Evolution is a basic, biological process

Soplar, I also believe that many observations have been accumulated over the millenia since Genesis was written. You yourself admitted that macro-evolution has never been observed. Are there some particular observations you have in mind? Well, the Flood destroyed the edenic paradise that existed. We live in a wrecked world. Why should we expect it to operate perfectly? The Bible records life spans of nearly 1000 years pre-Flood. Post-Flood life spans drop steadily and finally reach a new equilibrium between 60-100 years (according to the Bible). Obviously, something is wrong with the post-Flood world.We are apparently welcome to find cures for cancer; though I doubt the sincerity of the scientists, to which you refer. If there is no money to be made, there will be no cure found. Only medicines that can be patented will ever reach us.It's off-topic (and we can start a new thread if you like), but I would bet that cancer rates are very much lower (nearly non-existent) in areas that do not have good medical facilities...particularly areas that do not vaccinate the populations and that eat lots of vegetables and live low-mental-stress lives. That's not an assertion, but an "I betcha" type thing we could study a little, to whatever extent the Internet would allow.But, more interesting to me is that you think evolution explains things. What does evolution explain? Fossils result from geological events; not biological events; so evolution doesn't explain fossils, which only prove that many creatures "beat the odds" and found themselves in the amazing situations that are pre-requisite to fossilization. I am not sure that aging is a result of copying errors, but, even if it is, aging is NOT evolution. I'm pretty sure many cancers are a result of copying errors, but cancer is NOT evolution. What exactly does evolution explain?The evolutionist looks at almost any aspect among living creatures and says, "Random mutations and natural selection, working together, produced this." When coupled with your admission that macro-evolution has never been observed, I really have to wonder what is so explanatory about such a statement. It sounds more like yet ANOTHER BELIEF about HOW THINGS CAME TO BE.--TL

HappyAtheist,Soplar specifically said that evolution is observed under the microscope, and I am challenging that specific assertion. I really doubt that it is directly observed in any manner. What you describe is a setup that makes the idea that a mutation occurred to confer the resistance an easy inference to make, but it is very different than watching the whole process under the microscope. Are you certain that the bacterial DNA doesn't code for variableness in some fashion? It is my understanding that our immune system is able to do some neat things with DNA that cause random changes in certain structures in T-Cells or B-Cells or something like that (in the attempt to mirror some part of the invaders, generally, as I understood). Why can't the bacteria use some similar method to cause variants to be produced during miosis? In which case, it is not random mutations but pre-programmed random variableness.I get the impression that nearly ANYTIME you add an antibiotic to any bacterial population, you soon wind up with a resistant population (due to extermination of all non-resistant types). This just seems a little quaint to me if RANDOM MUTATIONS are the key factor.This message has been edited by TheLiteralist, 01-31-2005 05:46 AMThis message has been edited by TheLiteralist, 01-31-2005 05:47 AM

Your whole genome comparison comparison should make it fairly evident what sort of genetic changes have occurred. If all you detect are point mutations then it is very unlikely that any sort of genomic re-arrangement was involved. Your impression is incorrect. If it was then molecular biologists would have a much harder time of it. The usual method for producing large amounts of DNA is using an antibiotic resistant plasmid carrier in a bacterial line. If any bacterial population would evolve resistance when exposed to an antibiotic then we would not be able to screen for plasmid containing bacteria. It may be true when you have multiple exposures for very large populations, but it certainly isn't true for all populations.A comparison of antibiotic resistance based on initial concentration of the bacterial culture should answer the question of how the resistance arises. If the mechanism is along the pre-programmed variability spectrum you suggest then a much smaller initial concentration should have at least one resistant individual than if the resistance arises from random variation throughout the genome.I can't give you the right sort of figures off hand, but I'm sure that both systems could be modelled sufficiently to get some reasonable ball park figures, or at least the straight forward traditional random mutation could be, your model seems a little sketchy at the moment and therefore it may be rather hard to predict what the values would be, but the expected frequency of resistant bacteria should certainly be higher than in a traditional model.(Edited to add) Actually in retrospect there are some already recognised chromosome rearranging or mutation rate altering strategies which have been observed in bacteria under stress, the problem is that these are very rarely directional in anyway. If all you are doing is creating a new source of random variation I don't see how you are changing the situation in regards to the origin of the trait. Survival strategies relying in increased rates of random mutation still have random mutation as the key factor.TTFN,WKThis message has been edited by Wounded King, 01-31-2005 06:45 AM

Hi WoundedKing,First, let me thank you for your reply. I must be much more careful when responding to you...I think you actually know stuff (I don't necessarily...just lots of guessing)I have just been dying to get your general reaction (because this is your field) to my pre-programmed variability spectrum model (sounds so scientific when put that way ). For you to even hint that my "model" might be valid in some way astounds me (in a good way).You must understand that I have only a highschool level understanding of biology. I took no biology courses in college because I hated that subject (not because of evolution but because of the phenomenal array of facts that must be memorized for tests; chemistry was hated only slightly less; I loved physics and took level I of that in college).With you, not only because of your expertise, but also your willingness to consider my idea (such as it is), I am not actually wishing to "debate" but to "discuss." That being said, I do want to be clear that I am proposing a type of limited random variablness. In my mind, this could work two ways:

1. Any given bacterium has several variations possible in its DNA, but only one can be active in that bacterium. It's descendants might get the sequenced scrambled (the code would control this scrambling somehow) to make one of the other variations (of any particular structure) active, or
2. Certain segments of the DNA will be scrambled (within certain limits) during any given replication event. Again, which segments get scrambled, as well as how or when, would be controlled by the code in some fashion.

Is this more detailed description anything at all like what you were thinking I meant?I don't see a reason that any particular population (since my impression was incorrect, as you pointed out) should necessarily have the variation that confers resistance, but, I would agree that either of the two above methods, not being completely, utterly random in action, would seem to tend to produce higher frequencies of resistant bacteria in any given population. OTOH, I don't fully understand the plasmid idea. What little I've read about it intrigues me. Is resistance generally due to plasmids? Maybe the actual DNA structure of the bacterial variants has nothing to do with resistance. Maybe its only plasmids doing this and it happens concurrently with bacteria variating.Just a thought based on almost no knowledge of plasmids.Thanks again for your reply. I think any other comments you offer on this subject will be appreciated, too.--TL

WoundedKing, Well, I am a Creationist, and, as such, consider the genetic code to be a sort of physical/chemical programming language. Going from the assumption of an intelligently designed code, I began to wonder whether these ubiquitous random mutations I keep hearing about were actually a sort of pre-programmed randomness built into the genome for the sake of variation within the particular kind (whatever the Creator might consider a kind to be). In this case, I would expect the genome would probably never be affected in certain key areas (which would define the general kind in some way). However, certain areas would be frequently (though not necessarily always) targeted for change. So, the difference is whether the anti-biotic resistance and other variations/adaptations are a result of pure random mutations (changes in the genome that are not supposed to occur) or of purposeful random variableness (changes in the genome that are coded for somehow in the genome).(Edited to add: don't you also find it a bit intriguing (you might not) that we are able to continue to classify bacteria and algae and the like if they truly are randomly mutating at the rates I am hearing on this board? It really seems to me that there is some limiting factor, even in the bacteria as to what kinds of changes occur in the genome.)I don't know if I've stated it quite clearly yet...I've tried and tried to explain my idea, but you are the first to try to understand it at all. I don't know how clear I'm being about it.If the idea is incorrect for some reason, I'm not going to become an evolutionist; I just found the idea intriguing.--TL
PS: And I am not saying that random mutations cannot or do not occur. Only that they probably are not the main source of DNA variants among organisms and that when they do occur they will most likely be harmless but useless or harmful to the organism.
This message has been edited by TheLiteralist, 01-31-2005 08:27 AMThis message has been edited by TheLiteralist, 01-31-2005 08:29 AM

Disclaimer: Not a biologistFrom what I understand, when an experiment is done with antibiotic resistant bacteria, scientists can look at the genome of the bacteria before and after the experiment to see what genetic changes in particular are responsible for causing the resistence.If the reason for this change is due to true random mutation or some kind of programmed random mutation then how would we be able to tell the difference?In particular, I think we have actually been able to watch mutations happen when cells divide. Given that we can actually see a cause for change in the genome that is not caused by the genome but rather the process of dividing, why should we suspect programmed mutation rather than random ones?Also, in regards to your claim that the organelles of a cell are BELIEVED to be a result of evolution, what other objective conclusion would you have science hold. Given that they act like independent cells, are disjoint, and have characteristics of a cell such as DNA, why would you consider that a "belief" rather than simply the best objective theory we can come up with given what we know. It is not as if scientists hold this "belief" true in their hearts in the same way people of faith hold true to belief in God.

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By the way, for a fun second-term drinking game, chug a beer every time you hear the phrase, "...contentious but futile protest vote by democrats." By the time Jeb Bush is elected president you will be so wasted you wont even notice the war in Syria.
-- Jon Stewart, The Daily Show

Hi, TheLit, Never take my word for something you don’t understand. Your comment isn’t unreasonable. My comments, however, were not an assumption. Nuclear and mtDNA are fundamentally different. So different, in fact, that it is hard to see how they came about in the same organism. For example, shape: nuclear DNA is a folded string, mtDNA is a circle. That’s ALL nuclear in eukaryotes, and ALL mtDNA. Composition: mtDNA has different ribosomes than nuclear DNA — different rRNA, tRNA and mRNA. In addition, mtDNA doesn’t have introns — non-coding regions. Function: mtDNA codons often code for different proteins (or have different functions) than the same sequence in nuclear DNA. For example, the nuclear DNA sequence UGA is a stop codon that specifies the end of an exon (i.e., that designates the transcription of a protein is done). In mtDNA, UGA codes for the amino acid tryptophan. Inheritance: nuclear DNA is inherited (at least in sexual, diploid organisms) 50-50 from the male and female. mtDNA is inherited cytoplasmically (IOW, not only doesn’t it split during gametogenesis like nuclear DNA, but is passed on whole cloth during meiosis from one donor only). mtDNA replicates by simple fission (basic mitosis) when the cell itself divides, but the amount of mtDNA that is segregated into each new cell is random, unlike nuclear DNA which splits evenly. Additionally, an organism may have multiple mitochondria inside each of its cells. All the mitochondria are identical — and identically different from the nuclear DNA in the cell. The membrane proteins in mtDNA are unique to mtDNA and not found ANYWHERE else in the eukaryote cell (including electron transport enzymes and H+ATPase). Finally, mtDNA doesn’t bind to histones (basically protective proteins that insure accurate copying) and has a really sloppy repair mechanism. Please note that these are not assumptions: they’re observations.So the next obvious question is, why are these two forms of DNA so different?. As a creationist, you should appreciate the fact that simply answering, well, they obviously both evolved independently within the cell isn’t a good answer — especially since most creationists reject the idea that DNA could have formed by itself in the first place. Not only once but twice? In the same cell? Your answer would be that God did it that way. End of story, no reason to look further. However, with all respect, as an attempt to understand nature, that answer is somewhat, hmmm, unsatisfactory? One approach to answering the question would be to look around and see if there is anything else out there that has similar characteristics. Lo and behold, bacterial DNA is the only thing around that has all those characteristics! More specifically, cyanobacteria (for chloroplasts) and aerobic bacteria (for mtDNA).Now we have another problem, however. How in the world did something that bears more than a striking resemblance to bacteria get incorporated into eukaryotic cells? And to the point where the euk cell can’t live without it? There may be multiple hypotheses, but one prominent one says that an early euk (almost all free-living single-cell eukaryotes are predators, btw) engulfed a bacterium and somehow didn’t finish it off, with the net result that when the euk divided, the bacterium was passed on to the daughter cell. This is an idea called endosymbiosis. Pretty far-fetched, right? Not necessarily. It is, after all, testable. As early as 1966, a biologist named Kwang Jeon at the University of Tennessee infected amoeba with a lethal bacteria. Although most of his amoeba died, a few managed to live — and reproduced with the bacteria inside them. Within a few years, Jeon found that the amoeba couldn’t live without the bacteria and further tests (where he removed the bacterial genome from the amoeba) showed that the newly uninfected populations quickly started dying. Re-infecting the same amoeba got it going again (cured it). Lynn Margulis, the principal proponent of serial endosymbiosis, discusses this particular experiment in great detail in an article in Natural History magazine (Bacterial Bedfellows, 1987, 96:26-33).All this is all very well and good, however. To make a stronger case, we need to see if there is any specific bacterial genome whose sequences match (more or less) mtDNA. Guess what? We found it in the epidemic typhus-causing bacteria Rickettsia prowazekii. Here’s an article you might find interesting that supports my contention: Andersson SG, Zomorodipour A, Andersson JO, Sicheritz-Ponten T, Alsmark UC, Podowski RM, Naslund AK, Eriksson AS, Winkler HH, Kurland CG, 1998 The genome sequence of Rickettsia prowazekii and the origin of mitochondria, Nature 396:109-110

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We describe here the complete genome sequence (1,111,523 base pairs) of the obligate intracellular parasite Rickettsia prowazekii, the causative agent of epidemic typhus. This genome contains 834 protein-coding genes. The functional profiles of these genes show similarities to those of mitochondrial genes: no genes required for anaerobic glycolysis are found in either R. prowazekii or mitochondrial genomes, but a complete set of genes encoding components of the tricarboxylic acid cycle and the respiratory-chain complex is found in R. prowazekii. In effect, ATP production in Rickettsia is the same as that in mitochondria. Many genes involved in the biosynthesis and regulation of biosynthesis of amino acids and nucleosides in free-living bacteria are absent from R. prowazekii and mitochondria. Such genes seem to have been replaced by homologues in the nuclear (host) genome. The R. prowazekii genome contains the highest proportion of non-coding DNA (24%) detected so far in a microbial genome. Such non-coding sequences may be degraded remnants of 'neutralized' genes that await elimination from the genome. Phylogenetic analyses indicate that R. prowazekii is more closely related to mitochondria than is any other microbe studied so far.

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Whew. I hope this is a better explanation of why I made the statement concerning bacteria and eukaryote organelles. Chloroplasts have the same history, except their genome is closer to blue-green algae. Umm, bacteria didn’t evolve into mitochondria. They represent formerly free-living bacteria that shed some of their duplicative functions (especially concerning replication) when they became endosymbionts with eukaryotes. Neither can live without the other, as Jeon’s experiment showed once the process continued to its logical conclusion. And Jeon’s experiment (and others since) have shown that it is actually a relatively fast process, all things considered. So yeah, endosymbiosis has been observed. Not the exact duplication of mtDNA, but the process itself. On the contrary, as I showed, recourse to the idea of creation is a dead end. It simply begs the question — or at best causes us to shrug our shoulders and say God works in mysterious ways or words to that effect. Recourse to evolution actually provides an explanation for the observations. Is it totally correct and do we know all the answers to this question? Probably not — but we’re working on it. Unlike creationists, who have already given up trying to figure out nature.This post has already gotten pretty long. I’ll address the macroecology question in a later post. Yep. Pharomachrus mocinno, family Trogonidae, the resplendant quetzal, is my favorite bird. One of my signal triumphs during my stint in the tropics was developing an effective management and conservation plan to save a cloud forest preserve from illegal logging. One of the keystone species in that forest was the Northern Resplendant Quetzal (P.m. mocinno). Absolutely the most magnificent bird I have ever encountered.

Actually, they do apply. Let me take just one — island biogeography. I asked You said This is actually one component of the answer — very good. However, it has more to do with the origin of the islands themselves rather than how far they are away from the nearest continental landmass. Even distance is of lesser importance than origin. Bali and Lompok, for instance, are less than 20 miles apart, but they have very different biotic assemblages (well, at least as concerns mammals) even though the habitats, climates, etc are almost identical. Continental islands (islands that were once part of a continental landmass) have more organisms overall and more species for the same surface area (i.e., higher biodiversity) than oceanic islands (islands that were never tied to a continent, or that separated due to plate tectonics such a long time ago that the distinction is moot). However, oceanic islands have orders of magnitude more endemics than continental islands, (an endemic is a species that is found there and nowhere else on Earth), even though they have fewer actual species (the exceptions being very large, ancient continental islands such as Madagascar which separated from the nearest continent a very VERY long time ago). Why is that, do you think?How about some specifics? Take a look at the Hawaiian silversword alliance. These plants consist of some 28 distinct species, all endemic. They are different enough from one to another that taxonomists place them in three distinct genera. Was it multiple colonisations of these oceanic islands? Nope: molecular phylogeny shows that this alliance is monophyletic (IOW, these 28 species in three genera descended from a single common ancestor!). Since they exist nowhere else, what explains the high diversity of these plants? How about land snails on islands? The Hawaiian islands are especially rich in snails: around 1000 species. How many are endemic? 99+%!So what is the explanation for all these observations? A creationist might claim that God made them that way. If that was the case, God got really creative on islands, to the exclusion of mainland continental masses. And made an incredibly subtle distinction between the fauna of continental and oceanic islands, while still impoverishing even the continental islands' biodiversity and increasing the number of endemics. Odd, no? Riddle me this: why in the world would God put a flightless pigeon on Mauritius, or flightless rails on St. Helena (not just one, but 9 different species found nowhere else)? Why not put actual trees on St. Helena rather than using overgrown daisies to fill that niche (complete with woody bark)? The creation account simply doesn’t make sense.OTOH, evolution explains all these observations quite handily — although there’s a lot of dispute over the details of how it actually happened. If you want to understand the natural world — why it is the way it is — rather than simply cataloguing natural history, evolution is the key to understanding. Conservation and the preservation of our vanishing natural heritage requires understanding the dynamics of populations, communities and ecosystems. Those dynamics are best explained by evolution — not creation from nothing followed by variation within a kind.edited: Forgot an "and"This message has been edited by Quetzal, 01-31-2005 15:00 AM

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Now we have another problem, however. How in the world did something that bears more than a striking resemblance to bacteria get incorporated into eukaryotic cells? And to the point where the euk cell can’t live without it? There may be multiple hypotheses, but one prominent one says that an early euk (almost all free-living single-cell eukaryotes are predators, btw) engulfed a bacterium and somehow didn’t finish it off, with the net result that when the euk divided, the bacterium was passed on to the daughter cell. This is an idea called endosymbiosis. Pretty far-fetched, right? Not necessarily. It is, after all, testable. As early as 1966, a biologist named Kwang Jeon at the University of Tennessee infected amoeba with a lethal bacteria. Although most of his amoeba died, a few managed to live — and reproduced with the bacteria inside them. Within a few years, Jeon found that the amoeba couldn’t live without the bacteria and further tests (where he removed the bacterial genome from the amoeba) showed that the newly uninfected populations quickly started dying. Re-infecting the same amoeba got it going again (cured it). Lynn Margulis, the principal proponent of serial endosymbiosis, discusses this particular experiment in great detail in an article in Natural History magazine (Bacterial Bedfellows, 1987, 96:26-33).

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That's amazing! Do you have a link to any of the papers? I tried to google it, but came up blank? I've always been intereseted in this subject ever since I was 14 and played a video game who's main plot revolved around endosymbiosis.

Was that game Parasite Eve?One of my top 10 favorites of all time. Just curious.

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By the way, for a fun second-term drinking game, chug a beer every time you hear the phrase, "...contentious but futile protest vote by democrats." By the time Jeb Bush is elected president you will be so wasted you wont even notice the war in Syria.
-- Jon Stewart, The Daily Show

Yes, it was. It was also the reason why I became an Engineer. I thought that endosymbiosis theory was a bunch of made up stuff to make the game look scientific. However, once I took AP Bio and learned about the theory, that sealed the deal.

A lot of papers are not on line, or available only with subscription. I came across Jeon's original work referenced by Margulis as I noted. However, Jeon is still active, and still trying to kill off his amoeba: Jeon, KW 2004, "Genetic and physiological interactions in the amoeba-bacteria symbiosis", J. Euk Microbio, 51:502-508,

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Amoebae of the xD strain of Amoeba proteus that arose from the D strain by spontaneous infection of Legionella-like X-bacteria are now dependent on their symbionts for survival. Each xD amoeba contains about 42,000 symbionts within symbiosomes, and established xD amoebae die if their symbionts are removed. Thus, harmful infective bacteria changed into necessary cell components. As a result of harboring X-bacteria. xD amoebae exhibit various physiological and genetic characteristics that are different from those of symbiont-free D amoebae. One of the recent findings is that bacterial symbionts control the expression of a host's house-keeping gene. Thus, the expression of the normal amoeba sams gene (sams1) encoding one form of S-adenosylmethionine synthetase is switched to that of sams2 by endosymbiotic X-bacteria. Possible mechanisms for the switching of sams genes brought about by endosymbionts and its significance are discussed.

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He's also still at U. Tennessee if you want to try and email him for a copy of the original paper.Here's an earlier abstract that apparently refers back to his original work:Jeon, KW, Jeon MIS, 1976, "Endosymbiosis in amoebae: recently established endosymbionts have become required cytoplasmic components", J Cell Physiol 89:337-44

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A strain of large, free-living amoeba that became dependent on bacterial endosymbionts which had infected the amoebae initially as intracellular parasites, was studied by micrurgy and electron microscopy. The results show that the infected host cells require the presence of live endosymbionts for their survival.Thus, the nucleus of an infected amoeba can form a viable cell with the cytoplasm of a noninfected amoeba only when live endosymbionts are present. The endosymbiotic bacteria are not digested by the host amoebae and are not themselves used as nutritional supplement. While the host amoebae are dependent specifically on the endosymbionts, the latter can live inside amoebae of different strains, indicating that their dependence on the host cells is not yet strain specific.

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Hope this works for you. A decent academic library might be able to get ahold of the actual papers if you want to read them.

Hi Quetzal,Well, I'll have to go over that other stuff about mitochondria and chloroplasts again (as it's all new info for me). My main thought is that nothing about this is random mutations working together with natural selection; and, therefore, is not evolution at all. But I'll need to re-read it all.But about the islands...
It might be a little helpful if you first know that most Creationists would look to the Flood for an explanation of any biologic assemblages anywhere on earth today--particularly land-dwelling, air-breathing animals had to radiate from the ark. We might also conclude that God did make the basic kinds of animals on the ark particularly able to variate within their respective kinds (I can show you the verse that hints at this, if you wish).The islands themselves are thought to be a result of the Flood. Any birds or mammals would have had to have traveled their and then variated (so we would definitely expect to see organisms on these islands being mainly variations of certain kinds--they got there a few centuries after the Flood and have been variating for a few millenia). How did they get there? Creationists believe that the oceanic water levels were initially much lower than today and that they have steadily been increasing for various reasons. If you lower the water levels not too much (150 ft, I hear) there are land bridges connecting much of what are separated by water today. So they just walked, crawled, etc. Other creatures (birds, not the flightless ones, unless they lost the ability to fly after reaching the island, and fish) could fly or swim.I guess trees had a time getting over to St. Helena, but daisies made it over there (bird droppings perhaps?). Also, giantism is largely gone in all creatures in general, but I suppose that it could exist in a few organisms yet (the big daisies). The giantism aspect of many organisms seems to have had a time making it in the post-Flood world (but was rampant in the pre-Flood world).All from the Creationist/Flood Model POV, of course, and I wouldn't expect any evolutionist to suddenly go, "Oh wow, I never thought of it like that! Here, let me change sides now."Interesting history of your namesake Quetzal.--TL

Certainly the initial engulfing of the future endosymbiont is a good example of Lamarckian inheritance, but the subsequent changes the bacteria have undergone from free-living to obligate endosymbiont can mostly be ascribed to random mutation and natural selection.A good review of evolutionary changes in the mitochondrial genome is Kurland and Andersson(2000)
TTFN,WK

Well I guess this depends on what Soplar meant by "directly observed". I have no idea if mutations can be observed occuring as the cell divides and reproduces, but even if it can i'm certain that it can't be tracked in billions of cells all at once. I doubt that this is the kind of "observed" that Soplar meant. More likely, he meant that the conditions of the experiment are controled to such an extent that we will be able to look at the end result and know what happened using our knowledge of how bacteria reproduce and how DNA works. Both of these things would be assumptions in the context of the experiment, but they will be directly known and tested from other areas of biology. Well not being a biologist I should probably leave this to Wounded King and the others who know more than me, but what the heck. I'll have a stab at it.Your model could work in one of two different ways that I can think of, either proactively or reactively. Either the variation will occur each time the bacteria reproduce, thus maximizing the number of different variations in the population. I can see two (possible) problems with this. Firstly, as I think has already been mentioned, this would lead to a higher than average mutation rate both in frequency and location in the genome and would be detectable. Secondly (and this is something i've just thought of so if i'm wrong i'm sure someone will correct me), but it would make the whole process useless in protecting the population because when the correct variation in the genome was found to infer resistance, what would stop it from being reshuffled when the bacteria reproduces again? There would be nothing to make the offspring resistant if the parents were, unless you're proprosing some mechanism to stop the reshuffling.Secondly is reactively (which I think is what you were implying), the reshuffling only occurs if the bacteria is in the presence of something harmful. If you measured the number of genomic differences (from the original bacterial genome that the colony started from) immediately before the antibiotic was introduced and then a few generations after the number should be very much smaller the first time than the second time. This would indicate that introducing the bacteria caused the changes to occur. I'm assuming this is not what is observed.Another possible implication from an ID/Creationist POV (for both proactively and reactively), is that if the variations were programmed into the DNA intelligently, you would expect there to be little to no directly harmful or neutral variations resulting. Neither of these would be of any use whatsoever. You would expect the number of potentially helpful mutations to be very much higher than evolutionary biology would predict. Again, I assume this is not what is observed. I have no idea if resistant strains are produced every single time, or even how long it takes for a resistant strain to appear on average. I imagine there are some different predictions for evolution and creation that can be made though. For example, from an evolutionary perspective I imagine the potency of the antibiotic will be relevant. If it is capable of killing all non-resistant bacteria in a very short time then I imagine there is less chance of the population becoming resistant than if it takes a while for the antibiotic to kill them all. From a creationary perspective where the changes are non-random I imagine the potency of the antibiotic shouldn't have as much of an effect, the resistance will always arise.Anyway thats my stab into the relative unknown. I'd be interested to know how much of what I wrote is actually meaningful