In a message dated 9/15/2000 9:39:53 AM Pacific Daylight Time,
nalonso@megatribe.com writes:
<< Sure. But in the case of IC that's what you have to show. We all agree that
design can sometimes be infered quite reliably. IC does not eliminate
natural
processes as a cause, it claims that it does but it has not shown this. It
does not even show that ID is a plausible and useful alternative.
You seem to overestimate the power of ID and IC. Perhaps that's caused by
the
unsupported claims like the ones you make above?
Nelson:
Can you show how what I say above is not supported? You have to first
support your claim that IC systems can evolve. You cannot evolve something
that is totally ineffective below the sum of it's parts. >>
FMA:
You are trying to switch the burden of proof again.
Nelson:
No, the burden was to produce a system that cannot arise via chance and
natural selection. >>
Not the burden of proof is to show that an IC system cannot arrise through
chance and natural selection. And even if it could, this would not prove
design merely disprove Darwinian evolution as a mechanism here.
There can be no functional precursor if you cannot reduce
<< an irreducible system since the you cannot show an effective precursor. Now
if you want to say "it could have evolved" you have to give me a pathway to
work with. I have proposed my pathway, namely intelligent design.
>>
That's not a pathway. It's a place holder for ignorance. I have shown how an
IC system could arise naturally (Robison). Others include
Terry Gray
"A key first step is a gene duplication event that allows the preservation of
the original functional protein, but provides a second copy of the gene that
can be altered by mutation, providing a source of new material on which
selection can operate. There are multiple versions of globin genes that differ
by only a few amino acids in insects and molluscs of the organisms mentioned
above. In humans alpha and beta hemoglobin exist in gene clusters
containing multiple copies of each type gene. In the alpha cluster there are
two identical copies of the alpha gene, two copies of the alpha-like zeta
globin (found in fetal hemoglobin), and one alpha-like pseudogene, that
appears not to be expressed. In the beta cluster there five different
beta-like
genes and one beta-like pseudogene. It appears from various lines of argument
that these have arisen by gene duplication followed by mutations.
Some of the mutated copies appear to be functionless, whereas some of them
appear to have new functions, i.e. in fetal hemoglobin with altered
oxygen binding. These gene duplications are pre-adaptations, i.e. changes
that occur for other reasons, but once they have occurred they provide
the necessary conditions for some selectable function.
Sea lamprey globin evidences what might be the next intermediate stage. Sea
lampreys have a separate myoglobin for oxygen storage and a
hemoglobin-like molecule for oxygen transport. Lamprey hemoglobin is dimeric
rather than tetrameric. It does display cooperative oxygen binding,
though. Lamprey deoxyglobin forms dimers which dissociate upon oxygen
binding. The dimer contacts are in exactly the region of the molecule
where one alpha-beta dimer interacts with the other alpha-beta dimer. This is
the region that modulates the 15¡ rotation and the cog-slipping effect
that was described above. Murray Goodman and co-workers cite evidence from
their sequence comparisons that suggest that mutations
accumulated in this region of the molecule at four times the rate for the
molecule as a whole during the evolution of this new function. Clearly,
cooperativity of oxygen binding is a consequence of dimerization. But dimer
formation is the result of greasy patches on the surface of the protein,
which could well have arisen by a few amino acid substitutions (or even one
as is the case in deoxyhemoglobin S fibers in sickle-cell anemia). Dimer
formation would have been a Darwinian pre-adaptation to the evolution of
cooperative oxygen binding.
The next step in hemoglobin evolution is the result of a gene duplication of
the ancestral hemoglobin-like gene into the modern alpha and beta globin
genes. Again, the original oxygen transporting function could be preserved,
while mutations acted upon the second copy of the gene. The very
similar but slightly different version of the globin allowed for the
formation of the alpha beta dimer which upon interaction with another
alpha-beta
dimer allowed the preservation of the tetramer structure even upon
oxygenation. Again Goodman's group believe that their sequence comparison
data suggests that the alpha-beta dimer interface accumulated mutations at
nearly twice the rate for the whole molecule during the evolution of this
new function. Again, the gene duplication event and the alpha-beta dimer
formation are pre-adaptations to the formation of the complex tetramer.
In the 450 million years since the origin of the hemoglobin tetramer there
has been ample time to finely tune the primitive transport function. And
there does appear to be additional evolution, especially related to the rise
of warm-blooded creatures and, as I already mentioned in my discussion
of the gene structure of the human alpha and beta gene clusters, the rise of
placental mammals and special adaptations utilized in oxygen transport
there.
Hemoglobin is a marvelous molecular machine. When we look at it in all its
complex features, many of which we haven't even discussed today, we
might imagine that it's like a mousetrap: you take one part away and it
doesn't work any more. That may, in fact, be true with the modern finely
tuned version. But I have shown a plausible evolutionary scenario based on
the structural, mechanistic, genetic, and sequence data concerning
globins from all parts of the animal kingdom. "
Lindsay
"The above exchange happened in 1997. As of 1999, Behe has simply avoided the
goalposts. I do not know of a public acknowledgement that
some of his examples, such as clotting have been convincingly explained.
Instead, in September 1999 he said "The point in dispute is whether natural
selection can produce major innovations." But surely his book holds up the
immune system as a major innovation, and as of 1998 it was no longer
disputable that evolution could have caused that. "
"Rebuttal of Example: Cilia and Flagella
Although Behe describes these on pages 59-72, it isn't clear exactly what the
irreducible systems are, and why they can't be reduced.
Suppose we took flagellin, which in E. coli K-12 is a chain of 497 amino
acids. What if we chop out a third of those? If the "system" is irreducible
then removing these parts should make it stop functioning. But that has been
done, and the flagellum still worked fine [1]. So is this reduced system
Irreducible? Apparently we don't have a good way to know, since the method
applied to the original system gave a wrong answer.
Flagellin is also used for "active transport" inside cells, but a cutdown
version with 183 aminos will do that [2]. This implies that there was some
earlier molecule that was only used for transportation. Evolution replaced
that molecule with flagellin, and flagellin was then co-opted into its
flagella
role because it was lying around.
So, there is evidence suggesting evolutionary scenarios leading to a
flagella. Behe tries to ridicule these on page 66, but the best he can do is
demand detail. As Behe points out on page 62, microtubules are involved in
transport, and in simpler ways than their use in flagella. Just from his
description, one would guess that transport came first, and in fact we're
quite sure that flagella were not present in the original ancestral cell.
Since
this is an area of ongoing research, there is every reason to believe that
further evidence will be found that suggest or constrain the sequence of
events. Here is one guess, based on current knowledge:
Let us imagine a bundle of tubulins serving a structural function at the
cell membrane, sticking out and causing a projection (but a static
one) from the cell surface. Let's call such a projection a microvillus
(to choose a name at random :-)). One of the consequences of
these microvilli would be an increase in the surface to volume ratio of
the cell. Surely, even Behe might be able to come up with a
reasonable selective environment where such microvilli might be favored,
even if they could not move at all. Now one, as Behe points
out, might envision motor molecules involved in transport along the axis
of these fiber bundles (for precisely the reasons one might
expect microvilli to form in the first place). Linking some of the
bundles might allow some minor movement of the microvilli at levels
that would be insufficient to cause cell motility. But movement, by
creating microcurrents, might have uses without being sufficient to
move the organism. Under conditions that select for more vigorous
movement, you might well get the emergent property of motility.
I have previously given a highly speculative, but similar, possible
pathway to produce flagella via non-motile, but still functional
intermediates.
Can I prove these scenarios? Nope. Are they totally out of line? Well,
if you look for evidence of these intermediate states, you need
to ask whether tubulins are involved in maintaining cell structure in
microvilli, whether pilins have utility, whether there are protein
transport pores, etc in current organisms. This, of course, is not
direct evidence. It is evidence like that that Darwin presented for the
eye. It is evocative, possible, and is congruent with natural law
mechanisms. But it is the only type of evidence that anyone has in these
cases.
Posted 1 Sep 1997 on Usenet's talk.origins by Howard Hershey
It is also difficult to accept that a flagella represents Intelligent Design,
when it is so different from a cilia or an undulopodia. And why do archae and
bacteria use a very different flagellin? What kind of intelligent designer
doesn't re-use designs, or even components?
Rebuttal of Example: Clotting
In my ignorance section, I pointed out some problems with Behe's attack on
the article by Russell Doolittle. Doolittle has written his own response
which points out that there are animals with simpler molecules, as you'd
expect if the molecular evolution happened in one line of descent but not in
another. Doolittle ends by showing that lab animals can get along fine
without parts of this "irreducible" system.
George Acton wrote a slightly more technical response and says that it's
"like reading a discussion of the Shroud of Turin that totally omits any
mention of the radiocarbon dating studies."
Rebuttal of Example: Immune System
Behe spends Chapter 6 on the immune system, and on page 137 he talks about
scientists who have "gamely" tried to explain the system. The
scientific efforts have paid off. There is now a detailed theory as to how
the system could have been started. And, there is now experimental
evidence that the theory is correct. Work continues, demonstrating that the
theory of evolution is fertile, and not (as Behe put it) "sterile".
Rebuttal of Example: Bombardier Beetle
There is a good analysis of the bombardier beetle at the talk.origins
archive.
The main problem with Behe's analysis is that he doesn't seem to know what
data to look for. Any evolutionist would have immediately proposed a
whole list of things to be investigated. Do we have a tree of descent of
related species? Which of them secrete what chemicals? Which ones have
specialized bladders? - and so on. All of these would be useful as raw
material for constructing hypotheses and for ruling hypotheses out. But Behe
just cries out for more detail of the final answer. It's as if he doesn't
know how to attack these problems.
"
Niall Shanks
"Biological systems exhibit complexity at all levels of organization. It has
recently been argued by Michael Behe that at the biochemical
level a type of complexity exists -- irreducible complexity -- that
cannot possibly have arisen as the result of natural, evolutionary
processes, and must instead be the product of (supernatural) intelligent
design. Recent work on self-organizing chemical reactions
calls into question Behe's analysis of the origins of biochemical
complexity. His central interpretative metaphor for biochemical
complexity, that of the well-designed mousetrap that ceases to function
if critical parts are absent, is undermined by the observation
that typical biochemical systems exhibit considerable redundancy and
overlap of function. Real biochemical systems, we argue,
manifest redundant complexity - a characteristic result of evolutionary
processes. (.We would like to thank George Gale for helpful
comments, as well as the anonymous referees for Philosophy of Science.)"
"Redundant complexity is embodied in the discovery that biochemical processes
frequently do not involve simple, linear sequences of
reactions, with function destroyed by the absence of a given component
in the sequence. Instead, they are the product of a large
number of overlapping, slightly different and redundant processes. This
feature of these processes turns out to lie at the heart of the
stability that these processes manifest in the face of perturbations
that ought to catastrophically disrupt systems conceptualized from the
standpoint of Behe's central interpretative metaphor of the
well-designed, minimalist mousetrap -- the absence of any component of
which should render the system functionless. "
Redundancy
"It is a hallmark characteristic of evolved biochemical systems that there
are typically multiple causal routes to a given functional end,
and where one route fails, another can take over. The existence of
multiple isoforms of a given enzyme are evolutionary legacies --
legacies by means of which one and the same enzyme can be co-opted to
serve specialized functions in specialized tissues."
He concludes
"In the end, Behe overestimates the significance of irreducible complexity
because his simple, linear view of biochemical reactions
results in his taking snapshots of selective features of biological
systems, structures and processes, while ignoring the redundant
complexity of the context in which those features are naturally
embedded. Real biological systems are quite unlike economically
designed engineering artifacts such as mousetraps. His case against
evolution is a good example, in fact, of the perils of being "trapped"
by a metaphor."
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