RE: Evolution Statement

From: Moorad Alexanian (alexanian@uncwil.edu)
Date: Tue Dec 11 2001 - 20:15:37 EST

  • Next message: Howard J. Van Till: "Re: criticising scientific naturalism (fwd)...anecdote about science held hostage"

    I am glad you all dig me! :) But don't forget you heard it from me first: If
    something cannot in principle be measured by means of physical devices, then
    that something is not the subject matter of science. Moorad

    >===== Original Message From tikeda@sprintmail.com =====
    >[...]
    >I wrote:
    ><Thus we should not rule out the possibility that many of the older,
    >more disrupted lunar craters could have formed supernaturally and are
    >not the products of natural causes. (Or, pace Moorad: We never
    >saw the impact which produced Bessel crater, so why couldn't it have been
    >made by elves? Science can't apply to any crater formed before 10000 BC,
    >because there weren't modern humans or instruments to record it. Let it
    >forever be an enigma!)>
    >
    >.end speculations here...>>
    >
    >
    >Bob replied:
    >>Tim,
    >>I don't know why you threw in the concept of the supernatural in your
    >>moon example, which I suppose was meant to address my statement. Did
    >>I say anything about the supernatural? No. So why do you?
    >
    >That was more of a dig at Moorad than you. However, I do not see why
    >the idea of descent with modification becomes more problematic the further
    >one goes back in the history of life. Perhaps if one goes very far back,
    >say around the eubacterial, archaebacterial, eukaryotic split, that
    >question may apply, but not for most of what has happened since then.
    >
    >[...section removed...]
    >
    >
    >Tim: <Genetic variation is the major change agent. What locks a particular
    >change into a population or affects its frequency in a population includes:
    >natural selection, neutral drift, and other factors. It is actually a hot
    >debate about which of the two, selection or drift, are the most influential
    >agents of change. Certainly neutral mutations accumulate in a genome faster
    >than selective ones.>
    >
    >>While I can understand the mechanism of selection, I find it difficult to
    >>understand what drives neutral drift. I'd appreciate it if you would explain
    >>it. It seems to me to be a radical departure from natural selection. What is
    >>the significance of their "faster accumulation in the genome" that you
    >>mention?
    >
    >Nothing 'drives' neutral drift. It's simply variation that accumulates
    >in the absence of selection. For example, point mutations in the third
    >position of many codons are effectively neutral because the changes often
    >don't alter the amino acid sequence of proteins made. Similarly, there can
    >be changes made to proteins which have little or no effect on the immediate
    >viability of the organism. These are changes which can occur "under the
    >radar" of selection and pools of such variations can be supported in
    >a population with no immediate cost. These variations accumulate in the
    >population at approximately the rate of mutation (the majority of mutations
    >being neutral or negative), and that average rate is far greater than
    >rate of accumulation of positive mutations through selection.
    >
    >Where does neutral drift fit in? One necessary factor for evolution
    >is the existence of variation within a population. Evolution won't happen
    >if species can't "move about in genomic space". Selection can "drive"
    >systems to particular locations (optima) in these "spaces", or neutral
    >drift can allow systems to "drift" across the landscape in "non-directed"
    >steps. One of the questions is: How much of the change which accumulates
    >during evolution resulted from neutral mutation and how much can be
    >attributed to selection?
    >
    >[Note: Sometimes, as conditions change, variations which might once
    >started out neutral may actually have some affect on survival.]
    >
    >[...text removed...]
    >Tim: <<Reversibility is irrelevant and in fact, many of the changes are not
    >reversible at the genetic level. Remember that there is a gaping chasm
    >between genotype and phenotype. The mapping between the two domains is
    >anything but linear in all but the rarest situations. Point mutations
    >can confer antibiotic resistance. However, given the odds of hitting that
    >exact site again to exactly reverse the point mutation, it's more likely
    >that a mutation that eliminates resistance will occur in another
    >portion of the genome. Thus a phenotypic reversal (short-term or otherwise)
    >does not equate to a genomic "reversal". And we have a recently described
    >case where a bacterium acquired streptomycin resistance in a "long-term"
    >manner such that loss of the resistance, even in the absence of the
    >antibiotic, was selected against (A secondary mutation occurred which
    >effectively "locked in" the first one). So, we can say that ratchet-like
    >evolutionary progression has been observed even over short timescales.>>
    >
    >>One case doth not a theory make.
    >
    >But one case doth destroy a blanket refutation...
    >(Further, the emergence of second-site suppressors is pretty commonly
    >observed. Some examples have become common in bacterial genetics
    >lab courses).
    >
    >> Moreover this is not a ratchet-like
    >>evolutionary progression, as you claim. It is step one. Has anything
    >>been observed that builds on step one to produce step two? Unless it
    >>has you do not have a progression. You have merely a locked-in
    >>bacterium.
    >
    >The case I've described involved two-steps. First, the bacterium
    >acquired resistance to streptomycin. This is wonderful for such strains
    >when there is streptomycin around: All the wild-type strains which would
    >otherwise compete for food die. But the resistance carries a slight
    >penalty when no streptomycin is around. Strains carrying that mutation
    >tend to grow slightly slower and are thus handicapped against their
    >wild-type counterpart in an antibiotic-free environment. As a result,
    >these streptomycin resistant strains were not expected to persist in
    >the "outside" environment, where there is little of the antibiotic
    >around.
    >
    >However, there is a secondary mutation which can occur that eliminates
    >the growth handicaps of the resistant strains. This "suppressor" mutation
    >allows the bearers to not only grown when streptomycin is around but
    >also to grow as fast as the wild-type strains when the antibiotic is
    >absent.
    >
    >Interestingly, this second mutation, by itself, also inhibits growth
    >rates. Only when teamed with the streptomycin resistance mutation
    >do the two mutations persist in the population. Strains missing either
    >one of the two mutations tend to be eliminated. This is an example
    >of lock-in (or ratcheting).
    >
    >
    >
    >Tim: <<I suspect that true reversibility is a relatively uncommon
    >phenomenon. Should we be surprised? I think not. In the mind-bogglingly
    >huge morphology- or genetic-space available to organisms, it's not
    >likely that one could take more than a couple steps in any direction
    >and then return to exactly the same starting place.>>
    >
    >>I suspect you are overstating your case. Does your "bacterium [that]
    >>acquired streptomycin resistance" that you mentioned earlier have
    >>"mind-bogglingly huge morphology- or genetic-space available to it"? I
    >>doubt it. If so, tell mme what it is.
    >
    >E. coli has a genome of about 4.6 megabases. At four possible nucleotides
    >per base, that's a genome-space of about 4^(4.6E6) elements. But let's
    >start with one particular genome and calculate some odds of exactly
    >reversing a single point mutation. That's one in 4.6 million. What are
    >the odds of hitting anything else? Those are = 1 - 1/4.6E6 (or ~0.99999978).
    >So, long before you've reversed a _single_ mutation, you've probably hit
    >millions of other sites in the genome. That is the nature of genetic
    >irreversibility.
    >
    >Because most phenotypic traits (such a beak lengths) can be modified by
    >more than one gene (comprising thousands of bases/gene), odds are that
    >any phenotypic "reversals" aren't going to be genetic reversals.
    >
    >
    >[...text removed...]
    >Tim; <<Nobody is failing to acknowledge the hierarchical pattern of life and
    >discontinuities. These are what led to the conclusion of descent with
    >modification in the first place.>>
    >
    >>Your first sentence in the above paragraph is simply not true. Read the
    >>statement that Dick Fischer presented and see if you can find hierarchical
    >>organization and discontinuities in it. Moreover, evolution abhors a
    >>discontinuity. Many evolutionary biologists are busy trying to iron them
    out.
    >
    >From that statement:
    >[...]
    >"Nonetheless, no scientific hypothesis other than common descent
    >with modification can account for and make predictions about the
    >unity, diversity, and properties of living organisms." [...]
    >^^^^^ ^^^^^^^^^ ^^^^^^^^^^
    >
    >Unity: hierarchical pattern of life
    >Diversity and properties: variations = discontinuities. There are
    >bears, dogs and cats. They are distinct entities now disconnected
    >from each other by breeding barriers.
    >
    >Perhaps we are talking about slightly different things when use the word
    >"discontinuity". I think of it as the _appearance_ of gaps between related
    >species, rather than the _actual existence_ of gaps. True, evolution would
    >have problems with actual gaps. But the appearance of gaps (where there
    >really are none), is not unexpected, as Keith Miller explains elsewhere.
    >
    >
    >Tim: <<Discontinuity is a product of speciation (a mechanism of evolution)
    >and extinction.>>
    >
    >>Show me.
    >
    >Keith Miller described why (partially) in a recent post and many times in
    >the past. See: http://www.calvin.edu/archive/asa/200112/0080.html
    >
    >Reiterated: Speciation reduces genetic exchange between populations
    >of organisms. After speciation, the separate populations may travel
    >on separate trajectories (i.e. diverge) and the amount of visible
    >divergence tends to increase over time. Also "intermediate" species
    >become extinct along the way. So while bears and dogs may appear very
    >different today, that was not the case for their progenitors. Similarly,
    >while extant mammals are clearly distinguishable from reptiles today,
    >the earliest mammals where not easy to differentiate from related
    >reptilian groups.
    >
    >
    >Tim: <<Such discontinuities tend to manifest more in the
    >morphological arena than the biochemical one. Also, hierarchical
    >organization is a manifestation of the rates of change and the nature
    >of speciation and organismal genetics. Understanding the timing and details
    >of specific steps behind evolution is real challenge, IMHO.>>
    >
    >>Although these words may make sense to you, they don't to me.
    >
    >Sorry, I wrote that too fast...
    >
    >1) Common descent with modification is a process that generates
    > nested hierarchies.
    >2) Organisms often (but don't always) differ more on the surface
    > (morphology) than they differ from a biochemical viewpoint. E.g.
    > Mammals may look different and live in different environments but
    > the underlying "hardware" is pretty similar.
    >3) The apparent distances between branches of the phylogenetic
    > tree of life reflect variations in the rates of change over
    > time. As long as the rates of morphological and genetic changes
    > are not too great, patterns deduced from morphological comparisons
    > can be expected to be consistent with the patterns created on the
    > basis of genetic comparisons.
    >
    >And finally: Understanding the timing and details of specific steps
    >behind evolution is real challenge in the study of evolution.
    >
    >
    >>I think our brief discussion illustrates my point that the statement
    >>presented by Dick is incomplete, and I add, even misleading. It suggests
    >>that evolutionary theory is a done deal. I continue to hold that descent
    >>with modification needs a robustly supported mechanism (which in my view it
    >>doesn't have) and in addition, an unambiguous refutation of intelligent
    >>design, to substantiate its claim to be the all encompassing theory it wants
    >>to be.
    >
    >Descent with modification has an extremely robust mechanism and can be
    >paraphrased as follows: "If your parents didn't have children, neither
    >will you."
    >
    >How the variations accumulated and what mechanisms fixed a particular
    >variation in a population are definitely open questions.
    >
    >Regarding the unambiguous refutation of intelligent design: That is
    >simply impossible. One may as well ask: "What could an intelligent
    >designer not do?"
    >
    >Regards,
    >Tim Ikeda (tikeda@sprintmail.com)
    >
    >
    >
    >--------------------------------------------------------------------
    >mail2web - Check your email from the web at
    >http://mail2web.com/ .



    This archive was generated by hypermail 2b29 : Tue Dec 11 2001 - 20:16:20 EST