You asserted the mutations are 'ingrained' into the viruses. E. Coli is a bacteria firstly and secondly show me some data proving that E. Coli contains an ingrained bacteria so that it can take in citrate. Provide the study stating that
1. E. Coli contains this sort of genetic 'ingraining' for citrate coding.
2. The experiment above is false.
3. The qualified and trained biologists willing to provide scientific data as to why the graphs and results on this 20 year experiment are false let alone the entire experiment is false.
4. E. Coli is a virus, E. coli 0157:H7 is a gram-negative bacterium, one which can cause illness. It is not a virus.
Your statement no benificial mutations exist is refuted by this experiment. This is clearly a closed discussion and I am satisfied I have provided information you are unable to refute. I know quite alot about natural selection and evolution, that is why I provided evidence for natural selection the driving mechanism in the theory of evolution. Since you have provided no evidence for your argument and I have provided a 25 year detailed study against your argument, you seem to be unable to discuss this.
A
New Scientist article proclaims:
‘Lenski’s experiment is also yet another poke in the eye for anti-evolutionists, notes Jerry Coyne, an evolutionary biologist at the University of Chicago. “The thing I like most is it says you can get these complex traits evolving by a combination of unlikely events," he says. “That’s just what creationists say can’t happen."’
1
The many comments posted on the
New Scientist website shows just how excited the atheists are about this report. They are positively gloating.
The context
In 1988, Richard Lenski, Michigan State University, East Lansing, founded 12 cultures of
E. coli and grew them in a laboratory, generation after generation, for twenty years (he deserves some marks for persistence!). The culture medium had a little glucose but lots more citrate, so once the microbes consumed the glucose, they would continue to grow only if they could evolve some way of using citrate. Lenski expected to see evolution in action. This was an appropriate expectation for one who believes in evolution, because bacteria reproduce quickly and can have huge populations, as in this case. They can also sustain higher mutation rates than organisms with much larger genomes, like vertebrates such as us.
2 All of this adds up, according to neo-Darwinism, to the almost certainty of seeing lots of evolution happen
in real time (instead of imagining it all happening in the unobservable past). With the short generation times, in 20 years this has amounted to some 44,000 generations, equivalent to some million years of generations of a human population (but the evolutionary opportunities for humans would be far, far less, due to the small population numbers limiting the number of mutational possibilities; and the much larger genome, which cannot sustain a similar mutation rate without error catastrophe; i.e. extinction; and
sexual reproduction means that there is 50% chance of failing to pass on a beneficial mutation ).
As noted elsewhere (see ‘
Giving up on reality’), Lenski seemed to have given up on ‘evolution in the lab’ and resorted to computer modelling of ‘evolution’ with a program called
Avida (see evaluation by Dr Royal Truman,
Part 1 and
Part 2, which are technical papers). Indeed, Lenski had good reason to abandon hope. He had calculated[SUP]1[/SUP] that all possible simple mutations must have occurred several times over but without any addition of even a simple adaptive trait.
Lenski and co-workers now claim that they have finally observed his hoped for evolution in the lab.
The science: what did they find?
In a paper published in the
Proceedings of the National Academy of Science, Lenski and co-workers describe how one of 12 culture lines of their bacteria has developed the capacity for metabolizing citrate as an energy source under aerobic conditions.
3
This happened by the 31,500[SUP]th[/SUP] generation. Using frozen samples of bacteria from previous generations they showed that something happened at about the 20,000[SUP]th[/SUP] generation that paved the way for only this culture line to be able to change to citrate metabolism. They surmised, quite reasonably, that this could have been a mutation that paved the way for a further mutation that enabled citrate utilization.
This is close to what Michael Behe calls ‘The Edge of Evolution’—the limit of what ‘evolution’ (non-intelligent natural processes) can do. For example, an adaptive change needing
one mutation might occur every so often just by chance. This is why the malaria parasite can adapt to most antimalarial drugs; but chloroquine resistance took much longer to develop because
two specific mutations needed to occur together in the one gene. Even this tiny change is beyond the reach of organisms like humans with much longer generation times.
4 With bacteria, there might be a chance for even three coordinated mutations, but it’s doubtful that Lenski’s
E. coli have achieved any more than two mutations, so have not even reached Behe’s edge, let alone progressed on the path to elephants or crocodiles.
Now the popularist treatments of this research (e.g. in
New Scientist) give the impression that the
E. coli developed the ability to
metabolize citrate, whereas it supposedly could not do so before. However, this is clearly not the case, because the citric acid, tricarboxcylic acid (TCA), or Krebs, cycle (all names for the same thing) generates and utilizes citrate in its normal oxidative metabolism of glucose and other carbohydrates.
5
Furthermore,
E. coli is normally capable of utilizing citrate as an energy source under anaerobic conditions, with a whole suite of genes involved in its fermentation. This includes a citrate transporter gene that codes for a transporter protein embedded in the cell wall that takes citrate into the cell.
6 This suite of genes (operon) is normally only activated under anaerobic conditions.
So what happened? It is not yet clear from the published information, but a likely scenario is that mutations jammed the regulation of this operon so that the bacteria produce citrate transporter regardless of the oxidative state of the bacterium’s environment (that is, it is permanently switched on). This can be likened to having a light that switches on when the sun goes down—a sensor detects the lack of light and turns the light on. A
fault in the sensor could result in the light being on all the time. That is the sort of change we are talking about.
Another possibility is that an existing transporter gene, such as the one that normally takes up tartrate,[SUP]3[/SUP] which does not normally transport citrate, mutated such that it
lost specificity and could then transport citrate into the cell. Such a loss of specificity is also an expected outcome of random mutations. A loss of specificity equals a
loss of information, but evolution is supposed to account for the creation of new information; information that specifies the enzymes and cofactors in new biochemical pathways, how to make feathers and bone, nerves, or the components and assembly of
complex motors such as ATP synthase, for example.
However, mutations are good at
destroying things, not creating them. Sometimes destroying things can be helpful (adaptive),
7 but that does not account for the
creation of the staggering amount of information in the DNA of all living things. Behe (in
The Edge of Evolution) likened the role of mutations in antibiotic resistance and pathogen resistance, for example, to trench warfare, whereby mutations destroy some of the functionality of the target or host to overcome susceptibility. It’s like putting chewing gum in a mechanical watch; it’s not the way the watch could have been created.
Much ado about nothing (again)
Behe is quite right; there is nothing here that is beyond ‘the edge of evolution’, which means it has no relevance to the origin of enzymes and catalytic pathways that evolution is supposed to explain.
8
Bacteria 'evolving in the lab'? (Lenski, citrate-digesting E. coli)
