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Bacteria modify their lag time “just as much as they need to”

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From Science:

Populations of Escherichia coli grown in the lab quickly evolve tolerance when exposed to repeated treatments with the antibiotic ampicillin, according to a study published today (June 25) in Nature. Specifically, the bacteria evolved to stay in a dormant “lag” phase for just longer than three-, five-, or eight-hour-long treatment courses, before waking up and growing overnight until the next round of treatment began.

“I was very surprised that the bacteria are able to modify their lag time just as much as they need to,” said microbiologist Tom Coenye of the Laboratory of Pharmaceutical Microbiology (LPM) at Gent University in Belgium, who was not involved in the research.

Medical doctors have noted the same—the way bacteria manage clever strategies for hiding in the human body, via convenient dormancy.

They don’t think, but something seems to be doing their thinking for them. Not natural selection acting on random mutation because they evidently choose to avoid it whenever possible. That is, they avoid direct conflict with antibiotics, whether natural or human-directed.

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8 Replies to “Bacteria modify their lag time “just as much as they need to”

  1. 1
    ppolish says:

    “Playing Dead” is certainly much easier than evolving resistance. Safer too. All that randomness is a bit risky.

    Did microbes teach humans their Bear Safety techniques?

  2. 2
    phoodoo says:

    I posted this story over at skepticalzone, and their response was predictable: “Its not a problem for evolution, evolution can explain everything.”

  3. 3
    Joe says:

    phoodoo- the TSZ ilk don’t understand that ID is not anti-evolution. And they actually believe that evolutionary and genetic algorithms exemplify Darwinian evolution even though those algorithms employ goal-oriented targeted searches and Darwinian evolution 1) isn’t goal oriented and isn’t a search. “Oh but they are called ‘evolutionary’ algorithms!”, is their only imbecilic response to those facts.

    They also seem to believe that just because it is microevolution then that means the blind watchamaker didit.

    On another note- Natural selection does NOT act on random mutations. Random mutations are part of natural selection.

  4. 4
    Joe says:

    Oh, that “simple” non-teleological explanation– “It just happened, it just happened to work, so it was kept around”.

    Go ahead phoodoo- ask them what this non-teleological explanation is.

  5. 5
    phoodoo says:


    Their explanation now shifts to it being teleological, but its “teleonaturalism” rather than ‘teleomentalism”…..hahaha.

    I wish I made that up.

    In fact, to hear them tell it, this is exactly what evolution predicts, anti-biotic resistance (so why do we have to mess with the sloppy details about how, its so trivial.)

    If overnight the bacteria turned into anti-biotic slurping aardvarks made out of legos , they would say, what’s the problem, its exactly what we would expect. Go read a book about biology.

    Its not a problem for evolution!

  6. 6
    Gordon Davisson says:

    I don’t get why everyone seems to think this isn’t a simple case of random mutation + selection. All that’s happened here is that the duration of the “lag” phase got increased, and optimizing single variables like this is the sort of thing normal evolutionary mechanisms do quite easily. I’ll cite Mike Behe here:

    In arriving at the limits to Darwinism, I emphasized that that mechanism would certainly work if gradually-increasing, serial, beneficial mutations could do the job.

    …and as far as I can see, that’s exactly what we have here. I see no sign of any new function, new complexity, multiple coordinated changes, or anything like that. Mind you, I haven’t read the original paper (has anyone else?), but according to the summary:

    Exploring the genetic basis of this adaptation, the researchers identified three genes that seemed to play a functional role in antibiotic tolerance. While the exact mechanism of how mutations in these genes may have lengthened the bacteria’s lag time is not yet known, two of the genes are part of pathways that were previously implicated in bacterial persistence, including an antitoxin in a common toxin-antitoxin module that may help regulate that bacteria’s growth.

    “The way the toxin-antitoxin module is built, [there are] two entities that interact strongly with each other,” said Balaban: the toxic stops the cell from growing, until the antitoxin accumulates to high enough levels to neutralize the toxin. Although it remains to be experimentally demonstrated, this system could serve as an ideal lag-time adjuster. “If you alter the balance of toxin-antitoxin, bacteria stop growing for certain periods of time.”

    So any mutation that increased production of the toxin or decreased production of the antitoxin (or changed their effectivenesses in the correct direction or…) would extend the lag phase, and thus decrease the bacteria’s vulnerability to the antibiotic, and thus be selected for. Mutations that do any or all of these things will tend to accumulate until the lag phase takes long enough to evade the treatment course, at which point the selection pressure drops off…

    AIUI the only surprising things are how far they were able to extend the lag phase, and how quickly it happened.

    BTW, the linked summary is in The Scientist, not Science. You should probably fix that.

  7. 7
    bornagain77 says:

    “I don’t get why everyone seems to think this isn’t a simple case of random mutation + selection”

    Perhaps because it is a case of directed mutations instead of ‘random’ mutation?!?

    As is pretty much the case with all supposed ‘random mutations’ that Darwinists point to for evidence:

    Revisiting the Central Dogma in the 21st Century – James A. Shapiro – 2009
    Excerpt (Page 12): Underlying the central dogma and conventional views of genome evolution was the idea that the genome is a stable structure that changes rarely and accidentally by chemical fluctuations (106) or replication errors. This view has had to change with the realization that maintenance of genome stability is an active cellular function and the discovery of numerous dedicated biochemical systems for restructuring DNA molecules.(107–110) Genetic change is almost always the result of cellular action on the genome. These natural processes are analogous to human genetic engineering,,, (Page 14) Genome change arises as a consequence of natural genetic engineering, not from accidents. Replication errors and DNA damage are subject to cell surveillance and correction. When DNA damage correction does produce novel genetic structures, natural genetic engineering functions, such as mutator polymerases and nonhomologous end-joining complexes, are involved. Realizing that DNA change is a biochemical process means that it is subject to regulation like other cellular activities. Thus, we expect to see genome change occurring in response to different stimuli (Table 1) and operating nonrandomly throughout the genome, guided by various types of intermolecular contacts (Table 1 of Ref. 112).

    Shapiro on Random Mutation:
    “What I ask others interested in evolution to give up is the notion of random accidental mutation.”

    New Research Elucidates Directed Mutation Mechanisms – Cornelius Hunter – January 7, 2013
    Excerpt: mutations don’t occur randomly in the genome, but rather in the genes where they can help to address the challenge. But there is more. The gene’s single stranded DNA has certain coils and loops which expose only some of the gene’s nucleotides to mutation. So not only are certain genes targeted for mutation, but certain nucleotides within those genes are targeted in what is referred to as directed mutations.,,,
    These findings contradict evolution’s prediction that mutations are random with respect to need and sometimes just happen to occur in the right place at the right time.,,,

    How life changes itself: the Read-Write (RW) genome. – 2013
    Excerpt: Research dating back to the 1930s has shown that genetic change is the result of cell-mediated processes, not simply accidents or damage to the DNA. This cell-active view of genome change applies to all scales of DNA sequence variation, from point mutations to large-scale genome rearrangements and whole genome duplications (WGDs). This conceptual change to active cell inscriptions controlling RW genome functions has profound implications for all areas of the life sciences.

  8. 8
    Gralgrathor says:

    Perhaps because it is a case of directed mutations instead of ‘random’ mutation?

    Quoting Shapiro doesn’t do anything to support that. He’s not exactly an authority on genetics, him frequently showing signs of not understanding the Central Dogma and all.

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