Summations Only

Well no it doesn't. Thinking of genetic inheritance in terms of heterozygous or homozygous is fine for humans and pea plants since they are diploid organisms, but bacteria only have a single chromosome.Traditionally bacteria have been categorised into species by their morphology but also by the biochemical reactions they can perform including which sugars they can ferment/assimilate. We can use this method because it is fairly stable what chemical reactions different species of bacteria can perform, which is what makes the Lenski experiment so significant.Of course now with more widespread use of genetics to profile bacterial species we are seeing that, although what we define as a species are very closely related at the genetic level, there is still significant divergence, sometimes enough to identify different species. So for example you get the Enterobacter cloacae complex or Burkholderia cepacia complex, each thought to be a single species but now shown to be several species sharing the same biochemistry i.e. the same phenotype.So you can see there's a lot more to bacterial species than just morphology. You look at E.coli under the microscope and you'll see gram negative bacilli, but if look at Pseudomonas or Bacteroides they are also gram negative bacilli. Would you therefore regard those organisms as all pretty much the same thing?By comparison a great deal of the diversity we see in metazoa is not a result of novel mutations, but instead can be accounted for simply by changes in gene expression during development. You bring up the transition of a leg to a fin, yet during development a limb is already fairly fin like, it just requires genes to be expressed at the right time to control cell death between what will become fingers and toes. And for the record hox genes don't define how a limb develops, they lay out the body plan in the early stages of development so that other genes involved in limb development know where to be expressed. It's not as straight forward as a gene missing a few mutations to get from anaerobic uptake to aerobic uptake of citrate. As I understand it for citrate to be utilised it requires a cofactor such as glucose or glycerol as a reducing agent. Therefore the presence of oxygen interferes with this reaction, which is why it only occurs in anoxic conditions.{Started writing this reply a couple of days ago, so sorry to Taq and Catholic Scientist for repeating some of their points}

This is the image of a human limb bud at 6 weeks. As you can see it's a fairly flat plate like structure. It is known that controlled cell death causes this plate of tissue to become divided into five sections to form fingers. It is easy to see how changes in expression could instead cause this plate to elongate into a fin. Yes Haeckel got it wrong that the embryonic form replays ancestral species in our evolution, but some of his ideas do hold true.Also I find it interesting that you view this sort of change as impossible, yet in Message 216 you pass off the transition from a completely herbivorous to an omnivorous diet as no big deal.Anyway sorry this was a bit rushed and I'll have to get back to your other post later.Edited by Malcolm, : No reason given.

I can see how it could be used in that way, however it is not the commonly used definition. There is a risk in non-biologists, not necessarily yourself but others reading this, in equivocating the heterozygosity of a bacterial population with the heterozygosity of an individual diploid organism.
The other reason the bacteria in this experiment should not be referred to as heterozygous is that all the bacteria originated from a single bacterial cell so are there was no genetic variation between or within populations. Here is the initial paper where Lenski described the establishment of his long term experiment.
As I mentioned above all subsequent populations originated from a single common ancestor of an E.coli B clone. This carried no plasmids, harboured no bacteriophages and was asexual so could not form pilli to exchange genetic material. In other words any changes seen in the cells are solely the result of mutations. This initial population was used to seed 12 daughter populations, 6 were arabinose negative and 6 were arabinose positive after a spontaneous mutation. Well you did refer to morpholological stasis in E.coli showing lack of speciation, so I thought it worthwhile pointing out that morphology was just one aspect of defining a bacterial species. Citrate uptake is probably better defined as part of the phenotype.
As for E.coli being an identifiable species, it is not that straight forward. It has been found there is a great deal of variation amongst E.coli strains, in fact one comparison of 61 sequenced genomes showed only 20% homology. This study also indicated the related Genus Shigella should be classified as strains of E.coli, and conversely E.coli O157 is more closely related to Shigella than it is to other E.coli.But this topic isn't about speciation, so I don't really want to carry on with this line of discussion. I just find it fascinating since I work in a hospital microbiology lab and we do hundreds of bacterial identifications on a daily basis. I have read the citations, and yes it does involve the manipulation of pre-existing genes, but I think you are paying too much attention to what the gene does and not enough on how it accomplished it. The rearrangements of the genome described in the citations are fairly significant with the potential of these changes inserting into an essential gene rather than next to a useful promoter region. What I find interesting is that the rearrangements described are similar to hypothesised rearrangements for the evolution of the bacterial flagellum which is usually referred to by creationists/IDists as impossible. As I said the hox genes define the layout of the segments in the developing embryo. This in turn affects which genes are expressed depending on which section they find themselves in. So genes that are involved in leg development will be expressed if they find themselves in the right section of the embryo. As an example, consider antennapedia in Drosophila. A mutation in a hox gene has caused legs to form in place of the antennae, because the mutation has caused those cells to think they are part of the thorax, so have expressed genes for structures found in the thorax.From Message 231: You keep on saying it is 'scientifically impossible' but don't say how. Look back to the image I posted in Message 228 showing the blob of cells destined to become a human hand and arm. We have identified the pattern of gene expression that accomplishes this, so we can see with a change in gene expression during development the controlled cell death between the digits may not happen and tissue can elongate to form a fin, just as you'd normally have elongation to form the arm. And all this is accomplished without any new genes or rearrangement of gene 'blocks', just adaptation of already established gene pathways. All I will say to this is to point out that experiments involving fruit flies or E.coli as models to identify the functions of specific genes, not to induce speciation. Sorry what?! I was sort of thinking of the transition to an omnivorous diet in terms of gene expression influencing development of the gastrointestinal tract.

You are correct that CitT was already present, and with the duplication of this gene created a second copy next to a promoter that would activate associated genes in the presence of oxygen. This occurred at 31,500 generations which coincides with the ability to uptake citrate albeit poorly, and subsequent duplications improved this effect. But this isn't the most interesting part. They resurrected earlier generations of the e.coli from frozen stores and inserted plasmids multiple duplicates of the new promoter-gene complex. What they found was that adding the plasmid the bacteria would evolve the ability to uptake citrate, but only after generation 20,000.Therefore other mutations must have occurred at or before 20,000 generations to allow citrate uptake to later evolve, even although these earlier mutations did not have a direct effect on citrate uptake. I'm sure we'll see more on this research in the future.
Anyway you can read more about it in this arcticle that gives some more details about the research.Edited by Malcolm, : No reason given.

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've not used Enterotube but looks like the same principle as Biomerieux's API system we've used, which also lists E.coli as 0% citrate positive. With these methods it is the pattern of reactions to many biochemical tests which identify the bacteria. For API, there are usually 20 tests which generate a profile number which you enter into a web-based server which calculates the accuracy of the identification and highlights any contraindicated tests. So for something like citrate a positive citrate for E.coli would push the percentage probability of the ID down. Can't think I've seen this happen, but then I've not been paying particular interest in citrate. Now we use cards in the automated Vitek system which contain even more biochemical tests but again the same principles apply, with any inconsistent results being highlighted. However, couldn't find their criteria for different biochemical tests in this method, but then it is being constantly updated.I would say that I've found that biochemical tests are fairly consistent. For example we use MacConkey agar which causes lactose fermenting bacterial colonies to appear pink. There is a number of bacterial species are never found to be lactose-fermenters, such as Salmonella, so this is a good presumptive diagnostic test. So I would say it is consistent to describe cit- as an identifying characteristic of E.coli. An earlier paper by Blount mentions previous examples of cit+ E.coli. The majority of these were the result of acquiring plasmids from other species that contained the relevant genes for citrate uptake, but only a single documented example of the ability resulting from changes in an E.coli chromosome. This is probably why Enterotube is open towards the possibility of cit+ E.coli, even if it may be transitionary depending on other bacteria present.