Darwin's creation myth must be true, since scientists have observed bacteria involve into . . . bacteria!

An article on the significance of Lenski's E. Coli (subheadings and footnotes in the original).  After two decades and tens of thousands of generations, Darwinists still cannot show what they claim has been occurring for billions of years.  And that proves they're right!:

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."'

[. . .]

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. 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 that all possible simple mutations must have occurred several times over but without any addition of even a simple adaptive trait.


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.

This happened by the 31,500th generation. Using frozen samples of bacteria from previous generations they showed that something happened at about the 20,000th 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. 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.

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. 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, 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), 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.

When "proof" for macroevolution isn't, it's probably time to rethink one's position

It's interesting. I've been having a little discussion with one person in particular at another site over Darwinism. I've pointed out that no empirical (observable) evidence exists demonstrating either abiogenesis (Life arising from non-life by only random, natural processes) or one aspect of macroevolution (random, minor genetic mutations resulting in newer, more complex program, structure, and function; for this I use the term "vertical speciation") to be true.

He admitted that no one can observe macroevolution occur (in this case, a light-sensitive spot evolving eventually into a human eye). He also offered numerous links to evidence of microevolution (minor changes within species) and lateral speciation (changes in an organism that result in it being unable to reproduce with its cousins, but still being the same kind of animal).

Following is some of that proof showing "exactly . . . how" macroevolution (vertical speciation) has no empirical support.

Admissions of no evidence for macroevolution occurring, ridiculous leaps in logic, and mistaking correlation for causation, from here:

In summary, there is no barrier to species forming. This may not be enough to show that large-scale macroevolution occurs . . . For if there is enough change to form new species, and each species is slightly different from its ancestor, then simple addition shows that many speciation events can cause large-scale evolution over enough time . . . .

We can test a particular claim of macroevolution. We can test, for example, if weasels are more closely related to red pandas than bears are (Flynn and Nedbal 1998, Flynn et al. 2000). This is a test of a particular evolutionary tree or scenario. It tests a historical reconstruction. If shown, on the basis of the evidence and the best data, to be wrong, then that history has indeed been falsified. But can we test the idea of common descent? It is not possible to show that something never occurred, but it is very easy to show that where it ought to occur, it either has or it hasn't. Science will not retain a bad idea when it is shown repeatedly not to explain what we have a right to expect it to explain (this is one reason why creationism was dropped from science back in the 1850s). If macroevolution persistently were shown to run counter to the data, then science would drop it and look for another solution.

Moreover, science has to an extent falsified the initial conception of macroevolution. The original idea was that evolution formed only tree-like patterns – species split like branches. A growing consensus has argued that both hybridisation (species recombining) and lateral genetic transfer (genes crossing the taxonomic boundaries individually or as part of symbiotic organisms that are taken into the "host" taxon's cellular machinery) are more common than we had previously thought. Macroevolution of species is still regarded as the most common way that the diversity of life has developed, but the "tree" now has "vines" that hang across the branches of single celled organisms (Fig. 4).

From here:

The researchers conclude that the presence of the full three-component signaling system may have played a role in the development of metazoan organisms whose cells could communicate with each other in complex ways.

"It shows how evolution might work," says Wendell Lim, a researcher at the University of California, San Francisco, who was one of the authors of the paper. "Probably there was an ancestor to these organisms that first developed these chemicals."

From here:

Nothing—not even the Plague—has posed a more persistent threat to humanity than viral diseases: yellow fever, measles, and smallpox have been causing epidemics for thousands of years. At the end of the First World War, fifty million people died of the Spanish flu; smallpox may have killed half a billion during the twentieth century alone. Those viruses were highly infectious, yet their impact was limited by their ferocity: a virus may destroy an entire culture, but if we die it dies, too. As a result, not even smallpox possessed the evolutionary power to influence humans as a species—to alter our genetic structure. That would require an organism to insinuate itself into the critical cells we need in order to reproduce: our germ cells. Only retroviruses, which reverse the usual flow of genetic code from DNA to RNA, are capable of that. A retrovirus stores its genetic information in a single-stranded molecule of RNA, instead of the more common double-stranded DNA. When it infects a cell, the virus deploys a special enzyme, called reverse transcriptase, that enables it to copy itself and then paste its own genes into the new cell’s DNA. It then becomes part of that cell forever; when the cell divides, the virus goes with it. Scientists have long suspected that if a retrovirus happens to infect a human sperm cell or egg, which is rare, and if that embryo survives—which is rarer still—the retrovirus could take its place in the blueprint of our species, passed from mother to child, and from one generation to the next, much like a gene for eye color or asthma.

When the sequence of the human genome was fully mapped, in 2003, researchers also discovered something they had not anticipated: our bodies are littered with the shards of such retroviruses, fragments of the chemical code from which all genetic material is made. It takes less than two per cent of our genome to create all the proteins necessary for us to live. Eight per cent, however, is composed of broken and disabled retroviruses, which, millions of years ago, managed to embed themselves in the DNA of our ancestors. They are called endogenous retroviruses, because once they infect the DNA of a species they become part of that species. One by one, though, after molecular battles that raged for thousands of generations, they have been defeated by evolution. Like dinosaur bones, these viral fragments are fossils. Instead of having been buried in sand, they reside within each of us, carrying a record that goes back millions of years. Because they no longer seem to serve a purpose or cause harm, these remnants have often been referred to as “junk DNA.” Many still manage to generate proteins, but scientists have never found one that functions properly in humans or that could make us sick.

Then, last year, Thierry Heidmann brought one back to life. Combining the tools of genomics, virology, and evolutionary biology, he and his colleagues took a virus that had been extinct for hundreds of thousands of years, figured out how the broken parts were originally aligned, and then pieced them together. After resurrecting the virus, the team placed it in human cells and found that their creation did indeed insert itself into the DNA of those cells. They also mixed the virus with cells taken from hamsters and cats. It quickly infected them all, offering the first evidence that the broken parts could once again be made infectious. The experiment could provide vital clues about how viruses like H.I.V. work. Inevitably, though, it also conjures images of Frankenstein’s monster and Jurassic Park.

From here, a short video purported to show "exactly . . . how" the eye evolved from a light-sensitive spot into a human eye, but in actuality offering only a chart showing a progression in the complexity of various organism's eyes and a bit of "ontogeny recapitulates phylogeny," a discredited evolutionary propaganda piece.

Also offered was Lenski's experiments with E. coli. Though noteworthy for showing over twenty years that the bacteria developed the ability to consume citrate without the help of plasmids, it was still just E. coli, not a newer, more complex eukaryote.