Summations Only

Is the following representative of what you would consider a novel mutation?(letters indicate gene sequences and associated codes)Original organism: A B C D E F G H I JOrganism after mutation: A B C D E K F G H I JYou do realize this is how creation ex nihilo works, not evolution, don't you? Evolution uses existing materials to develop new features and new functions for existing features. It doesn't create something from nothing. If you wonder how the information got there in the first place, that is a different subject. This topic is discussing how evolution creates novel features using existing information.Essentially you are committing the straw man fallacy, but with a unique twist; instead of setting the straw man up and beating on it (which is the common way this fallacy is executed), you set the straw man up and say that he can kick the ass of the current theory. So those here that are arguing against you, end up beating on your straw man that you yourself set up. Even if "new information" dropped from the sky and fell right into a cell, it would still require an energy input. So in your opinion, the only way to generate "new information" is ex nihilo creation. Your whole perception of "information theory" shows a complete lack of understanding about how genetic information works and is utilized.HBD

(herebedragons) Sorry but not a living soul on this planet can explain it scientifically. I will counter with adaptation uses existing materials to develop new features and new functions for existing features. But adaptation will never change one species into another. Adaptation is observed, evolution has never been observed. My point is scientific yours is speculation.The question begging an answer is where the "features" that existed beforehand came from if not from a creator. Now explain how citT evolved and speculate all you need to. It not only doesn’t but it cannot. Your ongoing strategy of compartmentalize and concur. Since evolution is speculation, you must replace it with adaptation. Unless we are talking about religion or philosophy. I am flattered, but really, I am not that clever. You are losing the debate because you are simply in the wrong. Try using the word of God to navigate science and you will enjoy the same rate of success I do.

Ah, I see. You've decided to simply declare yourself the winner, an achievement normally accomplished by building arguments around evidence, an approach you've avoided so far. There's only 12 messages left in this thread, better get started.This particular message was filled with the same empty assertions whose rebuttals you ignored. We could rebut them again, but you'll likely just ignore them again, so with only 12 messages left there seems little point.--Percy

Well you haven't really since my point was using terms like homozygous and heterozygous to describe the population of E.coli in this experiment would cause confusion, and this paragraph does pretty much prove my point. For example why do you expect 'to reduce the heterozygosity to zero' at the SNPs flanking the selected site (I assume this selected site is the genetic trait being fixed)? Why do you need to show a classic sweep to show evolution is occurring? How do you know if you've run across positive evidence if you don't know what evidence you are looking for or have misconceptions of what it should look like.This looks like you are just trying really hard to shoehorn your own 'definition' that novel mutations must be fixed while still trying to rule out mutations in E.coli as novel, even although others have pointed out that the cit+ trait was fixed in populations grown on citrate containing media since those lacking the specific mutations could not survive in that environment. You even accept the difficulty of fixation in sexually replicating organisms which again contradicts you're idea that genes must be fixed to be novel. There is nothing in biology that says genes must be fixed in a population. There will be variation, and given a spread of environmental selective pressures a population can experience, this means that sub-populations will carry sub-sets of this variation depending on the local environment.
As for the question of adaptive change the problem is you're comparing the single-celled E.coli to multi-celled organisms. The perceived adaptive change is not at the cellular level, it is how that colony of cells interacts with each other to create structures. Answer yes to what, I didn't notice a question? Anyway we're not that kind of operation. We're a diagnostic lab, so we don't define what the species are, we just identify bacteria and what antibiotics are effective so doctors can treat the patient. The only reason I brought it up was to show that there is a lot of variation in E.coli and although we still describe it as a single species, albeit subdivided into strains, it would be possible to identify enough variation to segregate into separate species, just as we have with species which have been more recently identified, such as Acinetobacter baumanii and A.calcoaceticus, with the variation of A.genomospecies 3 straddling the two so we can't assign it to one or the other. And yet it is still easier to describe E.coli as one species because it has been known for so long and the phenotypic variation is so well documented. And if you keep on changing the names you will confuse the doctors
Anyway, before I get carried away, in general people get hung up on speciation. Really defining a species (or subspecies or strain) is a tool for categorising, so that we know we are talking about the same thing. It is just easier for multi-cellular organisms since expanses of time have allowed enough variation in morphology or even behaviour to be distinct. It's harder to define as species when the organisms you're dealing with subtle differences using techniques that are only coming into main-stream use. But if you want to discuss this further you should propose a new topic. I'm not going to get into the issues of using computer programming as an analogy for genetics, and others have covered the problems with assuming the only process in evolution is random change. But note that you state that the numbers showing up in the wrong place could be disastrous. Now consider those changes described in Lenski's E.coli which you describe as not novel, there is duplication of promoter and gene sequences being reintegrated into the genome along with SNPs and other indels. All this rearrangement has the probability of inserting something into the wrong place, with the disastrous outcome being the death of that particular cell. But there is other cells in that colony retaining the previous mutations and they have the potential of further mutations that aren't detrimental. Sounds like some form of selection that occurs naturally.Also what are you referring to as hypermutation, how does it differ from normal mutation? And as for the term somatic if you are using this in the context of the E.coli then it doesn't make sense to describe it as somatic, but if you're discussing multi-cellular organisms then somatic mutations are not inherited. This is the problem of throwing around technical terms which only serves to confuse matters as it's not immediately apparent that you know what the terms mean, just as discussed above about homozygous/heterozygous. The point was it is the hox genes that define the digit placement, because as shown by my Drosophila example and your chickens toes, mutations of the hox genes did not cause deformed digits, they caused replication of digits in positions they were not supposed to be. The hox genes define how cells divide and interact with their neighbouring cells and which genes to express. For example look at the earliest stages of embryo development, with the cells separating into the ectoderm, endoderm and mesoderm. This differentiation then defines what tissues the daughters cells become, and as development continues so does this differentiation and specialisation, as the pattern of expression of hox genes coordinates what genes in the dividing cells are expressed. Gradual changes in this pattern of expression will affect the structures these tissues form, including changing a hand into a fin, or altering the gastrointestinal tract to exploit alternative food sources. This is more subtle changes in timing of expression, nothing as extreme as the example in Lenski's E.coli of a chunk of the genome being reshuffled to land a citT gene next to a new promoter region. Well given that science is based on evidence this restatement of your view seems somewhat redundant, and you would have done better to describe your evidence that actually shows it's impossible. I have done Biology at university, and although the courses I've done were not specifically about genetics, there was still a lot of genetics involved, and from what I have learned I would have to say that it is indeed possible. Of course it's nothing as simplistic as an SNP, but as I described above with the hox genes it doesn't need new information, just reinterpretation of what is already there. However, we can see with a duplication of a hox gene and subsequent adaptation a new structure could arise. I've already covered this above, but I'd just like to ask why you view this example of adaptions to a specific diet as a 'trait'? You do realise that these adaptions are under the influence of hundreds of gene interactions and consequently there will be a great deal of variation. There is not going to be any fixation, rapid or otherwise. It just means that when food is scarce, those that are better able to take advantage of what's available will survive, and those that can't will die. And that is common to both bacteria and multicellular eukaryotes.Anyway I'll let others continue the topic as they're doing a better job of refuting you than I am.Edited by Malcolm, : No reason given.

I don't see how changing the terms changes anything. So should we change the discussion to how does adaptation produce novel features? Oh and let's change "novel" to "different".So now the question is: How does "adaptation" produce "different" features. Does that correct the "errors" in terminology? The question may indeed beg the answer, but that is not what the thread is about. Biological evolution (notice the forum we are in) assumes preexisting material. Do you assume that new features are created ex nihilo on the fly. Or that all creatures are essentially the same as they were when they were first created? You can't actually believe this. Lol! The debate hasn't even begun! I don't know what you mean by "novel" or "evolution" or "species" or "adaptation" or "scientifically" or just about anything else you have said. I do use the Word of God to navigate my life. So if I use it to navigate my life and within my life I engage in science, then I am using the Word of God to "navigate science." Other than that I don't know how else I should be using it to "navigate science." How would you apply the Bible to the issue we have been discussing, the "adaptation" of citrate utilization in e-coli?But if by success you mean "denying reality", I just can't accept that as success.If the whole point you are trying to make is that the "adaptation" of citrate utilization cannot be extrapolated to the sort of evolution that results in changing an arm into a wing, you may have a valid argument. But you are not going to advance that argument by equivocating on definitions, denying clear facts and submitting baseless assertions.HBD

So do you really believe this crap or are you just scoring debate points?'Cause I could explain evolution to you... but you seem to just want to oppose any sense of it rather than try to understand it.So? Yea or nay?

Using your definitions, all you need is adaptation in order to produce new species. Every single DNA difference between any two species is just a modification of what was already there. The evolution of terrestrial tetrapods? The fish already had swim bladders and fins. These were just adapted to moving about on land and breathing air. According to you, this isn't evolution. This is adaptation. In fact, using your definition of evolution we do not even need evolution to produce the biodiversity we see today from a simple replicator. All we need is adaptation.What this really boils down to is semantics. What we call evolution you call adaptation. A rose by any other name . . . What you describe as adaptation is exactly what we describe as evolution. Evolution is descent with modification. You are claiming that adaption is descent with modification. They are the same.

Just ran across this abstract:

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Proc Natl Acad Sci U S A. 2012 Oct 16;109(42):16894-9. doi: 10.1073/pnas.1211831109. Epub 2012 Oct 3.
Transforming a drug/H+ antiporter into a polyamine importer by a single mutation.
Brill S, Falk OS, Schuldiner S.
SourceDepartment of Biological Chemistry, Alexander A. Silberman Institute of Life Sciences, Hebrew University of Jerusalem, 91904 Jerusalem, Israel.

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Abstract
EmrE, a multidrug antiporter from Escherichia coli, has presented biochemists with unusual surprises. Here we describe the transformation of EmrE, a drug/H(+) antiporter to a polyamine importer by a single mutation. Antibiotic resistance in microorganisms may arise by mutations at certain chromosomal loci. To investigate this phenomenon, we used directed evolution of EmrE to assess the rate of development of novel specificities in existing multidrug transporters. Strikingly, when a library of random mutants of EmrE was screened for resistance to two major antibacterial drugs-norfloxacin, a fluoroquinolone, and erythromycin, a macrolide- proteins with single mutations were found capable of conferring resistance. The mutation conferring erythromycin resistance resulted from substitution of a fully conserved and essential tryptophan residue to glycine, and, as expected, this protein lost its ability to recognize and transport the classical EmrE substrates. However, this protein functions now as an electrochemical potential driven importer of a new set of substrates: aliphatic polyamines. This mutant provides a unique paradigm to understand the function and evolution of distinct modes of transport.
[emphasis mine]

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A single mutation changed the substrate specificity of the protein resulting in a novel form of antibiotic resistance.Edited by Taq, : No reason given.

Genesis 30:30-43 may address this, or more likely, not quite.

I came across this whilst using a new (to me) science only search engine:Scirus is the most comprehensive scientific research tool on the web. With over 460 million scientific items indexed at last count, it allows researchers to search for not only journal content but also scientists' homepages, courseware, pre-print server material, patents and institutional repository and website information.
Elsevier | An Information Analytics BusinessAnyhoo, I've now got some reading to do. darwin's tomatoes & the evolution of novel features : BioBlog: University of WaikatoQuintessence of Dust: How the bat got its wing

Tangle, as interesting as your examples are, surely they just show change in function, but not increased complexity. Yes deletions can change a species into a new one, disabling of a gene too. Adjustments to protein production can replace a function with a new one. But how do you add an extra functional gene? Whenever an added gene produces proteins the duplication of the proteins damages fitness to an organism. Have you got any examples of successful and natural increases to the number of protein producing genes?

It would appear that a gene duplication resulted in more complex brain morphology in humans:

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A team led by scientists at The Scripps Research Institute has shown that an extra copy of a brain-development gene, which appeared in our ancestors' genomes about 2.4 million years ago, allowed maturing neurons to migrate farther and develop more connections.
http://www.sciencedaily.com/...ases/2012/05/120503125720.htm

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It would also appear that gene duplication was involved in the vareity of eye complexity amongst Pancrustaceans:

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Overall, and when accounting for factors such as differential rates of whole-genome duplication in different groups, our results are broadly consistent with the hypothesis that genes involved in eye development and phototransduction duplicate at a higher rate in Pancrustacea, the group with the greatest variety of optical designs.
Gene duplication and the origins of morphological complexity in pancrustacean eyes, a genomic approach - PubMed

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Or you can do a simple google search for "gene duplication evolution" and check out the science for yourself. Plenty of papers to read out there.

Welcome mindspawn ... Here is an article about new functional sex genes in Drosophila. They discuss three ways that new genes arise and give examples of each. Tandem Duplication:

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This type of duplication typically includes the entire coding region of a gene, along with its flanking regulatory sequences.

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The new genes then specialize and the alternate splicing functions change and new protien producing genes are formed. Retrotransposons occasionally mRNA is reverse transcribed and stuck back into the parent DNA in a random position. It then relies on regulatory sequences that flank the new gene sequence. De novo gene evolution this one is rather interesting. A formerly non-coding section of DNA can be altered so that it begins to function.(Examples of the specific genes that were studied are given in the article.) This is just plain wrong. Do you have a source that supports this? So I take it you are thinking of genetic entropy?HBD

Taq, regarding that mice example, its assumed that the extra human brain gene is a duplication because of its similarity to the original. I believe in intelligent design, and so that extra gene appears to me designed in humans to add brain function. That gene was always there.Regarding Pancrustaceans, wasn't that study also done under evolutionary assumptions? Their conclusions were based on a phylogenetic tree which is assuming interrelationships based on comparing similarities and relative complexity with the underlying assumption of evolution. Without that I don't see much proof of increased complexity as opposed to a variety of creatures already designed like that.Edited by mindspawn, : Identify who I'm replying to

Thanks for the welcome herebedragonsWhen we observe two similar species, one that has an extra coding region :
1) The extra region could have evolved
2) The missing region could have devolved complexity
3) Both species could be designed like that (intelligent design)