Evolution Theory Issue - Great Debate -mindspawn and RAZD only

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. 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. 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. 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. 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? 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

This is long, because it is full of information and evidence. E. coli long-term evolution experiment

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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.

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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]

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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.

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(color added for emphasis)Note that because this is an asexual species there is no confusion between "mutation" and "genetic change" in our understandings. 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.

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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

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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.

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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'

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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.

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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.

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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.

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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.

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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).

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Icing on the cake polyploidy

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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.)

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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]

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Polyploidy may occur due to abnormal cell division, either during mitosis, or commonly during metaphase I in meiosis.

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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), ...

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Plains Viscacha Rat

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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]

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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]

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The species is threatened by destruction of its fragmented and restricted habitat.[1]

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Whole-genome duplications in South American desert rodents (Octodontidae)

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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.

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Molecular cytogenetics and allotetraploidy in the red vizcacha rat, Tympanoctomys barrerae (Rodentia, Octodontidae)

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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.

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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.

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more at link

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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

lol, I don't envy you. We don't get snow here , way too cold for me. Sorry, you have said this before, thanks for answering again. This is an assumption. Like I have said before, I agree with most processes of evolution. But not processes that involve the adding of coding genes. So some applications of those processes are merely theoretical in my eyes but don't work in the real world. I have no issues with the terminology. Edited by mindspawn, : No reason given.

I believe the horses have not been given enough time for one, and secondly the entire population has not been bred for speed. If all horses were bred only for speed, and most of the population was changed (as occurs in nature when a new trait becomes dominant throughout a population via selective pressure) then you can apply the horse example.But why keep arguing this point, I agree that the most significant changes occur rapidly , as per your "skew curve distribution", this makes sense. Even if we keep to that view, my point is made, variation through new gene combinations leads to new traits. (speed in horses). New gene combinations are one of the main sources of variation. 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. Let's discuss the evidence.Edited by mindspawn, : No reason given.

E-coli:
The citT is normally silent, being re-activated via duplication. The duplication event did not create an extra coding gene, just re-acti
vated an old silent gene that was already common in the population. Chlorella:
Did the chlorella example involve extra coding genes? This example of yours seems to be referring to multi-cellular life.Polyploid and tetraploid organisms are common. This rarely does add fitness because there is a certain genetic hardiness that comes from having "backup" chromosomes, the organism becomes less susceptible to damaging mutations. However as is consistently observed, if the duplicates are coding, then the organism loses fitness, it is the non-coding duplications of polyploidy and tetraploidy that sometimes add fitness. So these are not examples of additional coding genes.As Many Exceptions As Rules: Haploid, Diploid, And Those You Should Avoid I'm looking for additional coding genes, not silent copies.

Message 48That's too bad. I've got a lovely view outside my windows. 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 ... . And as I have said before denial does not change the facts, and opinion does not affect reality. Message 49First, 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). 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 variations are caused by new genetic sequences that result in new traits/functions/features. Again this is a stochastic process and it is not caused by selection. I 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. Indeed. Message 50As I said in Message 47: Right on cue. 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:

• 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. 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). 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. And yet, curiously, we still see cases where the organisms are fit, they survive, they breed.What this shows is that gene duplication occurs at many levels and is not a necessarily rare event, nor is it necessarily lethal. This is especially true in the plant kingdom. You're moving the goalposts.Enjoy.

Great! Yes the snowy landscapes make great viewing. I thought we have already agreed on selection. I also agree with what you are saying here regarding new features and new genetic sequences. The CitT gene is known to be responsible for the Cit+ phenotype:The Escherichia coli Citrate Carrier CitT: a Member of a Novel Eubacterial Transporter Family Related to the 2-Oxoglutarate/Malate Translocator from Spinach Chloroplasts - PMC As shown above, the trait already existed in the CitT gene, however this gene was normally silent in the population of your example: "This duplication immediately conferred the Cit+ trait by creating a new regulatory module in which the normally silent citT gene is placed under the control of a promoter for an adjacent gene called rnk. The new promoter activates expression of the citrate transporter when oxygen is present, and thereby enabling aerobic growth on citrate"The gene was normally silent, needing a promoter, when it was duplicated, this established a new but weak promoter for the gene which was then activated in aerobic environments. This whole description is about a citrate transporter gene normally silent that was then activated. The promoter sequence for the gene seems to have undergone a change, but NOT the gene itself. They do not discuss the other gene which appears to remain silent, and seems to be inverted which would disable it. I see this study as more about promoters than contributing towards any evidence of the evolution of coding genes. Yes, non-coding duplications are occasionally beneficial. This does not contribute towards this thread which is about additional beneficial coding genes. 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). You mention beneficial duplication, a process I believe in. You seem to be missing the word "coding" when you present your evidence. I said the following and fail to see why your reply does not mention coding regions:
"However as is consistently observed, if the duplicates are coding, then the organism loses fitness."I don't know how you have managed to miss the word "coding" in all my posts so far. When we defined what a coding gene is, we actually defined what a gene was, instead of delving into the word "coding". This is possibly my mistake as I always assumed that everyone who discusses these things already knows what a coding gene is, and assumed you noticed that I had deliberately used the phrase "coding gene" rather than just "gene" in most of my posts. I now see that this important definition has been left out.You get genes that code for proteins (they produce proteins) and you get pseudogenes that are dysfunctional. These pseudogenes are often described as "disabled" or lacking "expression" I am aware that pseudogenes sometimes add fitness, but my focus is on protein-coding genes because these have shown to have a high degree of functionality in the genome and are more easily counted and defined. Not at all. You have shown an unusual lack of interest in the word "coding" that I have been consistently using throughout the thread. Hopefully this is now sorted out, a coding gene is one that codes for proteins. Pseudogenes, silent genes, disabled genes are non-coding. Any evidence you put forward that the re-enabling or creating of pseudogenes adds to fitness is irrelevant to this discussion.In post 13 I emphasized that we were referring to coding genes, definitely no moving the goalposts: Proof of additional coding genes that are beneficial would help your case, that is what I have been asking for all the time. I have already agreed that non-coding regions add fitness (post 13), and I have also agreed with the process of re-activating of a de-activated gene adding fitness in my post 21: Even in post 1, you quoted me twice asking for proof of additional CODING genes, so this requirement has always been there from the start of this thread and there has been no moving of goalposts, maybe you have misunderstood my position.Edited by mindspawn, : No reason given.Edited by mindspawn, : No reason given.Edited by mindspawn, : No reason given.Edited by mindspawn, : No reason given.

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

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. 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.EnjoyEdited by RAZD, : clrtyEdited by RAZD, : No reason given.

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: 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 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. 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): 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

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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. ...

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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:

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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). ...

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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.

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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. ...

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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:

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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). ...

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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

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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.

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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.

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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.

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Note that all 12 isolates originate from a single clone colony.Now your job, seeing as you claim that ... ... 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:

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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).

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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. 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:

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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.

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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. ...

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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. 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: Coding, of course, can apply to more than proteins\polypeptides.In this case, of course, we are talking about encoding for transport proteins ... Grasping at straws? Please note that your article says:

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... a plasmid-linked gene encoding a citrate carrier ...

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Let me repeat (from Message 51): And add:

• You asked for it to be a coding gene: you got that.

EnjoyEdited by RAZD, : clrty

I find your manners pretty good, I find your comprehension of my position a little lacking, you are too focussed on my actual wording to have a real good understanding and debate on the core issues at stake. Fair enough.

I do appreciate that, no problem. I feel I did acknowledge that and said basically the same thing in my posts. I see you are not one to back down on a point, but you are really wasting your time with this particular example and showing that you are missing my whole point. You example fails to show that the duplicated gene was coding. In fact your article seems to indicate that the duplicated gene was inverted, which would disable it. I already said this. Maybe you like to blur the point with excessive posts, but please just move onto the next study, your current one is all about a duplication event that activated a promoter, but you fail to give any evidence that the duplicated gene itself was protein-coding. The normally silent gene was activated, this is no additional gene, but is a silent gene that activated using a new promoter sequence. In the end, we have a gene that was always there, being activated, and another gene being duplicated but non-coding. No additional coding genes.Edited by mindspawn, : No reason given.Edited by mindspawn, : No reason given.Edited by mindspawn, : No reason given.

Would you rather debate with someone else - like bluegenes - if so we can switch out.Enjoy

And yet you just blow off what I post. The duplication is "head to tail" -- indicating (to me anyway) that it comes directly after the other and in the same alignment. 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.EnjoyEdited by RAZD, : clrrtyEdited by RAZD, : subt

Suddenly or slowly, yes , I am asking for an explanation for how the number of coding genes can increase in number in an organism.