "Cit+ phenotype" in your article is a manufactured strain, made for the purpose of demonstrating that citT was the active transport coder for anaerobic conditions by making it work in aerobic conditions. The single modification to the gene made it work, isolating the function to the gene.
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 Tactivates expression of the citrate transporter when oxygen is present, and thereby enabling aerobic growth on citrate"
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.
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.
When the citT gene was duplicated it had a function\feature\trait that the parent population did not have. Remember our agreed definition of novel (Message 9):
Would you agree that a novel feature\function\trait would be one that did not exist in a previous generation?
Regarding novel features and functions, I don't see why you have included that in your list because I see no dispute there and do not feel it should be part of our terms of reference ...
Now let's return to the description of what occurred in the Lenski et al experiment:
Inaugural Article: Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli - PMC
quote:
The role of historical contingency in evolution has been much debated, but rarely tested. Twelve initially identical populations of Escherichia coli were founded in 1988 to investigate this issue. They have since evolved in a glucose-limited medium that also contains citrate, which E.coli cannot use as a carbon source under oxic conditions. No population evolved the capacity to exploit citrate for >30,000 generations, although each population tested billions of mutations. A citrate-using (Cit+) variant finally evolved in one population by 31,500 generations, causing an increase in population size and diversity. ...
Please note the complete absence of cit+ behavior for over 30,000 generations in all 12 isolated populations. Note that each population "tested billions of mutations" without enabling cit+ behavior.
The question is not that citT exists in the genome, but that in the "wild" E.coli strains the citT normally only works in an anaerobic environment, while this new strain has adapted to use it in an aerobic environment.
Now, from your article:
quote:
Under oxic growth conditions, most Escherichia coli strains are not able to utilize citrate due to the lack of a functional transport system. This is a key characteristic of E.coli among enterobacteria (15). ...
Enterobacteria live in intestines and do not need to be adapted to aerobic conditions. They are part of the fauna that help you digest food. Curiously, I worked with some E.coli back in the late '60's on an investigation of stream pollution in N. Carolina. They were\are used to test water for fecal contamination, because they naturally die off in aerobic conditions, and their presence in water demonstrates recent fecal contamination.
quote:
Under anoxic conditions in the presence of an oxidizable cosubstrate such as glucose or glycerol, Escherichia coli converts citrate to acetate and succinate. Two enzymes are specifically required for the fermentation of the tricarboxylic acid, i.e., a citrate uptake system and citrate lyase. Here we report that the open reading frame (designated citT) located at 13.90 min on the E.coli chromosome between rna and the citrate lyase genes encodes a citrate carrier. E.coli transformed with a plasmid expressing citT was capable of aerobic growth on citrate, which provides convincing evidence for a function of CitT as a citrate carrier. ...
In other words, the E.coli used in your article were modified in the lab -- "transformed with a plasmid expressing citT" ... not a "wild" strain:
quote:
Bacterial strains and growth conditions. E.coli DH5α (Bethesda Research Laboratories) was routinely used as the host for the cloning procedures. E.coli JM83 (38) was used for the preparation of chromosomal DNA by the method of Marmur (18). E.coli BL21(DE3), which contains the phage T7 RNA polymerase gene under the control of the lacUV5 promoter (33), served as the host for the expression of citT and citS from pET-derived plasmids (Novagen). ...
ie - this is not a "wild" strain of E.coli, nor does it's behavior with citT represent the behavior of "wild" E.coli in aerobic conditions.
Nor, apparently, is it related to the E.coli -- strain Bc251, isolated since 1966 -- used by Lenski et al in his experiment:
http://myxo.css.msu.edu/ecoli/strainsource.html
quote:
A 1966 paper* by Seymour Lederberg (Joshua's brother) describes the derivation of the T6r, Strr, r-m-, Ara- variant of E.coli B with which we work. See section 3 of the table on page 1031 of Lederberg's paper for that derivation. The strain was then given by Seymour to Bruce Levin when they were both on the faculty at Brown University.
By the time that I arrived in Bruce's lab, in April of 1982, the B strain was stored frozen. I took an aliquot to Irvine in the fall of 1985, and I re-froze a new stock from a single-colony isolate. In Irvine, I also selected the particular Ara+ variant that we now use as a spontaneous mutant on an MA plate.
Fresh single-colony isolates of the Ara- and Ara+ variants were frozen at -80C and designated as REL606 and REL607, respectively. I started the long-term experiment, which continues to this day, on February 24, 1988.
Note that all 12 isolates originate from a single clone colony.
Now your job, seeing as you claim that ...
The CitT gene is known to be responsible for the Cit+ phenotype:
... is to demonstrate that:
  1. this holds true for the founding population of the Bc251 strain used by Lenski
  2. that this is the same mechanism found by Lenski in his cit+ population, not a different mechanism,
  3. that this holds true for the common ancestor population between the two strains, Bc251 and JM83 (DNA source in your article)
From what I see there are 12x30,000 = 360,000 generations of E.coli that say you are wrong.
Note that the Lenski articled also says:
quote:
What physiological mechanism has evolved that allows aerobic growth on citrate? E.coli should be able to use citrate as an energy source after it enters the cell, but it lacks a citrate transporter that functions in an oxygen-rich environment. One possibility is that the Cit+ lineage activated a cryptic transporter (41), that is, some once-functional gene that has been silenced by mutation accumulation. This explanation seems unlikely to us because the Cit− phenotype is characteristic of the entire species, one that is very diverse and therefore very old. We would expect a cryptic gene to be degraded beyond recovery after millions of years of disuse. A more likely possibility, in our view, is that an existing transporter has been coopted for citrate transport under oxic conditions. This transporter may previously have transported citrate under anoxic conditions (43) or, alternatively, it may have transported another substrate in the presence of oxygen. The evolved changes might involve gene regulation, protein structure, or both (61).
Yes, non-coding duplications are occasionally beneficial. This does not contribute towards this thread which is about additional beneficial coding genes.
Trying to move the goalposts again.
The second coding gene is the critical element -- once that happens the cit+ behavior happens in those 30,000 generation old populations from the single lineage that has the two previous "enabling" mutations.
It is an additional beneficial coding gene.
Generations without the duplication do not have the novel beneficial behavior.
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).
Your claim is that the cit+ behavior was hidden\silent in the E.coli Bc251 strain and popped into use when needed.
What the Chlorella demonstrates - in spades - is what happens when hidden\silent traits are activated by an ecology\environment where it is a better adaptation than remaining hidden\silent.
By contrast, after some 30,000 generations and billions of mutations, the E.coli Bc251 strain does not exhibit this hidden trait.
Again from the Lenski article:
quote:
Other findings suggest that E.coli has the potential to evolve a Cit+ phenotype. Hall (41) reported the only documented case of a spontaneous Cit+ mutant in E.coli. He hypothesized that some complex mutation, or multiple mutations, activated cryptic genes that jointly expressed a citrate transporter, although the genes were not identified. Pos et al. (43) identified an operon in E.coli K-12 that apparently allows anaerobic citrate fermentation, and which includes a gene, citT, encoding a citrate—succinate antiporter. High-level constitutive expression of this gene on a multicopy plasmid allows aerobic growth on citrate, but the native operon has a single copy that is presumably induced only under anoxic conditions.
Despite this potential, none of the 12 LTEE populations evolved the capacity to use the citrate that was present in their environment for over 30,000 generations. During that time, each population experienced billions of mutations (22), far more than the number of possible point mutations in the ≈4.6-million-bp genome. This ratio implies, to a first approximation, that each population tried every typical one-step mutation many times. It must be difficult, therefore, to evolve the Cit+ phenotype, despite the ecological opportunity. Here we report that a Cit+ variant finally evolved in one population by 31,500 generations, and its descendants later rose to numerical dominance. ...
He disagrees with you, and not curiously, I find his argument more compelling than yours.
Note that reference 43 is your article, so Lenski is\was familiar with it and what it showed.
Note further that only two instances of E.coli using citrate are mentioned by Lenski -- as part of the normal review of existing literature that goes into writing a proper peer reviewed scientific article -- one of them involves the only other documented mutation, and the other involves a manipulated genome.
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.
Equivocation, imho, as we are talking about new genetic sequences that evolve to facilitate citrate metabolism, and I am unaware of mechanisms to do this without coding.
Now review Message 30:
What is a "coding gene" versus a "non-coding gene" and how do we tell them apart?
What I have in this regard is:
PHSchool.com Retirement—Prentice Hall—Savvas Learning Company
quote:
Concept 4: Basic Structure of a Protein-Coding Gene
A protein-coding gene consists of a promoter followed by the coding sequence for the protein and then a terminator.
The promoter is a base-pair sequence that specifies where transcription begins.
The coding sequence is a base-pair sequence that includes coding information for the polypeptide chain specified by the gene.
The terminator is a sequence that specifies the end of the mRNA transcript.
Coding, of course, can apply to more than proteins\polypeptides.
In this case, of course, we are talking about encoding for transport proteins ...
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.
Grasping at straws? Please note that your article says:
quote:
... a plasmid-linked gene encoding a citrate carrier ...
Let me repeat (from Message 51):
"I have been looking ... for some evidence that a gene can duplicate, and then produce a novel function in the duplicated coding gene that adds fitness. Haven't seen it yet,..."
  • You asked for a gene duplication event: you got that.
  • You asked for it to then provide a novel function: you got that.
  • You asked for it to show increased fitness: you got that.
And add:
  • You asked for it to be a coding gene: you got that.
Enjoy
Edited by RAZD, : clrty

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This message is a reply to:
 Message 52 by mindspawn, posted 02-11-2013 6:24 AM mindspawn has replied

Replies to this message:
 Message 57 by mindspawn, posted 02-18-2013 4:24 AM RAZD has replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


Message 58 of 65 (691004)
02-18-2013 9:00 PM
Reply to: Message 56 by mindspawn
02-18-2013 4:07 AM


Re: new topic perhaps
... , I find your comprehension of my position a little lacking, ...
Would you rather debate with someone else - like bluegenes - if so we can switch out.
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 ...
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This message is a reply to:
 Message 56 by mindspawn, posted 02-18-2013 4:07 AM mindspawn has not replied

  
RAZD
Member (Idle past 1404 days)
Posts: 20714
From: the other end of the sidewalk
Joined: 03-14-2004


(2)
Message 59 of 65 (691005)
02-18-2013 9:07 PM
Reply to: Message 57 by mindspawn
02-18-2013 4:24 AM


Denial and equivocation are not rebuttal arguments.
I do appreciate that, no problem.
And yet you just blow off what I post.
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. ...
The duplication is "head to tail" -- indicating (to me anyway) that it comes directly after the other and in the same alignment.
... 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.
Denial and equivocation are not rebuttal arguments. I'm sorry but if this is all I'm going to get in response then I have better things to spend my time on.
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?
Perhaps you need to elucidate what you expect to see from an evolutionary model, and then we can discuss how false or underinformed that idea is.
Enjoy
Edited by RAZD, : clrrty
Edited by RAZD, : subt

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:
 Message 57 by mindspawn, posted 02-18-2013 4:24 AM mindspawn has replied

Replies to this message:
 Message 60 by mindspawn, posted 02-19-2013 4:48 AM RAZD has replied

  
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