I have read the referenced document by Behe and it seems that the
distinction he is drawing is between mutliple "beneficial" mutations and
multiple "non-beneficial" mutations.
Since by beneficial we mean that it increases the survivability of the
organism, it is more likely that such traits would survive long enough
for other mutations to show up, the accumulation of the multiple
mutations being necessary for the ultimate trait in question.
However, if the multiple mutations are not beneficial they are less
likely to survive long enough for other required mutations to occur in
an individual.
Hence, beneficial mutations are correlated in some sense, assuming that
the sum of the multiple beneficial mutations is not detrimental, in
which case they will be anti-correlated.
However, the non-beneficial mutations are in a sense independent.
Suppose we have a group of bacteria with non-beneficial trait A. Such a
trait will not confer any survival advantage to them. Hence, their
relative population will remain unchanged, assuming that the remainder of
the population remains equally competitive. Now if a second mutation
should occur, it will be randomly distributed amongst the entire
population. So the probability of the two traits being in one individual
would be the fraction of those with mutation A. Assuming the situation
continues with traits A and B. The probability of an individual getting
mutation A, B, & C would be the fraction F_ab, with each subsequent
fraction decreasing over time since no advantage is conferred to the
cumulatively mutated individual.
But if the mutations confer advantage to individuals, then the
subsequently mutated individuals can produce larger and larger fractions
of individuals with the multiple mutations, until the multiply mutated
individuals dominate the population. This presumes, of course, that
individuals accruing the mulitple mutations do not become less survivable.
Such a limitation may restrict the sequence of the mutations, permitting
some and disallowing or disadvantaging others.
Finally, combinations of beneficial and non-beneficial mutations are
possible. But it seems that clearly multiple, esp. very large multiple,
mutations that are non-beneficial would be exceedingly unlikely, esp. when
compared to beneficial multiple mutations.
Anyway, I'm probably just repeating something that everyone already knows,
but it was good exercise for me. The only question is whether Lenski's
data actually supports the notion that the multiple mutations were
actually non-beneficial ones.
It ought to be possible to determine this by examining the temporal
populations of groups with the varying mutations. Should the fraction of
the mutated branch grow at the same rate as the rest of the population, it
appears that no increased survivability was conferred.
bill
On Wed, 14 Oct
2009, Schwarzwald wrote:
> Actually, Behe has a lot to say about this paper here:
> http://behe.uncommondescent.com/2008/06/multiple-mutations-needed-for-e-coli/By
> the way, I'd like to know where Behe claims that it's "impossible".
>
> Anyway, some selected quotes:
>
> "Now, wild *E. coli* already has a number of enzymes that normally use
> citrate and can digest it (it’s not some exotic chemical the bacterium has
> never seen before). However, the wild bacterium lacks an enzyme called a
> “citrate permease” which can transport citrate from outside the cell through
> the cell’s membrane into its interior. So all the bacterium needed to do to
> use citrate was to find a way to get it into the cell. The rest of the
> machinery for its metabolism was already there."
>
> "To get a feel for the clumsy ineffectiveness of random mutation and
> selection, consider that the workers in Lenski’s lab had routinely been
> growing *E. coli* all these years in a soup that contained a small amount of
> the sugar glucose (which they digest easily), plus about ten times as much
> citrate. Like so many cellular versions of Tantalus, for tens of thousands
> of generations trillions of cells were bathed in a solution with an
> abundance of food — citrate — that was just beyond their reach, outside the
> cell. Instead of using the unreachable food, however, the cells were
> condemned to starve after metabolizing the tiny bit of glucose in the medium
> — until an improbable series of mutations apparently occurred. As Lenski and
> co-workers observe: (1)
>
> Such a low rate suggests that the final mutation to Cit+ is not a point
> mutation but instead involves some rarer class of mutation or perhaps
> multiple mutations. The possibility of multiple mutations is especially
> relevant, given our evidence that the emergence of Cit+ colonies on MC
> plates involved events both during the growth of cultures before plating and
> during prolonged incubation on the plates.
>
> In *The Edge of Evolution* I had argued that the extreme rarity of the
> development of chloroquine resistance in malaria was likely the result of
> the need for several mutations to occur before the trait appeared. Even
> though the evolutionary literature contains discussions of multiple
> mutations (5), Darwinian reviewers drew back in horror, acted as if I had
> blasphemed, and argued desperately that a series of single beneficial
> mutations certainly could do the trick. Now here we have Richard Lenski
> affirming that the evolution of some pretty simple cellular features likely
> requires multiple mutations.
>
> If the development of many of the features of the cell required multiple
> mutations during the course of evolution, then the cell is beyond Darwinian
> explanation. I show in *The Edge of Evolution* that it is very reasonable to
> conclude they did."
>
> To read what Behe has to say about Lenski's discoveries with citrate, one
> would take away the idea that it supported and backed up what he spoke of in
> EoE.
>
> That said, it's a mistake to talk about how "scientists insist on rigor" -
> as if scientists all have a unified and therefore uncontroversial view about
> what counts as "science" or not. In fact, George Ellis (Isn't he an ASA
> member?) recently celebrated a birthday, in honor of which he invited a
> number of scientists and philosophers (Philosophers? Of all people?) to
> discuss whether appeals to a multiverse could be considered scientific. Some
> argued no, and some argued yes. On the 'yes' side included Max Tegmark, who
> favors the idea that all possible mathematically explicable universes exist
> (A type IV multiverse). Interesting stuff.
>
> Pay special attention to what this conversation means, however. No one, as
> far as I know, denied that multiverses were in principle beyond observation
> - at most, they could be inferred. Any support they could gain would be at
> best indirect, while the mere assumed existence of a multiverse inherently
> leads to certain absurdities (Paul Davies, among others, has some
> interesting things to say about this.) And it's admitted that entertaining
> explanations that lean upon multiverse speculations is not the same-old,
> same-old for science - indeed, it would be a loosening of established rules
> and practices. Sound familiar?
>
> Granted, multiverses are cosmology - Behe is dealing with microbiology.
> Still, the case is instructive since it deals with a general sense of what
> is and isn't admissible for a "scientific" explanation - and how in one area
> there are arguments to loosen those standards.
>
> On Tue, Oct 13, 2009 at 10:59 PM, Rich Blinne <rich.blinne@gmail.com> wrote:
>
>>
>>
>> On Mon, Oct 12, 2009 at 11:45 AM, Cameron Wybrow <wybrowc@sympatico.ca>wrote:
>>
>>> It does not seem to me obvious what the right answer is, nor do some of
>>> the greatest philosophers of science (who have wrestled quite seriously with
>>> teleological explanation) think it is obvious what the right answer is; TE
>>> people, on the other hand, just take for granted that consistency of method
>>> trumps adequacy of explanation every time.
>>>
>>>
>> The reason why scientists insist on rigor is that it produces adequate
>> explanations while those whom try to "expand" the scientific method to get
>> around the rigorous requirements -- in part to explain why they don't end up
>> in peer-reviewed journals -- in the end produce less adequate explanations.
>> So called adequacy is a way to get the camel's nose in the tent. For
>> example, ID proponents want to use abduction rather than induction, cf.
>> Chapter 7 Signature in the Cell. The reason why induction is superior for
>> scientific study is that through the process of falsification errors in the
>> original "adequate" explanations can be removed or "inadequate" explanations
>> can be reconsidered. In general, MN is used because it's easier to produce
>> falsifiable propositions but as I will show MN is not necessary in order to
>> be in bounds of tightly-demarcated science. ID fails demarcation not because
>> it considers the natural effects of the supernatural but because it isn't
>> empirical and inductive.
>>
>>
>> Take the drug resistance of the malaria parasite in EoE. Behe claimed that
>> the "odds" of producing a drug-resistant strain was in essence impossible.
>> First off, let's assume for the sake of discussion the God of Scripture. He
>> created the Universe, sustains it, and is a God of order (cf. 1 Cor. 14). We
>> know for a fact that currently Plasmodium is resisting previously successful
>> drug therapies -- and this next point is very significant -- after a delay
>> where the therapies were very successful. We also know that the genetic
>> difference between the old and new strains is something that wouldn't easily
>> be achieved by a single mutation. Behe concedes both common descent and
>> natural selection. He does not concede that abilility of so-called random
>> mutation to generate parasites to select from. This leaves us with three
>> possibilities:
>>
>>
>> 1. The drug-resistant parasites are the mutated descendants of the
>> non-drug-resistent ones. This Behe claims is impossible.
>>
>>
>> 2. The drug-resistant strains already existed and were merely selected once
>> the drugs were introduced. This appears to be what Behe prefers. But there's
>> a problem. The delay. If the drug resistant parasites are available to be
>> selected population genetics tells us that they start taking over quickly.
>> More on this later.
>>
>>
>> 3. The drug-resistant strains were created *de novo* by God after the
>> drugs were introduced. This possibility is not testable by science but is
>> the only option if 1 and 2 are eliminated. To use ID speak this is the most
>> "adequate" explanation. The theological implications of this are immense.
>> Behe claims that he is not out to prove the Christian God and this shows
>> that this is true. Behe has just proven an evil, pagan god. Tell all the
>> Christian doctors to pack it up because there is no way to know whether your
>> therapy will be directly thwarted by God.
>>
>> Fortunately this inevitable conclusion that no Christian including Michael
>> Behe would want is solved by plain ole mainstream science. See this paper by
>> Rich Lenski as part of the LTEE (long term evolution experiment). They have
>> taken several lines of E Coli bacteria for decades and gave it an
>> environment rich in citrate which E Coli does not normally metabolize. For
>> many many generations the E Coli did nothing with it and then after 20 years
>> (33,127 generations) E Coli that metabolized citrate appeared and started to
>> dominate.
>>
>> http://www.pnas.org/content/105/23/7899.full
>>
>> The role of historical contingency in evolution has been much debated, but
>>> rarely tested. Twelve initially identical populations of *Escherichia
>>> coli* were founded in 1988 to investigate this issue. They have since
>>> evolved in a glucose-limited medium that also contains citrate, which *E.
>>> coli* cannot use as a carbon source under oxic conditions. No population
>>> evolved the capacity to exploit citrate for >30,000 generations, although
>>> each population tested billions of mutations. A citrate-using (Cit+)
>>> variant finally evolved in one population by 31,500 generations, causing an
>>> increase in population size and diversity. The long-delayed and unique
>>> evolution of this function might indicate the involvement of some extremely
>>> rare mutation. Alternately, it may involve an ordinary mutation, but one
>>> whose physical occurrence or phenotypic expression is contingent on prior
>>> mutations in that population. We tested these hypotheses in experiments that
>>> “replayed” evolution from different points in that population's history.
>>> *We observed no Cit+ mutants among 8.4 × 1012 ancestral cells, nor among
>>> 9 × 1012+, indicating that some potentiating mutation arose by 20,000
>>> generations. This potentiating change increased the mutation rate to Cit+but did not cause generalized hypermutability. Thus, the evolution of this
>>> phenotype was contingent on the particular history of that population. More
>>> generally, we suggest that historical contingency is especially important
>>> when it facilitates the evolution of key innovations that are not easily
>>> evolved by gradual, cumulative selection.*
>>>
>>
>> The relevance to Behe's example is he assumed that a single probability of
>> a giant mutation was applicable. In short, Behe assumes the mutations are
>> statistically independent. Rather, what Rich Lenski showed was a
>> potentiating mutation which made the rare jump easier (cf. Figures 1 and 3
>> of the paper) and the mutations are thus not statistically independent.
>>
>> Viewed another way a prediction that something is impossible is falsified
>> by the existence of the impossible event. Unless you want to admit God
>> created a parasite deliberately to thwart drug therapy then the fact that
>> Plasmodium did mutate falsified Behe's "prediction". We see from Lenski et
>> al the prediction failed because Behe's view of mutation was flawed and
>> oversimplified. At least that's the way science normally operates but ID
>> wants it to be different so that normal falsification rules don't apply.
>>
>> Rich Blinne
>> Member ASA
>>
>
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Received on Thu Oct 15 00:55:38 2009
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