Was E. Coli Bacteria Evolving In the Lab?

In 1988, with one single microbe started an experiment conducted by Richard Lenski, who is an evolutionary biologist.  In 2008, evolutionists were tooting their horns claiming a new ability to subsist on citrate was proof that new traits can evolve! But there was a cost along the way  as a result of activating this so-called new trait through mutations.

Michael Behe, in his paper points out…

“By examining the DNA sequence of the E. coli in the neighborhood surrounding the IS [insertion sequence] elements, the investigators saw that several genes involved in central metabolism were knocked out, as well as some cell wall synthesis genes and several others.”

“In subsequent work, Cooper et al. (2001) discovered that twelve of twelve cell lines showed adaptive IS-mediated deletions of their rbs operon, which is involved in making the sugar ribose. Thus, the adaptive mutations that were initially tracked down all involved loss-of-FCT.”

“Several years later, when the cultures had surpassed their 20,000th generation, Lenski’s group at Michigan State brought more advanced techniques to bear on the problem of identifying the molecular changes underlying the adaptation of the E. coli cultures. Using DNA expression profiles, they were able to reliably track down changes in the expression of 1300 genes of the bacterium, and determined that 59 genes had changed their expression levels from the ancestor, 47 of which were expressed at lower levels (Cooper et al. 2003).”

“The authors stated that “The expression levels of many of these 59 genes are known to be regulated by specific effectors including guanosine tetraphosphate (ppGpp) and cAMP-cAMP receptor protein (CRP)” (Cooper et al. 2003:1074). They also noted that the cellular concentration of ppGpp is controlled by several genes including spoT. After sequencing, they discovered a nonsynonymous point mutation in the spoT gene. When the researchers examined ten other populations that had evolved under the same conditions for 20,000 generations, they found that seven others also had fixed nonsynonymous point mutations in spoT, but with different substitutions than the first one that had been identified, thus suggesting that the mutations were decreasing the protein’s activity.”

After 20,000 generations, not much happened. But after a while, the types of changes taking place in the E. coli tended to decrease or eliminate protein function! Now we get to the ability of E. coli to metabolize citrate. This is where evolutionists love to toot their horn, “after a series of mutations “bacteria that use citrate dominate the population,” they say.

What they didn’t tell you is that E. coli already have the machinery to uptake and metabolize citrate (like a number of enzymes that normally use citrate and can digest it) but doesn’t do it under oxic conditions! The experiment wasn’t showing any evidence for a  biochemical pathway invented by the mutations which was entirely new! Instead, it was only activating its machinery with a cost under different conditions.

In other words, normal E. Coli lacks the ability to transport citrate through the cell membrane into the cell under oxic conditions. But Lenski’s E. Coli, the regulation mechanism of a citrate-transport gene lost its function thereby causing an over expression (turning the switch on) which then enables the bacteria to uptake the citrate under oxic conditions!

Last month, another story breaks, just like last time, evolutionists are tooting their horns once again. After 56,000 generations under some predetermined conditions such as plenty of oxygen but very limited food supply. Testing the bacteria with a small amount of glucose, to see how they would react. We see a revisit of the hype as shown below…

Science News

“Learning to eat citrate, also called citric acid, is as big an innovation for E. coli as developing eyes or wings would be for multicellular creatures, says evolutionary geneticist Paul Rainey of Massey University in Auckland, New Zealand, and the Max Planck Institute for Evolutionary Biology in Plön, Germany.”

It’s hardly an innovation! But what they are observing is nothing more than duplication and rearrangement of pre-exsiting information while loosing the regulation mechanism which then allowed the uptake of citrate by the E. Coli bacteria. Does this mean the bacteria was evolving in the lab? The answer is a resounding, no! The bacteria wasn’t evolving for the last 25 years along with its 56,000 generations!

3 thoughts on “Was E. Coli Bacteria Evolving In the Lab?

    ………………………………………….but not in practice.
    …………………………………………..but not in theory.

    >According to Michael Behe’s The Edge of Evolution, Richard Lenski’s citrate-slurping bacteria theoretically could only have been designed; mutations would have taken more then the age of the universe to occur. Yet they were observed continually for 20 years, without a single flash of divine intervention.
    >According to Michael Behe’s 2010 paper their genetic degeneration over the experiment theoretically weakened the bacteria significantly. Yet they proliferate, reaching colony densities hugely larger than when the experiment started.

    >According to Stephen Meyer’s Signature in the Cell, complex specified information can only affect a genome function when it is introduced by an outside intelligent agent. No such intelligent agents were observed skulking about in Lenski’s lab. In fact, neither Meyer nor anyone else has ever observed any intelligent agent fooling around with genomes anywhere…
    >Lenski’s bacteria managed to rearrange its genome so as to link two previous citrate genes by means of another, unrelated gene. All by itself. One of the previous citrate genes came under control of a promoter for the unrelated gene. Over a period of hundreds of generations, this rearranged area was duplicated several times, which amplified the citrate uptake greatly. All by itself. Among the vast number of single-point mutations that had occurred before the clone proliferation, some of them—Lenski is still not sure which ones—made it possible for the newly linked genes and promoters to work together to import citrate. All by themselves, and even though they had no idea what their “function” would be ahead of time..

    Lenski recently published a new paper.[1] tracing the history of this new function. An accompanying news article[2] notes—.

    The discovery of th Cit+ mutants in Lenski’s experiment has been a mote in the eye for those suggesting that major phenotypic innovations cannot be explained by microevolutionary (gradual) processes. Indeed, for anti-evolutionists, lack of mechanistic detail has even allowed room for divine intervention. After several attempts to politely address the concerns of one critic, Lenski has responded publicly in what has proven to be one of the most competent and direct defences of science vesus dogma for some time. It includes the memorable phrase “In other words, it’s not that we claim to have glimpsed ‘a unicorn in the garden’—we have a whole population of them living in my lab!”


    [1] Blount, et al., “Genomic analysis of a key in novation in and experimental Eschericia coli population,” Nature 489:513-517.(27 Sept. 2012)

    [2] “How the unicorn ot it horn,” Nature 489:504-505 (27 Sept 2012)

  2. But Lenski’s E. Coli, the regulation mechanism of a citrate-transport gene lost its function thereby causing an over expression (turning the switch on) which then enables the bacteria to uptake the citrate under oxic conditions!

    ……. while loosing the regulation mechanism which then allowed the uptake of citrate by the E. Coli bacteria.

    Michael, who put you up to this crap? Answers in Genesis?

    You should know better than to rely on a creationist source They’ll lie to you every time.

    Nothing lost its function; the bacteria is still capable of metabolizing glucose. A new function was gained. So much function that many biologists think the E. coli having it deserve to be given a new species name—-they are no longer E. coli.

    Your attempts to denigrate this advance are pitiful acts of sheer desperation.

  3. the evolutionist always says that a watch need a designer because it cant self rplicat. so if we will find a self replicat watch we need to say that is made by itself

    scientist even find a motor in bacteria called bacterial flagellum:

    and we know that a motor is evidence for design. even if its very small.

    check this site


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