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originally posted by: wdkirk
Seems like you posted to the wrong thread. This is a discussion on evolution not propaganda. Part of the discussion is how each views the evidence shown in order to come to a conclusion. Both sides are stating good material and a wealth of knowledge. Somewhere in between is common ground that they both share.
As for bible verses, I'd say you have found your own personal contribution of propaganda.
In June 2008 the popular science magazine New Scientist printed a story about Professor Richard Lenski's twenty-year project examining the evolution of E. coli. They reported that, as a result of several beneficial mutations, his organisms had acquired the ability to metabolize citrate — or more correctly an ability to transport it through the cell wall prior to metabolizing it. This was an entirely new ability for this species — an increase in complexity provided by a beneficial mutation. This beneficial trait was then fixed in the population by natural selection.
It is also important to notice that before acquiring this ability the bacteria acquired a previous potentiating mutation which, although it was not clearly beneficial at the time, subsequently allowed the descendants of that potentiated group the ability to process citrate after a further mutation. Furthermore frozen ancestors of that group, and only the frozen ancestors of that group, retained the ability to re-evolve that favorable trait.
His group did not use genetic engineering to modify the organism (to design it), it was produced entirely by the evolutionary process.
Adaptive evolution can cause a species to gain, lose, or modify a function; therefore, it is of basic interest to determine whether any of these modes dominates the evolutionary process under particular circumstances. Because mutation occurs at the molecular level, it is necessary to examine the molecular changes produced by the underlying mutation in order to assess whether a given adaptation is best considered as a gain, loss, or modification of function. Although that was once impossible, the advance of molecular biology in the past half century has made it feasible. In this paper, I review molecular changes underlying some adaptations, with a particular emphasis on evolutionary experiments with microbes conducted over the past four decades. I show that by far the most common adaptive changes seen in those examples are due to the loss or modification of a pre-existing molecular function, and I discuss the possible reasons for the prominence of such mutations.
They reported that, as a result of several beneficial mutations, his organisms had acquired the ability to metabolize citrate — or more correctly an ability to transport it through the cell wall prior to metabolizing it. This was an entirely new ability for this species — an increase in complexity provided by a beneficial mutation. This beneficial trait was then fixed in the population by natural selection.
Recently, Lenski's group reported the isolation of a mutant E. coli that had evolved a Cit+ phenotype. That is, the strain could grow under aerobic conditions in a culture of citrate (Blount et al. 2008). Wild E. coli cannot grow under such conditions, as it lacks a citrate permease to import the metabolite under oxic conditions. (It should be noted that, once inside the cell, however, E. coli has the enzymatic capacity to metabolize citrate.) The phenotype, whose underlying molecular changes have not yet been reported, conferred an enormous growth advantage because the culture media contained excess citrate but only limited glucose, which the ancestral bacteria metabolized. Blount et al. (2008) marshaled evidence to show that multiple mutations were needed in the population before the final mutation conferred the ability to import citrate; the activating mutation did not appear until after the 30,000th generation. As Blount et al. (2008) discussed, several other laboratories had, in the past, also identified mutant E. coli strains with such a phenotype. In one such case, the underlying mutation was not identified (Hall 1982); however, in another case, high-level constitutive expression on a multicopy plasmid of a citrate transporter gene, citT, which normally transports citrate in the absence of oxygen, was responsible for eliciting the phenotype (Pos et al. 1998). If the phenotype of the Lenski Cit+ strain is caused by the loss of the activity of a normal genetic regulatory element, such as a repressor binding site or other FCT, it will, of course, be a loss-of-FCT mutation, despite its highly adaptive effects in the presence of citrate. If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation. The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski's research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT.
originally posted by: ServantOfTheLamb
a reply to: TzarChasm
resist all you want, but posting poorly formulated attacks on a conspiracy forum is probably not the most effective approach.
....oh the irony...
Literally all you said is that cells are self-regulating, thermodynamically open systems which exchange matter and energy with its environment. Yes all of that is true, but again doesn't even attempt to solve the issue I've presented here.
I don't think you even know what the problem I've posed is.
Vertebrates supposedly came from invertebrates, do you want to explain how that is possible when their mitochondria use different coding languages?
Yes it does I've explained it numerous times if you can't understand it I can't help you.
Maybe if your first response didn't imply that millions of years explains away different coding languages in the mitochondria of vertebrates and invertebrates.
If you think you have something that shows I am wrong, then quit beating around the bush and explain it.
originally posted by: TzarChasm
i am more inclined to think that the dilemma is concerned with your education in mes. it is difficult to educate yourself when you are more focused on proving that you are smarter than the experts. resist all you want, but posting poorly formulated attacks on a conspiracy forum is probably not the most effective approach.
Every single one of those items listed is a not just a different sequence of genes, but they interpret the same codon's completely differently. That shows all the different coding languages and explains which codons are read how for each code. So yes it does acknowledge these things, but rather than state it as a number they have listed them out and explained how to read some of their codons, which is unique to that cell type or structure. So you'd have to count them, which it appears there are more than 19 now, surprise surprise. You are either being deliberately dishonest or you simply didnt scroll down on the NBCI link. You'll notice the vertebrate and invertebrate mitochondrial DNA is on that list. Its exactly what I was talking about in th OP.
So the truth is we don't know if that proves gain in function mutations are actually possible. If we are taking inference to the best explanation they are most like loss of function mutations or modification of function mutations.
Lenski's experiments have nothing to do with different coding languages inside of DNA. They have yet to do anything to show that new morphological features can arise via natural selection and random mutation. Why don't you just accept that I actually study this stuff and read peer reviewed sources, and that the dilemma I've pointed out isn't from lack of knowledge.