General fitness, health and nutrition · Public discussion

Get what you need

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General fitness, health and nutrition
Published
30 May 2004
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7 June 2004
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Jim Menegay
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  1. You can't always get what you want But if you try sometimes,
    well you just might find You get what you need

    M. Jagger/K. Richards

    Does a population whose survival is threatened by some
    environmental stress "evolve faster" than one which is not?
    Well sure. If there is a low frequency gene that usefully
    responds to the stress, Fisher's fundamental theorem and
    common sense agree that the frequency of this gene will
    increase faster when the stressor is actually present in the
    environment than when it is not.

    But some researchers go farther and claim that mutations
    leading to alleles that usefully respond to the stress are
    more likely when the stress is present. This idea is widely
    considered to be heresy. It apparently conflicts with one of
    the core axioms of neo-Darwinism - that mutation is
    "random". Nevertheless, apparently solid empirical results
    in microorganism systems repeatedly back up this claim of
    environmentally directed mutation.

    In a typical experiment, a strain of bacteria that is
    sensitive to some toxin is divided into two groups. One is
    exposed to moderate levels of the toxin, the other is not.
    Periodically, a sample is taken from both populations and
    cultured under high toxin levels. A check is made to see if
    there are any survivors. If so, then a beneficial mutation
    must have occurred. Such experiments repeatedly find that
    the beneficial mutations happen more frequently in the
    stressed population. And statistical analysis of the results
    suggests that it is not just a case of the stressed
    population having a higher mutation rate. There is a much
    lower tendency for a stress by one toxin to induce an
    immunity to a second, non-present, toxin.

    Results like these definitely challenge the neo-Darwinnian
    axiom, IMO. One frequently sees the label "Lamarckian"
    attached to these results - I suppose there could be debate
    over whether that label is appropriate. In any case, results
    like these have always puzzled me. What could be the
    mechanism?

    Well, I finally ran across a paper that suggests a
    mechanism.

    Wright BE. A biochemical mechanism for nonrandom mutations
    and evolution. J Bacteriol. 2000 Jun;182(11):2993-3001
    jb.asm.org2993

    Without endorsing what she says about evolution, I think
    that I can agree with what she says about mechanism.
    Basically, it is that DNA segments that are being actively
    transcribed are more at risk of mutation than segments that
    remain continually in double-stranded form.

    Suppose that we have a species of bacteria that have an
    inducible defense against a toxin. Two genes are involved
    here - one to sense the toxin and one to deal with it. Now,
    isolate a mutant strain that has a defect in the deal-with-
    it gene. Use this strain in your anti-neo-Darwinist
    experiment. Your control group never transcribes the
    defective deal-with-it gene, but your stressed group does -
    ineffectively, of course. But a back mutation to an
    effective deal-with-it gene is more likely in the stressed
    group than the control group.

    OK, it works for back mutation, but can this mechanism
    explain how immunity can develop in an environmentally
    directed way to a novel toxin. Yes it can, if the novel
    toxin is chemically similar to a known toxin that the
    microorganism can already deal with. If the gene to sense
    the known toxin is non-discriminating, it will respond to
    the novel stress by promoting the transcription of the deal-with-the-known-
    stress gene. And that gene can probably mutate to one that
    deals with the novel stress more readily that can some
    randomly chosen gene from the genome.

    It can be debated whether these ideas really challenge neo-
    Darwinism and whether they support neo-Lamarckism. But I
    like them because they tend to explain the origin of the
    signalling mechanism involved in inducible enzymes. A new
    inducible enzyme pair arises by the duplication and
    evolution of an old pair. The two genes involved in the
    communication do not have to originate separately and then
    later come to an agreement on the "signalling protocol".

    organisms. Recombination is also more likely in DNA segments
    that are actively being transcribed!

  2. Jim Menegay <[email hidden]> wrote or quoted:

    Quoted message said:

    But some researchers go farther and claim that mutations
    leading to alleles that usefully respond to the stress are
    more likely when the stress is present. This idea is
    widely considered to be heresy. It apparently conflicts
    with one of the core axioms of neo-Darwinism - that
    mutation is "random". Nevertheless, apparently solid
    empirical results in microorganism systems repeatedly back
    up this claim of environmentally directed mutation.

    [...]

    Quoted message said:

    In any case, results like these have always puzzled me.
    What could be the mechanism?

    Well, I finally ran across a paper that suggests a
    mechanism.

    Wright BE. A biochemical mechanism for nonrandom mutations
    and evolution. J Bacteriol. 2000 Jun;182(11):2993-3001
    jb.asm.org2993

    Without endorsing what she says about evolution, I think
    that I can agree with what she says about mechanism.
    Basically, it is that DNA segments that are being actively
    transcribed are more at risk of mutation than segments
    that remain continually in double-stranded form.

    [...]

    Quoted message said:

    organisms. Recombination is also more likely in DNA
    segments that are actively being transcribed!

    How come? Don't large orgainsims keep their germ-line DNA in
    insulated boxes, well away from the daily toil?

    ISTM that this effect would be much reduced in organisms
    with a germ/soma division, since they can take steps to
    insulate their germ line from the environment.
    --
    __________
    |im |yler timtyler.orgtimtyler.org [email hidden] Remove
    lock to reply.

  3. Jim Menegay <[email hidden]> wrote or quoted:

    Quoted message said:

    But some researchers go farther and claim that mutations
    leading to alleles that usefully respond to the stress are
    more likely when the stress is present. This idea is
    widely considered to be heresy. It apparently conflicts
    with one of the core axioms of neo-Darwinism - that
    mutation is "random". Nevertheless, apparently solid
    empirical results in microorganism systems repeatedly back
    up this claim of environmentally directed mutation.

    In a typical experiment, a strain of bacteria that is
    sensitive to some toxin is divided into two groups. One is
    exposed to moderate levels of the toxin, the other is not.
    Periodically, a sample is taken from both populations and
    cultured under high toxin levels. A check is made to see
    if there are any survivors. If so, then a beneficial
    mutation must have occurred. Such experiments repeatedly
    find that the beneficial mutations happen more frequently
    in the stressed population. And statistical analysis of
    the results suggests that it is not just a case of the
    stressed population having a higher mutation rate. There
    is a much lower tendency for a stress by one toxin to
    induce an immunity to a second, non-present, toxin.

    These experiments have been much-criticised:

    ``Basically Cairns (in Nature) and B. H. Hall (in Genetics)
    say that organisms can respond to environmental stresses by
    reorganizing their genes in a purposeful way. Such "directed
    mutation" shifts the course of evolution in a nonrandom way.

    Such a conclusion was like waving a red flag in front of
    the evolutionists. R. May, at the University of Oxford,
    complained, "The work is so flawed, I am reluctant to
    comment." On the other side, a University of Maryland
    geneticust, S. Benson, comments, "Many people have had
    such observations, but they have problems getting them
    published."''

    - science-frontiers.comsf064b07.htm

    ...and people have come up with explanations for the effect
    which do not involve directed mutations:

    ``Experimental evidence for an alternative to directed
    mutation in thebgl operon''

    nature.comcgi
    taf/DynaPage.taf?file=/nature/journal/v356/n6368/abs/356-
    446a0.html

    "Adaptive frameshift mutations" could also explain some
    such effects.

    Of course there is now a well-established mechanism for
    directed mutation in nature - namely genetic engineering.
    --
    __________
    |im |yler timtyler.orgtimtyler.org [email hidden] Remove
    lock to reply.

  4. Again I suggest this Model of Selection Pressure

    As environmental adaptation increases, stabilizing selection
    increases and disruptive and diversifying selection
    decreases,

    and vice versa

    As environmental adaptation decreases, stabilizing selection
    decreases and disruptive and diversifying selection
    increases.

    Tom

    << Does a population whose survival is threatened by some
    environmental stress "evolve faster" than one which is not?

  5. "Tim Tyler" <[email hidden]> wrote in message
    "]news:[email hidden]...

    Quoted message said:

    Jim Menegay <[email hidden]> wrote or quoted:

    Quoted message said:

    But some researchers go farther and claim that mutations
    leading to alleles that usefully respond to the stress
    are more likely when the stress is present. This idea is
    widely considered to be heresy. It apparently conflicts
    with one of the core axioms of neo-Darwinism - that
    mutation is "random". Nevertheless, apparently solid
    empirical results in microorganism systems repeatedly
    back up this claim of environmentally directed mutation.

    [...]

    Quoted message said:

    In any case, results like these have always puzzled me.
    What could be the mechanism?

    Well, I finally ran across a paper that suggests a
    mechanism.

    Wright BE. A biochemical mechanism for nonrandom
    mutations and evolution. J Bacteriol. 2000 Jun;182(11):2993-
    3001 jb.asm.org2993

    Without endorsing what she says about evolution, I
    think that I can agree with what she says about
    mechanism. Basically, it is that DNA segments that are
    being actively transcribed are more at risk of mutation
    than segments that remain continually in double-
    stranded form.

    [...]

    Quoted message said:
    Quoted message said:

    organisms. Recombination is also more likely in DNA
    segments that are actively being transcribed!

    How come? Don't large orgainsims keep their germ-line DNA
    in insulated boxes, well away from the daily toil?

    ISTM that this effect would be much reduced in organisms
    with a germ/soma division, since they can take steps to
    insulate their germ line from the environment.

    An excellent point. This mechanism does not apply to the
    larger metazoa. Animal fans will have to come up with a
    different mechanism if they wish to be neo-Lamarkian.
    Culture has been suggested as one mechanism.

    AFAIK, plants are large organisms that don't generally do
    germ line sequestration, though. Also, I'm not sure to what
    extent even germ line DNA gets transcribed for housekeeping
    functions in animals.

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