Irreducible Complexity

[Administrator2]

HELEN

Barbarian asked some interesting questions:
1. Is it essential that the creationist know which things are designed
a priori in order to say which is which? And if so, of what use is such
a thing?
2. What confidence do we have that ID will ever be useful?
3. Is there any thing that can be evaluated as to "design" without
knowing beforehand?


As any child grows, the concept of design becomes established, first of
all, through experience. Thus, by adulthood, a pile of scrap metal can
be distinguished from a car or a computer via this knowledge. So the
first understanding must be that we all do have some concept of what
design is and is not going into this thing as adults. It is with THIS a
priori knowledge of what design means that a number of scientists – and
regular folk – have looked at cells, leaves, bodies, and perhaps even
the earth itself and commented to themselves, “This really does not look
like an accident. This looks like intricate design!” Could they/we be
mistaken? Of course! Dawkins and others admit the biological world
shows signs of rather complex design but claim that is an artefact of
our imaginations and not representative of reality.

So the point is, who is right? Is that cell a product of intentional,
intelligent design or is it something which came about purely by
chemical chance in the right circumstances? There will be, and often
are, strong feelings one way or the other, based on presuppositions of
creation or evolution, but feelings are not facts, and science itself
would normally like to get a little closer to the facts than feelings
can take them.

Thus the idea of testing for design. We do have criteria for
determining that the Golden Gate Bridge shows intentional, intelligent
design while a log across a creek, while performing the same essential
function, does not. At least, not as a bridge… So what are those
criteria? Let me ask you: how would YOU determine such a thing APART
FROM EXPERIENCE AND PREVIOUS KNOWLEDGE? The ID tests which have emerged
so far include the Dembski filter and specified complexity. I
personally have played around with another more vague idea, that
concerns the ‘natural’ function or position of materials. If something,
say a rock, is doing something other than ‘just lying there’ as rocks
are prone to do when not being thrown through the air by a child,
earthquake, landslide, etc., then perhaps that rock is part of a
design. If the rock is part of a fountain, or a wall, or has been
sculpted – this is not something we see rocks ‘do’ in their ‘natural’
state. This might well indicate design. You can see this is still a
very rough idea and not at all polished and presentable yet, but I think
you can get the idea.

So the first answer is that no, no one needs to know what is designed
ahead of time, although from experience we may have some pretty good
clues.

Will ID ever be useful? Well, we use it everyday in our own lives as
far as manmade objects are concerned, so I assume you mean
scientifically where biology in particular is concerned. Yes, it will
be very useful for three immediately thought-of reasons: first to
correct the current reductionist tendency in science which assumes a
material, natural cause for all known effects. If science has any goal
anywhere within it regarding seeking out the truth of a matter, then
this is very important. Secondly, this would correct the allocation of
funds in a number of areas of research. Funds for abiogenesis research
could well be redirected into medical research, for instance. And
finally, the establishment of even the possibility of design in the
natural world would stop the current teaching from ripping apart the
faith of students bit by bit, which, from what I have seen in media,
texts, and in person, seems to be a major goal of science education at
this point. There is no need to destroy a student’s personal
foundations in the name of science, especially when science may well be
– and certainly has been historically – wrong.

Can design be inferred which is not known about ahead of time? Do you
want to ask a chaos theorist about that one? Do you see what I mean?
Remember the cell when described a hundred and fifty years ago? Just a
sort of blob. That did not need to be designed; that most certainly
could have just sort of happened. But with more knowledge we are seeing
something vastly more complex. So I guess partly I would have to ask
you what you mean by ‘ahead of time’. How far ahead of time? One most
probably would not test for design if one did not at least suspect it.

What puzzles me, quite honestly, are those who declare design to be
apparent but then deny it, which an awful lot of evolutionists do. Why
is the concept of intentional, intelligent design so evidently
frightening to them?

In the long run, I really do think it is for theological reasons and not
scientific ones. If things are not always materially, naturally caused,
then there may be a God. And if there is a God, then they may be
accountable for who and what they are. And yes, I agree, that can be a
very frightening thought to a rational man.

ID is essentially very scientific, using exactly the same scientific
method, including repeatability, which science declares must be used.
But it is rejected not because of this ‘peer review’ nonsense (were
‘memes’ peer reviewed first? And they are completely imaginary!), and
not because it is not based on rational, quantitative science, but
because of the implications if ANYTHING in the natural world can
possibly, objectively, be determined to be intentionally, intelligently
designed, and not simply a matter of chance/accident along with natural
forces.

 

[Administrator2]

NEILUNREAL

Helen wrote:

First "ID", or "intelligent design" is not a new proposal at all. It
is simply trying to take something that seems apparent, such as design in
nature, and seeing if we can test for it a little more objectively than
simple experience allows.

Whether I agree with ID or not, I don't have a problem with this view -- it
does, however, contain the seeds of my discontent. For ID to be science, it
is necessary to "see… if we can test for it a little more
objectively." But point/counterpoint arguments about supposed specific
instances of ID are exactly not the development of a general theory
of ID.

My scientific problem with "intelligent design" is that it seems very
difficult to recognize in the absence of a lot more theory about evolution
and dynamic systems. I say "intelligent design" in quotes, because the same
problem arises in purely materialistic terms when trying to determine
whether there are natural meta-operators which give evolution and
co-evolution a teleology (and other meta-hypotheses about evolution e.g.
Kauffman, Holland, et al). Right now, we can only recognize "design" in
very limited venues, such as noise vs. information in transmission channels.
(Another example is the ability to statistically test the probability of
membership in a given population.) Current scientific statements about
teleology -- whether "designed" or "naturalistic" -- must carefully balance
expert credibility against the highly conjectural nature of these
statements.

My philosophical problem with irreducible complexity is that it attempts to
prove a negative. How can you tell whether the irreducible complexity arose
by divine fiat or by some natural method you haven't yet thought of? How
can you ever be sure you've proven even a single case? Irreducible
complexity is useless as a philosophical tool unless there is some theory
which tells you how to distinguish unsolved natural cases from supernatural
cases. Statistical testing won't do the job, since you've made population
assumptions in ignorance. The operation of induction, deduction and proof
are never as cut-and-dried in real-world science as in mathematics. (For
philosophers: Hempel's paradox addresses similar epistemological issues.)

All this creates a metaphysical problem for me when things like intelligent
design and irreducible complexity are used as apologetic tools.
Scientifically entrenching around a system like Newtonian mechanics until it
becomes untenable is the way good Kuhnian paradigm change occurs.
Theologically entrenching around a system until it breaks is bad theology
and bad science. It pays to remember that in the Galileo controversy, the
geocentric system was the existing scientific paradigm. The Church
got herself into trouble by theologically taking a stake in what should have
been a scientific question.*

If a scientist wants to devote research effort to ways to recognize
intelligent design (if there are any), I don't have a problem with that. I
my opinion, any problem to which any scientist is willing to devote time and
money is a problem worth studying (though getting that time and money is
their problem). But while doing science, they must remain good scientists!

Helen wrote:

From what I can see, that is also its weakness, for experience with
design is what we have to go on anyway.

Also a touches on point I was trying to make. Good science requires a
degree of objectivity and detachment -- the profound desire to reach a
conclusion must coexist with the even more profound desire to accept
whatever conclusion the science reveals. I worry that incautiously mixing
metaphysics and science makes objectivity difficult and can cause laymen to
misconstrue the normal machinations of science. This worry applies equally
to scientists of all faiths and of no faith.

Thanks for your comments,

-Neil

* I'm not attempting to associate anyone on either side of the ID
issue with anyone on either side of the Galileo issue! This is just the
most widely-known example of what I'm trying to illustrate. For the record,
neither am I impugning the Catholic Church as an institution or
organization -- my point is that I see the Galileo thing as a mea
culpa and cautionary tale for all people of faith.

[ March 15, 2002, 02:35 PM: Message edited by: Administrator ]

 

[Administrator2]

THE BARBARIAN

It seems simple enough. If ID is a workable idea, one can take a section of
human DNA, and a hypothetical one that is randomly generated, and use it to
say which one is "designed" and which is merely random.
To say "Here, I've determined life is designed.", when one has previously,
on religious grounds, assumed it is designed, is not very convincing. The
question is, can anyone use ID to tell where the answer is not already
assumed or determined? So far, no one's been able to do that.

Until then, it's not hard to figure out why few scientists, including those
of us who are Christians, give it any credibility. If you don't think it
would work on determining whether specific DNA is designed or not, then
could you give even one example of any case where the answer isn't
previously assumed or known, where it does work? And then can we test it
to see?

Keep in mind, as in that case where a new metabolic pathway was formed, we
know for a fact that particular DNA wasn't designed, because it was observed
to evolve by natural processes. I'm sure someone might say "Well, God
designed the process." But that would only show that theistic evolution
plus ID is no better than theistic evolution alone.

If, on the other hand, you'd like to actually try to analyze a few DNA
sequences to say whether or not they were designed, I'd be pleased to
provide them.

 

[Administrator2]

JOHN PAUL

Pat:
It seems simple enough. If ID is a workable idea, one can take a section of
human DNA, and a hypothetical one that is randomly generated, and use it to
say which one is "designed" and which is merely random.

John Paul:
I guess it would seem simple enough if you didn’t understand what ID is and what ID isn’t. And the EF is and what the EF isn’t. (chicken-dance music in the background)

So this hypothetical DNA wouldn’t be DNA at all, it would just exist on paper or a computer? Is that what you are saying? I can see no use in doing such a comparison. If, on the other hand, you had random sequences of DNA arising in nature (outside of a living cell) and you wanted to compare those to a segment of human DNA, that would be different. But in your scenario, even the hypothetical DNA would be designed.

The EF relies on our ability to determine specificity. I touched on this in an earlier post when I mentioned ‘junk’ DNA:

If we limit ourselves to segments of DNA one could pick out a segment of alleged ‘junk’ DNA/ pseudo-genes and because of our lack of knowledge about the genetic code, use this seemingly random sequence as evidence that DNA couldn’t be designed because that segment apparently doesn’t code for anything. That would miss the point and count on our ignorance for support.

IOW, although some segments of an organism’s DNA have no apparent function, the full sequence of DNA for that organism, most certainly does.

And yes, the EF can be fooled. A person could design what would give all appearances to be random rock patterns. Only that person would know it was designed. In that case anyone, but that person, entering the data into the EF would come up with a different conclusion because although it was designed it did not exhibit specificity to that other person.

Pat:
To say "Here, I've determined life is designed.", when one has previously,
on religious grounds, assumed it is designed, is not very convincing.

John Paul:
I can’t say about other people, but for me I became more religious once I made the determination life could not have originated via purely natural processes. Yes, I had my doubts. I weighed the evidence, heavily, and made my choice. After making that choice I at first felt guilty because I had those doubts, but now I am thankful for them. I don’t think the Lord wants blind sheep. We already bit from the tree/ fruit of knowledge (Adam’s original sin), no turning back. To survive we must understand. To understand we must study, research, develop, etc.

So your premise is demonstrate-ably wrong. The materialistic naturalists pretty much had me convinced, but I grew out of it.

Why is it OK to say life is the product of purely natural processes without substantiating evidence? That’s not convincing at all. Double-standards there Pat.

Pat:
The question is, can anyone use ID to tell where the answer is not already
assumed or determined?

John Paul:
That is what I demonstrated.

Pat:
So far, no one's been able to do that.

John Paul:
That’s incorrect. I did just that with DNA. I have no idea if it was designed, I wasn’t there. But, thanks to the EF, I can safely infer that is was.

All the EF is, is a process guide. It guides you through the process of differentiating design from natural processes. It is only as good as the data it is fed. Guess what Pat? Humans provide that data. Assumptions are made in science and biases influence conclusions. Welcome to the real world.

The ‘Giant’s Causeway’ in Ireland was once thought to be the product of design, and may have, at one time, passed through the EF as such. Now, with our current geological understanding we see it as a result of a natural process. The EF only works as good as the people operating it. No doubt about that.

That is why much thought and effort is going into refining the concept of Complex Specified Information and how it pertains to biological organisms.

Pat:
Until then, it's not hard to figure out why few scientists, including those
of us who are Christians, give it any credibility.

John Paul:
ID-type processes are already in use in several fields. So I don’t know what you are talking about. The only way around ID is to ignore it.

The Biologist:

http://www.creationequation.com/Archives/TheBiologist.htm

Are you saying it’s OK for a Christian to twist Scripture? Didn’t I expose you for doing just that? Talk about lacking credibility. Even with my religious convictions I would not have dared try to pull-off what you posted about the Genesis reference to a Special Creation (i.e. complex metazoans amongst the first inhabitants- humans separate from all other).

Pat:
If you don't think it would work on determining whether specific DNA is designed or not, then
could you give even one example of any case where the answer isn't previously assumed or known, where it does work? And then can we test it to see?

John Paul:
It would be nice if you applied those standards to the current paradigm. How can we determine if DNA (or life) originated via purely natural processes? And then can we test it to see?

Again I point you to Dr. Behe:

”Might there be an as-yet-undiscovered natural process that would explain biochemical complexity? No one would be foolish enough to categorically deny the possibility. Nontheless, we can say that if there is such a process, no one has a clue how it would work. Further, it would go against all human experience, like postulating that a natural process might explain computers. Concluding that no such process exists is as scientifically sound as concluding mental telepathy is not possible, or that the Loch Ness monster doesn’t exist. In the face of the massive evidence we do have for biochemical design, ignoring that evidence in the name of a phantom process would be to play the role of the detectives who ignore an elephant.”

from the next paragraph:

”Our ability to be confident of the design of the cilium or intracellular transport rests on the same principles to be confident of the design of anything: the ordering of separate components to achieve an identifiable function that depends sharply on the components.”

But yes, the EF’s intention is to aid us in differentiating between a naturally produced object and a designed object. Once that is determined, design or not, that is where the backing should go. Sure, keep some people around to try to falsify that premise, but put the bulk of the resources behind the EF’s output.

Pat:
Keep in mind, as in that case where a new metabolic pathway was formed, we
know for a fact that particular DNA wasn't designed, because it was observed
to evolve by natural processes.

John Paul:
Are you going to provide a reference for that or not? I have asked and you have not complied. Also you should keep in mind that if that particular DNA were the result of a designed process, it wouldn’t be due to natural processes. And don’t forget Dr. Spetner’s hypothesis.

Pat:
I'm sure someone might say "Well, God designed the process." But that would only show that theistic evolution
plus ID is no better than theistic evolution alone.

John Paul:
No. Theistic evolution is a cop-out. ID flat out says the CSI exhibited in living organisms is the result of intentional design and sets out to understand that design. ID gives us mechanisms like Dr. Spetner’s Non-Random Evolutionary Hypothesis, that help us understand a population of organisms’ limit in the variety it can achieve, how it can achieve it and why it may have to.
Theistic evolution just kind of mumbles around and accomplishes little, if anything, different from atheistic evolution.

Pat:
If, on the other hand, you'd like to actually try to analyze a few DNA
sequences to say whether or not they were designed, I'd be pleased to
provide them.

John Paul:
It has become apparent that you don’t understand ID or the purpose of the EF. The EF is satisfied that DNA of living organisms can be inferred to have at one time, been designed. The EF cannot tell us what happened to that design after eons of replication, mixing and environmental pressures.

ID is an inference based upon the available evidence. Until you can demonstrate that purely natural processes can bring about CSI or life itself, that inference will stand un-falsified.

One more thing. What is the positive evidence that life can originate from non-life via purely natural processes? If there isn’t any, why is it ‘scientifically’ OK to dogmatically declare that it did? That is what you are doing by denying the design inference and ignoring the irreducible complexity of life itself.

God Bless,

John Paul

[ March 19, 2002, 11:43 AM: Message edited by: Administrator ]

 

[Administrator2]

HELEN
Barbarian, the concept of IC lies NOT in the sequencing, but in the
function. DNA 'works' because the cell knows what to do with it. In
this sense, I suppose, it could be said that the cell itself can tell
the difference between what is intelligently designed and what is random
nonsense genetically.

We should be as smart as our cells!

 

[Administrator2]

JOE MEERT

Helen:ID has nothing to do with any religious
paradigm

and then later:

And
finally, the establishment of even the possibility of design in the
natural world would stop the current teaching from ripping apart the
faith of students bit by bit, which, from what I have seen in media,
texts, and in person, seems to be a major goal of science education at
this point.

JM: Forgive me if I find these statements confusing. On the one hand, you
doubt ID as independent of religion and then you tout its inclusion into the
currriculum as rescuing the faith of students. Which is the real position?
This is one of the reasons ID faces an uphill battle it's claims don't hang
together. Suppose as an instructor I want to teach that the Intelligent
designer is really Satan dressed up as a Martian? Or heck, suppose I just
want to assert that the intelligent designer is Satan. Would that be
allowable? I mean at some point a student is going to ask about the
identity of the designer. Are you willing to allow teachers to invent their
own designer or is the next step to introduce GOD? Make no mistake about
it, Phillip Johnson has made it clear what he wants out and what he wants in
and it is very religious. Again, I ask, how many non-Christians are
affiliated with the ID movement and how many of them think something/one
other than god is the designer?

 

[Administrator2]

HELEN

I don't know if this is IC or not, but these two proteins must work together
to accomplish anything...

Nature -- February 7, 2002 -- Volume 415, Issue 6872, pp. 659-662
Mechanism of force generation by myosin heads in skeletal muscle
Gabriella Piazzesi,et al

Muscles generate force and shortening in a cyclical interaction between
the
myosin head domains projecting from the myosin filaments and the adjacent
actin filaments. Although many features of the dynamic performance of muscle
are determined by the rates of attachment and detachment of myosin and
actin, the primary event in force generation is thought to be a
conformational change or `working stroke' in the actin-bound myosin head.
According to this hypothesis, the working stroke is much faster than
attachment or detachment, but can be observed directly in the rapid force
transients that follow step displacement of the filaments. Although many
studies of the mechanism of muscle contraction have been based on this
hypothesis, the alternative view-that the fast force transients are caused
by fast components of attachment and detachment -has not been excluded
definitively. Here we show that measurements of the axial motions of the
myosin heads at ångström resolution by a new X-ray interference technique
rule out the rapid attachment/detachment hypothesis, and provide compelling
support for the working stroke model of force generation.

 

[Administrator2]

THE BARBARIAN

John Paul: It has become apparent that you don't understand ID or the
purpose of the EF. The EF is satisfied that DNA of living organisms can be
inferred to have at one time, been designed. The EF cannot tell us what
happened to that > design after eons of replication, mixing and
environmental pressures.

Barbarian: It is clear that EF is easily satisfied, but requires a prior
assumption of design on the person doing the analysis. Why not simply call
it "faith" and let it be? If I understand you correctly, you are telling me
that there is no way to test the supposition. If there is a way, I would be
very pleased to hear about it.

ID is an inference based upon the available evidence. Until you can
demonstrate that purely natural processes can bring about CSI or life
itself, that inference will stand un-falsified.

The problem is that there seems to be no evidence for ID. Can you give me
an example where it is invoked where there has not been a prior assumption
of design? Such an assertion is not only unfalsified, it is unfalsible, and
hence not science.

One more thing. What is the positive evidence that life can originate
from non-life via purely natural processes?


Let's see.... the fact that RNA can be auto-catalytic, the nature of basic
biochemical processes that seem to indicate an original low oxygen
environment, followed by a higher oxygen tension, the existence of
archaebacteria, which all seem to be extreme anaerobic thermophiles, the
fossil record, which shows a progression of early cellular life from simple
to more complex, ... and so on. There's not enough evidence for it to be a
given, yet (and maybe there never will be) but no honest person familiar
with the research says that there is no evidence for it.

If there isn't any, why is it scientifically OK to dogmatically declare
that it did?

It wouldn't be. But you are incorrectly assuming that's what scientists are
doing. First, there is evidence to support the theory, and I'm certainly
not dogmatically insisting the theory is correct. I do accept what Genesis
has to say about it, but that is not a scientific statement, merely my
faith in God's Word.

[/i}That is what you are doing by denying the design inference and ignoring
the irreducible complexity of life itself. [/i]

No. I'm just waiting until some one shows me that it can actually
demonstrate design. I've pointed out to you before that we have directly
observed irreducible complexity evolve, so irreducible complexity cannot be
evidence for design.

Again, is there any instance where the EF works prior to determining whether
something is "designed" or not?

 

[Administrator2]

SCOTT PAGE

Helen:
Barbarian, the concept of IC lies NOT in the sequencing, but in the
function. DNA 'works' because the cell knows what to do with it. In
this sense, I suppose, it could be said that the cell itself can tell
the difference between what is intelligently designed and what is random
nonsense genetically.

The function of DNA is dictated by the 'sequencing', so in reality, the sequence of DNA is very important. As such, one should think that a 'filter' that is purported to be able to tell what is 'Designed' and what is not, biologically speaking, should certainly be able to tell whether or not a given sequence of DNA is designed, a random conglomeration of nucleotides, or arose naturally.

The cell only 'knows' what do do with the DNA because the DNA tells the cell what to do.

Of course, the creationist has already provided for themselves a way out, as John Paul so explicitly demonstrated above:

"So this hypothetical DNA wouldn’t be DNA at all, it would just exist on paper or a computer? Is that what you are saying? I can see no use in doing such a comparison. If, on the other hand, you had random sequences of DNA arising in nature (outside of a living cell) and you wanted to compare those to a segment of human DNA, that would be different. But in your scenario, even the hypothetical DNA would be designed."

John Paul also mentioned something interesting regarding creationist physicist Lee Spetner's 'non-random evolutionary hypothesis.'

Some interesting issues regarding that (courtesy of Sumac,):

Posted on: 10:18 am on May 25, 2001
: The phenomenon discussed in the two articles was first described by John Cairns and colleagues (1). I won't present the experiments in detail (unless someone is really interested), but it helps to know that the Cairns experiments were essentially repeats of experiments that had been performed and published over 40 years previous (2). All of the experiments were designed to test whether mutations occurred independent of or in response to selection. Luria and Delbrück's data unquestionably demonstrated that mutations can and do occur independent of selection. Cairns et al.'s data were not as clear cut.

: The key difference between the experiments was that Cairns et al. used a non-lethal selection while Luria and Delbrück used a lethal one (Luria and Delbrück selected for phage resistance; Cairns et al., selected for lactose utilization). Non-lethal selection was important because it allowed the bacteria to remain viable in a so-called stationary state for long periods of time in the selection medium. Although stationary cells are not growing, they are anything but dormant. Stationary cells actively break down and rebuild proteins and other biomolecules and they continuously sample their environment while waiting for any opportunity to begin growing again.

: The vast majority of mutations observed in the Cairns experiments did occur independent of selection, confirming previous conclusions. However, if the bacteria were left in the selection medium for long periods of time (days or weeks), a small number of new colonies would begin to grow suggesting that they contained mutations that occurred after exposure to the selection medium. These low frequency mutations appeared to be specifically responsive to the selection medium which led to the hypothesis that perhaps they were directed to occur by the selection.

: Directed mutation was just one hypothesis of several. Cairns et al. actually favored a model in which a trial-and-error mechanism searched for mutations that would allow the cells to grow. In a commentary that accompanied Cairns's article, Franklin Stahl suggested the possibility that the scavenging state of stationary cells may be conducive to an overall increase in mutation rate (3). Stahl proposed that as soon as a 'good' mutation occurred, normal growth would resume and the mutation rates (and types of mutations) would return to normal.

: Over the next several years following Cairns's discovery, other studies using different types of non-lethal selection were published with similar results. However, none of the studies could demonstrate that the mutations were actually directed to occur. Your first article (the Foster review, ref. 4) compiled data from a number of studies and weighed the data against the hypothesis of directed mutation. Although Foster seemed to like the idea, she was quick to note that directed mutation is "the aspect that is the least supported by the experimental evidence." In the end, Foster favored a model that is a combination of Cairns's and Stahl's hypotheses: the overall mutation rate increases and temporary mutations are tested for benefit against selective pressures.

: From her concluding remarks: The evidence suggests that the role of selection in the mutational process is not to "direct" the process, but to define success. While this may appear to be just a version of "you get what you select for," there is an important distinction. If the idea of transient genetic variants is correct, it is not the organism, but its informational molecules that are under selection. Thus, a nondividing cell is, potentially, multiphenotypic, a characteristic previously thought to be true of the population, not the individual. If a bacterium can, either by design or accident, increase its genetic variability under stress while maintaining its genome more or less intact, this is clearly of evolutionary significance.

: Unfortunately, Foster was sometimes a bit overzealous in pushing her favorite model – even to the point of subtly misrepresenting data (I suspect unintentionally). For instance, when discussing Barry Hall's work on trp reversion (5), she stated, "Hall found no sequence changes in the Trp+ revertants other than the reverted bases themselves, a result which none of the current models for directed mutation can explain." Superficially, this statement is true. Hall didn't find any other sequence changes because he didn't look for other sequence changes. He only sequenced the regions of the genes (TrpA and TrpB) that contained the original trp- mutations. Furthermore, in the TrpA gene, most of the changes were not reversions to the original wild-type sequence, but were other changes that restored enzyme activity. Hall recognized the limitations of his data and acknowledged the possibility that other mutations would be present in the revertants even though he hadn't looked for them. The possibility of second-site mutations was especially likely in a couple of cases where the mutations in TrpA couldn't possibly restore enzyme activity on their own.

: Now to your second article (6). Foster and Trimarchi used the same experimental set-up as Cairns, but took it one step further. Bacteria containing a mutant form of the lacZ gene were selected for growth on lactose as before. The lacZ genes from late-appearing revertants were then sequenced and the mutations were analyzed. Out of a total of 54 revertants, six had multi-base insertions and four had multi-base deletions in lacZ. Three of the revertants retained the mutant lacZ gene suggesting that the phenotypic reversion was due to a mutation elsewhere in the genome. The most interesting result was that 41 of the revertants contained single base deletions within lacZ. These deletions were scattered throughout the lacZ gene (41 deletions at 10 different positions) and were found almost exclusively in regions of the gene that contained repeats of a single nucleotide (for instance, CCCC). Coincidentally, another group had been doing pretty much the same thing and published their paper in the same issue of Science (7). Rosenberg et al. identified 86 mutations at 41 different positions, 57 of which were single base deletions spread out over 14 positions. The remainder were larger deletions, insertions, or duplications. The single base deletions discovered by Rosenberg et al. were also predominantly located at regions of repeated nucleotides. Unfortunately, neither Foster and Trimarchi nor Rosenberg et al. looked at mutations outside of the lacZ gene.

: Since that time, more work has been done to understand how stationary bacteria adapt to specific selection media. Huxter presented some of those papers above. The big question was: are the mutations incurred by stationary phase bacteria really directed to occur in specific genes or is the apparent direction an artifact of the experimental set up? In 1997, Torkelson et al. demonstrated that it is the latter (8). Mutations in revertant bacteria are not localized to specific genes, but accumulate throughout the entire genome. The unique nature of these mutations (i.e. the preponderance of single base deletions) is most likely due to increases in specific types of oxidative damage and diminished fidelity of repair and recombination (9, 10). The appearance of specificity comes from the fact that as soon as a positive hit occurs, the bacterium leaves stationary phase and begins to grow on the selective medium. Stahl was right.

: I know I took a long time to get here, but I wanted to (hopefully) make it clear why the examples you provided are not examples of directed mutation. Two facts are worth repeating: 1) the mutations that lead to phenotypic reversion are varied and scattered throughout the relevant genes – they can even be extragenic, 2) unselected mutations accumulate throughout the genomes of revertants. These two facts are clear indications that the mutations leading to reversion are not directed.

: I'll end with two quotes. In a more recent review (11), Foster wrote: Because nonselected mutations arise and persist in the population during selection, a stress-associated general mutational state, strictly speaking, does not meet the original definition of adaptive mutation. However, here I will continue to call the selected mutations "adaptive" to distinguish them from nonselected mutations occurring during selection. This meaning of "adaptive mutation" is the same as that used by evolutionists to distinguish beneficial from neutral or deleterious mutations.

: And finally, from a news article that accompanied your second article (12): What hasn't been narrowed down, however, is a name for this phenomenon. Cairns originally used the term "directed mutation", which to many scientists implied that the bacteria themselves were directing which mutations arose. Others have called it "Cairnsian", "stationary phase" and "starvation-associated" mutation. Foster and Rosenberg both used "adaptive" in print, but on the job in Rosenberg's lab, they call it SPAM–Selection-Promoted Additional Mutations. Foster's idea: Just call it "Fred."

:
: References:
: 1. Cairns, J., Overbaugh, J., and Miller, S. (1988) The origins of mutants. Nature 335:142-145
: 2. Luria, S.E., and Delbrück, M. (1943) Mutations of bacteria from virus sensitivity to virus resistance. Genetics 28:491-511
: 3. Stahl, F.W. (1988) A unicorn in the garden. Nature 335: 112-113
: 4. Foster, P.L. (1992) Directed mutation: between unicorns and goats. J. Bacteriol. 174:1711-1716
: 5. Hall, B.G. (1991) Adaptive evolution that requires multiple spontaneous mutations: mutations involving base substitutions. Proc. Natl. Acad. Sci., USA 88: 5882-5886
: 6. Foster, P.L. and Trimarchi, J.M. (1994) Adaptive reversion of the frameshift mutation in Escherichia coli by simple base deletions in homopolymeric runs. Science 265: 407-409
: 7. Rosenberg, S.M., Longerich, S., Gee, P., and Harris, R.S. (1994) Adaptive mutation by deletions in small mononucleotide repeats. Science 265: 405-407
: 8. Torkelson, J., Harris, R.S., Lombardo, M.-J., Nagebdran, J., Thulin, C., and Rosenberg, S.M. (1997) Genome-wide hypermutation in a subpopulation of stationary-phase cells underlies recombination-dependent adaptive mutation. EMBO J. 16: 3303-3311
: 9. Bridges, B.A., Foster P.L., and Timms A.R. (2001) Effect of endogenous carotenoids on "adaptive" mutation in Escherichia coli FC40. Mutat Res 473: 109-119
: 10. Harris, R.S., Feng, G., Ross, K.J., Sidhu, R., Thulin, C., Longerich, S., Szigety, S.K., Hastings, P.J., Winkler, M.E., and Rosenberg, S.M. (1999) Mismatch repair is diminished during stationary-phase mutation. Mutat. Res. 437: 51-60
: 11. Foster, P.L. (1998) Adaptive mutation: has the unicorn landed? Genetics 148: 1453-1459
: 12. Culotta, E. (1994) A boost for "adaptive" mutation. Science 265: 318-319

osted on: 2:49 pm on November 1, 2001
:<b>(1988) "Adaptive evolution that requires multiple spontaneous mutations. I. Mutations involving an insertion sequence," Genetics, vol. 120, pp. 887-897. In the last, Hall investigated the occurance of the precise deletion of IS103 in the presence of saline. 2 mutations had to occur in order for Hall's strain to metabolize salacin. The sequence IS103 had to be precisely deleted, then the right nucleotide had to be changed or else a sequence called IS1, or another one called IS5, had to be inserted into the cryptic regulatory gene. Hall tried to measure the spontaneous rate of the precise deletion of IS103 but found it to low to measure (he gave it a probability of less than 2 in a trillion). In the absence of saline these two mutations occur in the same cell with a chance less than 10 to the -19th. If the two are indeed independent of each other, then the chance of the rifgt double mutation in at least one cell of the population in two weeks (many generations of bacteria) is about one in 30 million. But wait! In two weeks Hall found that 60% of his colonies underwent both mutations and could metabolize salacin. Imagine that. Just looking at the IS103 deletion, which was to low to measure before, 89% of the colony underwent that deletion in 8-12 days. </b>

: It is true that Hall's initial data concerning the bgl operon could be interpreted as directed mutation. However, as we saw with the Cairns model, critical evaluation of the data and additional experimentation have shown that Hall's results were artifacts of the experiment and are not really evidence of directed mutation.

: As with the Cairns experiments, Hall was studying the reversion of a mutant phenotype back to the wild-type phenotype. The E. coli strain used for these studies(chi342LD) is a derivative of the K12 strain and was selected for its inability to metabolize salicin (a beta-glucoside sugar). The bgl operon (the unit of genes that metabolize beta-glucosides) of chi342LD contains two mutations: a point mutation in bglR and an insertion in bglF (Hall refers to this insertion as IS103 in early papers and IS150 in later papers...does anyone know why the nomenclature changed?). In order for chi342LD to metabolize salicin efficiently, these two mutations must be compensated for somehow.

: The experiment in the original paper (Hall, Genetics 120: 887-897, 1988) was fairly simple. Essentially, Hall plated chi342LD on medium that contained salicin as the sole carbon source and looked for bacteria that could grow. Hall found that, during a period of two to three weeks on the selection medium, approximately one out of every 100,000,000 cells plated would acquire mutations that could overcome the two defects in the bgl operon. Many, but not all, of the revertants contained deletions that excised all or a part of IS103 from bglF. Many, but not all, of the revertants contained point mutations in bglR.

: The quote (from who?) above is deceptive for a number of reasons. First, the observed deletions of IS103 were not "precise". Deletions of variable size were detected by Hall and others. The only common feature of these deletions were that they retained the reading frame of bglF and removed the STOP codons in IS103. In addition, there was no specificity to the revertant mutations in bglR. A number of different mutations all gave rise to the Sal+ phenotype.

: Another deceptive statement in the quote concerns the 60% number. While it is true that 60% of the colonies plated on the selective medium acquired mutations, only one or a few cells in each colony were actually revertants. Hall described these events as "papillae" which means that a single cell began to grow while the remainder of the colony remained in stationary phase. The rate of reversion was not 60%; it was 0.000001% (10-8 x 100). This is still several orders of magnitude faster than the reversion rate without selection, but I will get to that in a moment.

: The last sentence in the quote is not only deceptive, it is outright wrong. Hall found that between 1% and 10% of the cells in each colony acquired a deletion that removed all or a part of IS103 from bglF, not 89% (where did that number come from?!?). Of these, only a very small number acquired the second mutation necessary for complete phenotypic reversion. The rate of acquisition of the second mutation was similar to the normal rate of reversion in bglR.

: So what's going on? As we discussed before, it has been shown that cells in stationary phase have a much higher rate of mutation than growing cells and that the high mutation rate is especially apparent when one looks at deletions. Deletion of all or a part of IS103 from bglF occurs more often in cells plated on the selection medium because deletion rates in general are higher. Mittler and Lenski (Nature 356: 446-448, 1992) showed that chi342LD cells that had excised IS103 from bglF could grow slowly on salicin even if there was no reversion in bglR. Just a little growth on salicin would be enough to provide an advantage to IS103 deletions versus other types of deletions and, thus, would allow for an enrichment of these mutations in the population. The second mutation - reversion of bglR on selection medium - occurred at rates similar to reversion without selection.

: Therefore, it looks like what is really happening is that an increased rate of non-specific deletions, together with the normal rate of non-specific point mutations, combine to give the appearance of an induced phenotype. But it is really just an artifact of the selection. The selection does not induce a specific type of mutation, it only allows the "correct" ones to grow once they occur.

Posted on: 8:31 am on June 14, 2001
: I think it is worth noting that the debate among scientists over whether or not the phenomenon discovered by Cairns is the result of directed mutation is being hashed out in journals such as Nature, Science, PNAS, Genetics, Journal of Bacteriology, Mutation Research, EMBO Journal, etc. There are a few scientists such as Hall who favor the directed mutation interpretation (despite the fact that the evidence seems to be against them), yet they do not have any trouble publishing their data and opinions about the data in these mainstream journals. Directed mutation runs against the current paradigm, yet the editors of the journals feel that the data are compelling enough to be worthy of debate. So, you see, there is no conspiracy by evolutionists to keep conflicting data out of mainstream journals. The conspiracy is to hold conflicting data to the same standards of quality as supporting data. If directed mutation turns out to be a real phenomenon (and I'm not yet convinced that it is), then it must be incorporated into the paradigm. Even the most diehard evolutionists understand this.

[of note - these posts had been presented to John Paul before]

Also from me (this originally appeared here: http://geocities.com/huxter4441/williams2.html. I have changed some wording to make it applicable to Spetner’s ‘hypothesis’) :

Using DNA sequence data from Common chimp and bonobo, we can see that they differ by about 0.8%. If we assume that this rate is consistent across the genome, then we should expect there to be a difference of about 24 million nucleotides, or 12 million per species. Some have argued in the past that this number is off by some 20% due to polymorphism, so let us apply that here. That leaves us with 19.2 million differences.
YECs believe in a literal interpretation of the King James version of the bible, and so believe that all extant diversity is the result of hyperevolution after the Flood of Noah, which most creationists seem to put at about 2,500 –4,500 years ago. Let us go with the older date, 4,500 years ago.

Chimps have a generation time of around 10-15 years, so this means that a maximum of about 450 generations have come and gone since the flood waters subsided. If we assume that the rate of evolution has been stochastically consistent over time, then we should expect an average of 42,600 nucleotide changes to become fixed in the chimp population, or about 21,300 in each lineage (chimp v. bonobo) in the allotted time – PER GENERATION.
Clearly, only a fraction of these changes would be of the beneficial variety, but we should consider that many deleterious mutations, especially the very deleterious ones, will have been removed via selection (I will ignore that for the sake of simplicity). Creationists accepts ReMine's claim that non-beneficial changes actually require longer to reach fixation, and we will ignore that as well. Pro-ReMine creationists unquestioningly accept Haldane's model, which puts a 'speed limit' on evolution of the fixation of 1 beneficial mutation per 300 generations, the chimp-bonobo descent from an original kind requires a fixation of some 21300 mutations per generation, or about 6.4 MILLION times faster than allowed by Haldane's model (if I did the math right).

Section added for the Baptist Board:

The notion behind NREH is that the “information is already there” in the genome, and some environmental change induces some suite of mutations that activates or deactivates genes already in the genome, producing multiple species formt he original Kind.

Let us take the chimp-bonobo example. The fact that they seem to differ by so many substitutions is in itself sufficient to severely damage if not outright falsify what appears the be Spetner’s central tenet, for if these extant creatures descended from some original ‘chimp kind’, in the YEC timeline of a generous 4,500 years ago (post-flood), then there is no possible way that the observed changes could have occurred. Even if we much too generously assume that half of the observed difference is due to polymorphism, we still havce some 6 million differences per lineage to account for. 6 million changes in 4,500 years= 13,333 per year, or 133,330 per generation to be accounted for (as opposed to 1 every 300 generations under the Haldane model). This works out to roughly 2 million times faster than allowed in Haldane’s model, which creationists seem to embrace. Keep in mind thatnon-beneficial mutations take LONGER to reach fixation in a population than do beneficial ones, so I am being very generous here. (looks like I made a math error in my earlier analysis – either way, it doesn’t help the creationist position much!).
So, young earth creationists have a choice – regardless of whether or not they accept the NREH/directed mutation scenario, they either have to:
1. reject the use of Haldane’s model as an argument against evolution

or

2. abandon their hope of trying to use genetics/science to claim that YECism is scientifically tenable.

 

[Administrator2]

THE BARBARIAN

Helen:
Barbarian, the concept of IC lies NOT in the sequencing, but in the
function. DNA 'works' because the cell knows what to do with it. In
this sense, I suppose, it could be said that the cell itself can tell
the difference between what is intelligently designed and what is random
nonsense genetically.

Suppose I make a few random changes in the gene for cytochrome c. Most
changes will still permit the enzyme to work, but a few will not. Will a
cell see the non-functional ones as nonsense and the functional ones as the
result of "design"? By your yardstick, it would. But neither are designed.

The DNA that was modified by natural selection to make a new, IC metabolic
pathway would appear to be designed, but it was not. It was merely evolved
by natural selection.

We come back to the basic problem. Stuff that looks to be designed often
isn't. And so far, the "filter" hasn't been able to distinguish one from
the other. Unless the answer was predetermined.

To be useful, this has to work. John Paul talked about forensics and fire
investigation and archaeology as examples. I have a little experience in
the second; we look for things like the direction in which a light bulb
melted out to point to the origin of the fire, scorch marks for signs of
accelerants, remains of fuses, and so on. But none of this is different
than the same old scientific method that's been around for years. In
archaeology, we can look at a broken piece of flint, and see whether it is
natural or designed by specific signs, the striking platform, the bulbar
scar, and ripple marks. Skilled workers can look at waste and know what
toolmaking tradition was involved. Yet, the "Filter" can't tell "designed"
from random DNA.

That's a serious problem. I'm aware that Intelligent Design admits to
common descent,and an ancient universe, and is compatible with modern
evolutionary theory. But I can't take it seriously, until it can show some
kind of usefulness.

 

[Administrator2]

JOHN PAUL

Helen:
Barbarian, the concept of IC lies NOT in the sequencing, but in the
function. DNA 'works' because the cell knows what to do with it. In
this sense, I suppose, it could be said that the cell itself can tell
the difference between what is intelligently designed and what is random
nonsense genetically.

Scott Page:
The function of DNA is dictated by the 'sequencing', so in reality, the sequence of DNA is very important. As such, one should think that a 'filter' that is purported to be able to tell what is 'Designed' and what is not, biologically speaking, should certainly be able to tell whether or not a given sequence of DNA is designed, a random conglomeration of nucleotides, or arose naturally.

John Paul:
Actually I already covered that:

John Paul:
It has become apparent that you don’t understand ID or the purpose of the EF. The EF is satisfied that DNA of living organisms can be inferred to have at one time, been designed. The EF cannot tell us what happened to that design after eons of replication, mixing and environmental pressures.

IDists and Creationists do NOT debate that CSI (complex specified information) can arise from CSI. The debate is how did the CSI originate?

Scott Page:
The cell only 'knows' what do do with the DNA because the DNA tells the cell what to do.

John Paul:
Peer-reviewed reference please.

Scott Page
Of course, the creationist has already provided for themselves a way out, as John Paul so explicitly demonstrated above:

John Paul:
As usual the evolutionists try to cover themselves when the facts are revealed. Let’s take a look:

"So this hypothetical DNA wouldn’t be DNA at all, it would just exist on paper or a computer? Is that what you are saying? I can see no use in doing such a comparison. If, on the other hand, you had random sequences of DNA arising in nature (outside of a living cell) and you wanted to compare those to a segment of human DNA, that would be different. But in your scenario, even the hypothetical DNA would be designed." [/I]

John Paul:
How is that providing a way out? What I stated is a fact. It was obvious that the person who set up this (ahem) ”test” was merely erecting a strawman. Excuse me for exposing it.

Scott Page:
John Paul also mentioned something interesting regarding creationist physicist Lee Spetner's 'non-random evolutionary hypothesis.'

John Paul:
You did know he is also a bio-physicist. Wouldn’t want you to misrepresent his credentials.

Scott Page:
Some interesting issues regarding that (courtesy of Sumac,):

John Paul:
Before we go there let’s take a look at what I actually stated regarding Spetner’s Non-Random Evolutionary Hypothesis: (note- what I said has nothing to do with what sumac posted)

Is the minimal function of each step of the building process in any way related to the minimal function of the finished product? IOW, if the finished product’s function is for people to live in or gather in, and the only function of the intermediate steps is to achieve that goal, how can that be used as an example of Darwinian step-by-step processes used to achieve perceived IC?
If this is what occurs in living organisms it would be evidence for Dr. Spetner’s Non-random Evolutionary Hypothesis in that it would appear to be a directed function.

and

Yup, design is one way to get around perceived IC and that is what Pat has shown. Thanks Pat.

Is that how evolution works? By building something it can’t use until it is finished building it? How would NS know what it (the organism) is building? And why would the intermediate steps be selected, unless NS was also privy to the ‘plans’?

No wait, I got it. The organism called the psychic hotline to find out what the environment was going to be in the future. Armed with that information it directed the population to concentrate so that they could collectively recombine their gene pool for the best chance of survival. We already know single-celled organisms can communicate and work together (slime molds and other colony-like adjustments are good examples of this), so except for the psychic hotline bit, it could work. But that would be a sign of directed mutations and would also be support for Dr. Spetner’s non-random evolutionary hypothesis.

And

But on the other hand we have Dennett stating in the PBS series Evolution that there is no way to predict what would be selected for at any point in time. If a population of organisms could duplicate a gene that also provides an immediate benefit to the organism, it would be foolish not to look at the implication of directed mutation. That is an organism sensing its environment and purposely (through some as yet unknown triggering mechanism) causing a recombination that allows the population to better survive.

Otherwise you would have an organism ‘building’ something it may not need because of the shifting eco-system. What would happen to neo-Darwinism if the bulk of (or any) mutations were found to be environmentally cued (i.e. directed)?

Did anyone see any reference to the references that Spetner uses in his book? I wrote it and have re-read it several times and I don’t see a one.

Scott Page:
[of note - these posts had been presented to John Paul before]

John Paul:
Note- I did not post any references that Spetner offers in his book- which is what sumac responded to months ago and I have not questioned, in this or any other post (yet). What I do find interesting is that Spetner has an ongoing dialog with the evolutionist Max, which can be read here:

http://www.trueorigin.org/spetner1.asp

and

http://www.trueorigin.org/spetner2.asp

Notice that Max does not bring up what sumac posted. If sumac is right he should bring this to Max’s attention and then Spetner could defend his position or eat crow.

Scott Page:
Using DNA sequence data from Common chimp and bonobo, we can see that they differ by about 0.8%. If we assume that this rate is consistent across the genome, then we should expect there to be a difference of about 24 million nucleotides, or 12 million per species. Some have argued in the past that this number is off by some 20% due to polymorphism, so let us apply that here. That leaves us with 19.2 million differences.

John Paul:
Questions- Do we know how much one common chimp can vary from another common chimp? What is the maximum nucleotide difference that two common chimps (or bonobos) can have? Can chimps and bonobos interbreed?

Scott Page:
YECs believe in a literal interpretation of the King James version of the bible, and so believe that all extant diversity is the result of hyperevolution after the Flood of Noah, which most creationists seem to put at about 2,500 –4,500 years ago. Let us go with the older date, 4,500 years ago.

John Paul:
First either something is literal or it is an interpretation. Literal interpretation would be an oxymoron.

Secondly literal Genesis Creationists offer their best-educated “guess” as to the timeframe of the Flood. This timeframe is in no way “etched in stone.” For example John Morris, in his book Young Earth puts the age of the Earth between 6,000 & 12,000 years based upon a literal Genesis. I have seen at least one other go as high as 15,000 years.

All I am saying is that we have to take into consideration that a faulty assumption may be being made in Scott’s calculations.

Scott Page:
Chimps have a generation time of around 10-15 years, so this means that a maximum of about 450 generations have come and gone since the flood waters subsided.

John Paul:
That would assume your timeframe is correct and that chimps generation time hasn’t increased over the time since the Flood.

Scott Page:
If we assume that the rate of evolution has been stochastically consistent over time, then we should expect an average of 42,600 nucleotide changes to become fixed in the chimp population, or about 21,300 in each lineage (chimp v. bonobo) in the allotted time – PER GENERATION.

John Paul:
That assumption wouldn’t be realistic. Why? Because right after the Flood all the niches would be wide open, meaning the rate of evolution would have been much higher at that time.

Scott Page:
Clearly, only a fraction of these changes would be of the beneficial variety, but we should consider that many deleterious mutations, especially the very deleterious ones, will have been removed via selection (I will ignore that for the sake of simplicity). Creationists accepts ReMine's claim that non-beneficial changes actually require longer to reach fixation, and we will ignore that as well. Pro-ReMine creationists unquestioningly accept Haldane's model, which puts a 'speed limit' on evolution of the fixation of 1 beneficial mutation per 300 generations, the chimp-bonobo descent from an original kind requires a fixation of some 21300 mutations per generation, or about 6.4 MILLION times faster than allowed by Haldane's model (if I did the math right).

John Paul:
But would Haldane’s model even apply to a population (or populations) of organisms that already has the genetic information available for the variation necessary for survival?

Scott Page:
Section added for the Baptist Board:

The notion behind NREH is that the “information is already there” in the genome, and some environmental change induces some suite of mutations that activates or deactivates genes already in the genome, producing multiple species formt he original Kind.

John Paul:
That is only part of it. If you had read his book you would have known that.

Why is it that some people think they can accurately comment on a book that they haven’t read?

Scott Page:
Let us take the chimp-bonobo example. The fact that they seem to differ by so many substitutions is in itself sufficient to severely damage if not outright falsify what appears the be Spetner’s central tenet, for if these extant creatures descended from some original ‘chimp kind’, in the YEC timeline of a generous 4,500 years ago (post-flood), then there is no possible way that the observed changes could have occurred. Even if we much too generously assume that half of the observed difference is due to polymorphism, we still havce some 6 million differences per lineage to account for. 6 million changes in 4,500 years= 13,333 per year, or 133,330 per generation to be accounted for (as opposed to 1 every 300 generations under the Haldane model). This works out to roughly 2 million times faster than allowed in Haldane’s model, which creationists seem to embrace. Keep in mind thatnon-beneficial mutations take LONGER to reach fixation in a population than do beneficial ones, so I am being very generous here. (looks like I made a math error in my earlier analysis – either way, it doesn’t help the creationist position much!).
So, young earth creationists have a choice – regardless of whether or not they accept the NREH/directed mutation scenario, they either have to:
1. reject the use of Haldane’s model as an argument against evolution

or

2. abandon their hope of trying to use genetics/science to claim that YECism is scientifically tenable.

John Paul:
First it must be shown that Haldane’s model applies to the NREH. It could but as it stands it applies to random mutations culled and directed by natural selection. Secondly you have to provide evidence that the assumptions you made are correct. Finally without knowing the differences in the pair of chimps aboard the Ark, any calculations from them could hardly be accurate.

Dissasortive mating can greatly increase the opportunity for new genetic combinations to arise, and thereby increase the overall level of genetic variation upon which selection can operate. Templeton, A.R., and B. Read. 1983. The eliminating of inbreeding depression in a captive herd of Speke’s Gazelle (pp. 241-61) in Schonewald-Cox, C.M., Chambers, S., MacBryde, B., and W.L. Thomas, eds. Genetics and Conservation. Benjamin/ Cummings Publishing Co., London, Amsterdam.

If chimps and bobnobos could interbreed at the time of the Flood, would that help the YEC case? I think it would.

Until you take all things into consideration I can’t see that your argument has any merit. It could, but it doesn’t as it is.

God Bless,

John Paul

 

[Administrator2]

HELEN

To Scott Page: the function of DNA certainly is dictated by the
sequencing, but that was not my point. My point was that the concept of
irreducible complexity does not lie in the sequence of any portion of
the DNA. On strictly mathematical grounds, any sequence is as probable
or improbable and any other sequence, so that is not the relevancy.
What my point was is that the function of the DNA requires the cellular
mechanism to ‘understand’ and deal with it in an appropriate way. And
this, in many cases, such as shape of the resulting cell, is NOT to be
found in the DNA, by the way. It truly does take a cell to make a cell,
and there is a distinct concept of irreducible complexity there. The
very fact that geneticists are looking to find the least amount of
genetic material necessary for cellular life and reproduction means they
are implicitly working with the concept of IC. There is a point at
which the genetic material cannot lose any more ‘parts’ without losing
its ability to program the workings of the cell. However, it must also
be remembered in the meantime that the genetic material without the cell
is useless – it cannot function. And the cell requires the membrane,
for instance, to be a cohesive unit capable of functioning. The cell
itself, then, is an example of irreducible complexity. This is the
point I was attempting to make. And this is why Pat’s ‘challenge’ to
show that one stretch of DNA is the product of intelligent design while
another is not is a challenge based on a lack of comprehension of what
is going on.

It requires the rest of the cell to see what that bit of DNA does – its
stochastic complexity ‘rating’ means nothing. What it does – its
SPECIFIED complexity, means everything, and until we can see what the
specification is, we cannot make any determination regarding possible
ID with the information now available to us.

And all of this, by the way, has nothing to do with mutations or even
natural selection. It has to do with the actual process of living and
replicating which is the business of any cell, mutated or unmutated,
naturally or artificially or non-selected. Sumac’s material was
therefore of no import where this discussion is concerned.

To Barbarian: In addition to the above material in light of your
challenge, a response concerning the following mis-statement:
I'm aware that Intelligent Design admits to common descent, and an
ancient universe, and is compatible with modern evolutionary theory.

ID does not ADMIT to any of the above! It has nothing to do with either
the concept of common descent or an ancient universe. Quit trying to
mix it up with YEC models. ID simply says, essentially, “We have reason
to believe that not everything is the result of material, natural
causes.” However, as far as ‘modern evolutionary theory’ I am not sure
what you mean. Evolutionary theory is so malleable that no matter what
I say about it you can disagree and pull out some quote or another. So
while ID is a wide enough umbrella to accommodate both common ancestry
as well as YEC, it does not really have anything to do with either. It
is simply about measurable indicators in natural phenomena that not
everything is the result of natural and material causes. To push it
further than that is either ignorant or deceptive.

Nor does it matter if you, personally, can take it seriously until you
think it shows “some kind of usefulness.” It is simply out to make the
point that science as we know it today has bound itself by philosophical
chains that prevent it from being what science should be: a search for
what is true, not just what fits a model that can be tested using our
limited resources and understandings.

 

[Administrator2]

JOHN PAUL

John Paul: It has become apparent that you don't understand ID or the
purpose of the EF. The EF is satisfied that DNA of living organisms can be
inferred to have at one time, been designed. The EF cannot tell us what
happened to that > design after eons of replication, mixing and
environmental pressures.

Pat:
It is clear that EF is easily satisfied, but requires a prior assumption of design on the person doing the analysis.

John Paul:
What is clear is your misunderstanding of the EF as it makes NO prior assumptions, at all, and neither does the person doing the analysis. Sure a person could make that assumption, I can’t prevent that and neither can the EF. But is not a requirement.

By stating “It is clear that the EF is easily satisfied”, because it can determine that DNA, which exhibits CSI in spades (and therefore can be inferred to have at one time been designed), tells me you misunderstand the processes involved in making that determination.

Pat:
Why not simply call it "faith" and let it be?

John Paul:
Because that would be a blatant misrepresentation.

Pat:
If I understand you correctly, you are telling me that there is no way to test the supposition.

John Paul:
I did not say or imply that so I would have to say you didn’t understand me correctly.

Pat:
If there is a way, I would be very pleased to hear about it.

John Paul:
That is what I did with DNA. What part of that EF example didn’t you understand?

Here it is again:

OK DNA enters box #1. Does DNA have a high probability of originating via purely natural processes? We have never observed DNA do this. That doesn't mean it can't happen but it just doesn't happen regularly. On to box #2.

Does DNA have an intermediate probability of originating via purely natural processes? Again DNA has never been observed originating via purely natural processes. Even if we put all the amino acids, sugars, and other chemicals we know are in living organisms into a flask, DNA does not form. On to box # 3

Does DNA have a small probability of originating by purely natural processes? For discussion sake we will say Yes. Things of small probability happen all the time. But we have only observed DNA in living organisms and not once arising outside of one. Is DNA specified? The DNA in living organisms is. So unless it is shown that any DNA sequence would give rise to a living organism, or easier yet, that any DNA sequence injected into an egg cell will give rise to life, the DNA in living organisms could be considered to be specified. Thus specified complexity is determined to be representative of DNA. From what we know, we only observe specified complexity arise via design.

The only thing that had to be determined ahead of time is what is specified complexity (or CSI as others call it). For a brief definition of specified complexity see the following article:

ID FAQ:
http://www.arn.org/id_faq.htm

ID is an inference based upon the available evidence. Until you can
demonstrate that purely natural processes can bring about CSI or life
itself, that inference will stand un-falsified.

Pat:
The problem is that there seems to be no evidence for ID.

John Paul:
Only if you ignore the evidence would that be so. Someone locked in a dark room all his life would say there is no evidence for the Sun. It appears ID critics are that person.

Pat:
Can you give me an example where it is invoked where there has not been a prior assumption of design?

John Paul:
You mean another example. I have already furnished one.

Pat:
Such an assertion is not only unfalsified, it is unfalsible, and
hence not science.

John Paul:
As has been made clear, such an assertion is NOT made.

One more thing. What is the positive evidence that life can originate
from non-life via purely natural processes?

Pat:
Let's see.... the fact that RNA can be auto-catalytic, the nature of basic
biochemical processes that seem to indicate an original low oxygen
environment, followed by a higher oxygen tension, the existence of
archaebacteria, which all seem to be extreme anaerobic thermophiles, the
fossil record, which shows a progression of early cellular life from simple
to more complex, ... and so on. There's not enough evidence for it to be a
given, yet (and maybe there never will be) but no honest person familiar
with the research says that there is no evidence for it.

John Paul:
First ideas are not evidence. Second, what is the evidence that the earth’s early atmosphere was reducing? You did know that the earth’s atmosphere is proposed to have been reducing because that is the only type of atmosphere that is conducive to the formation of the simplest of amino acids. And finally I offer this:

The RNA World by Brig Klyce:

http://www.panspermia.org/rnaworld.htm

The undreamt-of breakthrough of molecular biology has made the problem of the origin of life a greater riddle than it was before: we have acquired new and deeper problems. — Karl R. Popper, 1974

Yes sir, it appears that time and knowledge are the enemies of materialistic naturalists. I am very comfortable with that.

If there isn't any, why is it scientifically OK to dogmatically declare
that it did?

Pat:
It wouldn't be. But you are incorrectly assuming that's what scientists are
doing.

John Paul:
Materialistic naturalists are doing it. No assumption needed.

Pat:
First, there is evidence to support the theory, and I'm certainly
not dogmatically insisting the theory is correct.

John Paul:
In reality the evidence consists only of ideas. Which isn’t evidence at all.

Pat:
I do accept what Genesis has to say about it, but that is not a scientific statement, merely my faith in God's Word.

John Paul:
As I have shown earlier you do NOT accept what Genesis has to say about it. Genesis clearly speaks of a Special Creation in which organisms were Created separately and humans were Created as humans and were given dominion over the others.

That is what you are doing by denying the design inference and ignoring
the irreducible complexity of life itself.

Pat:
No. I'm just waiting until some one shows me that it can actually
demonstrate design.

John Paul:
First it is called the design inference for a reason. The reason being that until falsified it is safe to infer design from the evidence available.

Pat:
I've pointed out to you before that we have directly observed irreducible complexity evolve, so irreducible complexity cannot be evidence for design.

John Paul:
Wrong again. I have asked you for a reference that you have refused to provide. Why is that? Also I haven’t used IC to infer design or as evidence for design. I have used SC (or CSI).

Behe uses IC as a challenge to scientists to demonstrate that all biochemical systems can evolve in Darwinian step-by-step processes. Do you understand the difference?

Pat:
Again, is there any instance where the EF works prior to determining whether
something is "designed" or not?

John Paul:
Yes, I have already provided such an example with the DNA of a living organism. No prior determination of design was made and no amount of complaining will change that.

Helen:
Barbarian, the concept of IC lies NOT in the sequencing, but in the
function. DNA 'works' because the cell knows what to do with it. In
this sense, I suppose, it could be said that the cell itself can tell
the difference between what is intelligently designed and what is random
nonsense genetically.

Pat:
Suppose I make a few random changes in the gene for cytochrome c.

John Paul:
That would be “unnatural” intervention. Also you have missed both Helen’s and my point. Both of us are talking about the entire DNA sequence of a living organism and you keep bringing up bits and pieces to try to rebut our point. Apples and oranges Pat. Please try to stay focused.

Pat:
Most changes will still permit the enzyme to work, but a few will not.

John Paul:
I would be interested to know how you determined that most changes would still allow the enzyme to work, but only a few would not.

Pat:
Will a cell see the non-functional ones as nonsense and the functional ones as the
result of "design"? By your yardstick, it would.

John Paul:
I bring you back to this:

John Paul:
It has become apparent that you don’t understand ID or the purpose of the EF. The EF is satisfied that DNA of living organisms can be inferred to have at one time, been designed. The EF cannot tell us what happened to that design after eons of replication, mixing and environmental pressures.

What part of that do you not understand?

Pat:
But neither are designed.

John Paul:
Are you making the pre-determination that the original gene for cytochrome c arose via natural processes? Remember if it arose out of a designed DNA sequence, it too would be a product of design.

Also if you intervened, as you stated, that would be very similar to this:

And yes, the EF can be fooled. A person could design what would give all appearances to be random rock patterns. Only that person would know it was designed. In that case anyone, but that person, entering the data into the EF would come up with a different conclusion because although it was designed it did not exhibit specificity to that other person.

Pat:
The DNA that was modified by natural selection to make a new, IC metabolic
pathway would appear to be designed, but it was not.

John Paul:
Please provide the peer-reviewed reference that states the new metabolic pathway is IC. I have only read you saying it was IC. That hardly makes it so.

That CSI can arise from CSI is NOT the debate and is what you are presenting with that example.

Pat:
It was merely evolved by natural selection.

John Paul:
Natural selection acting upon what? A design? That would still be the product of design.

Also what was the mechanism? ID, random mutations culled by NS or Spetner’s NREH (which could be included in ID)?

Pat:
We come back to the basic problem. Stuff that looks to be designed often
isn't.

John Paul:
That would all depend. If the stuff that looks designed is derived from designed stuff it couldn’t be attributed to purely natural processes alone.

But I do agree there are objects that at first look give the appearances of design. That is why we have to follow the process flow of the EF and use all the knowledge available.

Maybe you can provide with an example of CSI originating via purely natural processes.

Pat:
And so far, the "filter" hasn't been able to distinguish one from
the other. Unless the answer was predetermined.

John Paul:
Using your logic archeologists and anthropologists know an object is an artifact before they thoroughly examine it. Sorry Pat, it doesn’t work that way.

Also the EF worked just fine on the DNA of a living organism without any predetermination.

Pat:
To be useful, this has to work. John Paul talked about forensics and fire
investigation and archaeology as examples. I have a little experience in
the second; we look for things like the direction in which a light bulb
melted out to point to the origin of the fire, scorch marks for signs of
accelerants, remains of fuses, and so on. But none of this is different
than the same old scientific method that's been around for years. In
archaeology, we can look at a broken piece of flint, and see whether it is
natural or designed by specific signs, the striking platform, the bulbar
scar, and ripple marks. Skilled workers can look at waste and know what
toolmaking tradition was involved. Yet, the "Filter" can't tell "designed"
from random DNA.

John Paul:
What is “random DNA”? I have asked and not received an answer. Why is that?

BTW, the methods you speak of are very similar to the methods used by IDists to determine design in living organisms. IDists just have to take it a step further.

Pat:
That's a serious problem. I'm aware that Intelligent Design admits to
common descent,and an ancient universe, and is compatible with modern
evolutionary theory.

John Paul:
ID makes no such admissions. It could care less about common descent or the age of the universe. IDists may make such admissions but that is separate from ID. Just like some IDists may infer God is the IDer but that too does not matter to ID.

Pat:
But I can't take it seriously, until it can show some
kind of usefulness.

John Paul:
And what exactly is the usefulness of thinking that all of life’s diversity owes it common ancestry to some as yet unknown population of organisms that just happened to have the ability to self-replicate? What is the usefulness of thinking that diversity arose from random mutations acted upon by natural selection, especially in the light of what Dennett stated on the PBS series Evolution that there is no way to predict what would be selected for at any point in time?

But to answer your question, Mike Gene’s website offers some insight.

Here is one article that discusses ID’s usefulness:

Using ID to Understand the Living World:

http://www.idthink.net/arn/pred/index.htm

There are other articles on ID and books written on the topic. Plenty of information on the topic. All that is required is time & research and you will find you question has been answered.

God Bless,

John Paul

 

[Administrator2]

SCOTT PAGE

JOHN PAUL

quote:
Helen:
Barbarian, the concept of IC lies NOT in the sequencing, but in the function. DNA 'works' because the cell knows what to do with it. In this sense, I suppose, it could be said that the cell itself can tell the difference between what is intelligently designed and what is random nonsense genetically.

Scott Page:
The function of DNA is dictated by the 'sequencing', so in reality, the sequence of DNA is very important. As such, one should think that a 'filter' that is purported to be able to tell what is 'Designed' and what is not, biologically speaking, should certainly be able to tell whether or not a given sequence of DNA is designed, a random conglomeration of nucleotides, or arose naturally.

John Paul:
Actually I already covered that:
quote:

John Paul:
It has become apparent that you don’t understand ID or the purpose of the EF. The EF is satisfied that DNA of living organisms can be inferred to have at one time, been designed. The EF cannot tell us what happened to that design after eons of replication, mixing and environmental pressures.

Then how can it possibly be of any use at all? If it cannot look at extant material – that’s all we have, right? – and tell if it was designed or not, how, EXACTLY, is this EF to be employed? Rhetorically?
And of most import, how, EXACTLY, is the EF “satisfied that DNA of living organisms can be inferred to have at one time, been designed”? That is the question! Yet you say:
“The EF cannot tell us what happened to that design after eons of replication…”
So please, with peer-reviewed support, of course, EXPLAIN exactly how the EF determined this by using only material that has been subject to eons of replication, mixing, and environmental pressure.

IDists and Creationists do NOT debate that CSI (complex specified information) can arise from CSI. The debate is how did the CSI originate?

That really does not seem to be a topic of ‘debate’ among creationists/IDists at all. They seem to ‘know’ that CSI must have arisen via supernatural/non-terrestial intelligent intervention, and have been expending large amounts of rhetorical energy trying to ‘prove’ this.

Scott Page:
The cell only 'knows' what to do with the DNA because the DNA tells the cell what to do.

John Paul:
Peer-reviewed reference please.

I don’t have any. I know how transcription and translation work. I know that there are multiple feedback mechanisms at work that influence/induce differential gene expression. The expression of genes alters the cell’s activity, just as the binding or various ligands does (by altering gene expression patterns, among other things). Better yet, since it appears that you seem to think that the cell ‘tells’ the DNA what to do, YOU could provide a peer-reviewed reference.

Scott Page
Of course, the creationist has already provided for themselves a way out, as John Paul so
explicitly demonstrated above:

John Paul:
As usual the evolutionists try to cover themselves when the facts are revealed. Let’s take a look:

quote:
"So this hypothetical DNA wouldn’t be DNA at all, it would just exist on paper or a computer? Is that what you are saying? I can see no use in doing such a comparison. If, on the other hand, you had random sequences of DNA arising in nature (outside of a living cell) and you wanted to compare those to a segment of human DNA, that would be different. But in your scenario, even the hypothetical DNA would be designed." [/I]

John Paul:
How is that providing a way out? What I stated is a fact. It was obvious that the person who set up this (ahem) ”test” was merely erecting a strawman. Excuse me for exposing it.

Yes, lets take a look at it. Sentence by sentence.

“So this hypothetical DNA wouldn’t be DNA at all, it would just exist on paper or a computer?”

How do you propose that the EF – or ANY analytical tool, for that matter, analyze DNA? Do you really think that technicians just pour some DNA into a machine and it spits out all sorts of information? The EF is at its heart a mathematical construct. How else is it to analyze DNA if not via inputting the sequence into a computer?

“I can see no use in doing such a comparison.”

And yet, as laid out, the EF should be able to tell the difference.

“If, on the other hand, you had random sequences of DNA arising in nature (outside of a living cell)…”

Therein lies the rub – please explain – supported with peer-reviewed documentation, of course – how ‘random sequences of DNA’ would arise in nature. In the past, I have explained to you –with citations – how the insertion of LINES and SINES for example are random in relation to the locus of insertion. You dismissed this because the insertion of these elements requires mediation by enzymes. I have little reason to doubt that you would employ a similar rationale if presented with any other scenario in which DNA was postulated to be assembled randomly, since any such assemble, certainly in a cell, will be enzyme-mediated.

“… you wanted to compare those to a segment of human DNA, that would be different. But in your scenario, even the hypothetical DNA would be designed.”

Exactly MY point. A segment of DNA – indeed, not even real DNA, i.e., existing only in a computer – that is random in its sequence, it seems to me, should be an easy target for the EF. Basically, this could act as a control. But you say that even this would be ‘designed’. How then shall we actually test the efficacy of the EF? You say by using naturally occurring random DNA sequences. Actually, there are plenty of them – they can be found in intergenic DNA and to a lesser extent in introns, especially larger ones. I predict that you will simply reject them as also being the products of design. Circularity writ large by assuming what you intend to demonstrate.

Scott Page:
Some interesting issues regarding that (courtesy of Sumac,):
John Paul:
Before we go there let’s take a look at what I actually stated regarding Spetner’s Non-Random Evolutionary Hypothesis: (note- what I said has nothing to do with what sumac posted)
</font><blockquote>quote:</font><hr /> Is the minimal function of each step of the building process in any way related to the minimal function of the finished product? IOW, if the finished product’s function is for people to live in or gather in, and the only function of the intermediate steps is to achieve that goal, how can that be used as an example of Darwinian step-by-step processes used to achieve perceived IC? If this is what occurs in living organisms it would be evidence for Dr. Spetner’s Non-random Evolutionary Hypothesis in that it would appear to be a directed function.

</font>[/QUOTE]I am unaware of any evidence at all that indicates that each supposed step in some process is geared toward reaching some biological goal. Are you? If so, please provide the peer-reviewed references. Your last sentence provides the link between what Sumac presented before and this thread – the concept of ‘directed mutation’, upon which Sopetner based his NREH. There is, in fact, a DIRECT relevance.

And </font><blockquote>quote:</font><hr />
Is that how evolution works? By building something it can’t use until it is finished building it? How would NS know what it (the organism) is building? And why would the intermediate steps be selected, unless NS was also privy to the ‘plans’?
No wait, I got it. The organism called the psychic hotline to find out what the environment was going to be in the future. Armed with that information it directed the population to concentrate so that they could collectively recombine their gene pool for the best chance of survival. We already know single-celled organisms can communicate and work together (slime molds and other colony-like adjustments are good examples of this), so except for the psychic hotline bit, it could work. But that would be a sign of directed mutations and would also be support for Dr. Spetner’s non-random evolutionary hypothesis.

</font>[/QUOTE]I would not characterize the co-option of proteins ‘making something it can’t use until it is finished.’ Of course, if the ‘intermediate steps’ – a phrase that has some undue connotations itself – ‘work’, then they are not really intermediate steps. This is like saying that the biplane was an intermediate step in the development of the Concorde. That is true if – and only if – the designers of the biplane wanted to build the Concorde but had to muddle their way through numerous intermediate steps to get there.
The ‘psychic hotline’ bit is cute, but seems to be a violation – or close to it – of the board rules. I can only speculate as to why you were not asked to re-submit your post without those references.
And again you mention ‘directed mutations’ – the very topic of the lengthy piece by Sumac. Directed mutations, the foundation of Spetner’s ‘hypothesis’, are not what they are made out to be.

And </font><blockquote>quote:</font><hr />

But on the other hand we have Dennett stating in the PBS series Evolution that there is no way to predict what would be selected for at any point in time. If a population of organisms could duplicate a gene that also provides an immediate benefit to the organism, it would be foolish not to look at the implication of directed mutation.

</font>[/QUOTE]That appears top be a non-sequitur. The whole issue of ‘directed mutation’, so I have gathered from numerous internet posts by various creationists, is that the genetic material is already there. A duplication of a gene produces an additional copy of a gene – by definition, something that wasn’t already there. So, in fact, it seems to me that it would be foolish to propose that a gene duplication falls under the definition of a directed mutation, especially since the concept of directed mutation is all but disproved.

What would happen to neo-Darwinism if the bulk of (or any) mutations were found to be environmentally cued (i.e. directed)?

Many mutations are environmentally cued, but not in the sense you seem to be implying. In order for there to be any ‘problem’ for ToE, it would have to be shown that:
-ONLY the ‘necessary’ genes/loci are being targeted by the environmental changes (already shown to be false)
-the genes/loci necessary to deal with the change were already there
(not demonstrated at all)

Scott Page:
[of note - these posts had been presented to John Paul before]

John Paul:
Note- I did not post any references that Spetner offers in his book- which is what sumac
responded to months ago and I have not questioned, in this or any other post (yet).
What I do find interesting is that Spetner has an ongoing dialog with the evolutionist Max, which can be read here:

http://www.trueorigin.org/spetner1.asp

and

http://www.trueorigin.org/spetner2.asp

Notice that Max does not bring up what sumac posted. If sumac is right he should bring this to Max’s attention and then Spetner could defend his position or eat crow.

I noticed that the bulk of Spetner’s replies there are insults. Spetner is merely trying to prop up his book and the belief system behind it. Of course, maybe Max is unaware of what Sumac refered to. Spetner surely is.

Scott Page:
Using DNA sequence data from Common chimp and bonobo, we can see that they differ by about 0.8%. If we assume that this rate is consistent across the genome, then we should expect there to be a difference of about 24 million nucleotides, or 12 million per species. Some have argued in the past that this number is off by some 20% due to polymorphism, so let us apply that here. That leaves us with 19.2 million differences.

John Paul:
Questions- Do we know how much one common chimp can vary from another common chimp? What is the maximum nucleotide difference that two common chimps (or bonobos) can have? Can chimps and bonobos interbreed?

That is what polymorphism is, John Paul, and that is why I took it into account. I do not know if they can interbreed or not. But that has nothing to do with my analysis.

Scott Page:
YECs believe in a literal interpretation of the King James version of the bible, and so believe that all extant diversity is the result of hyperevolution after the Flood of Noah, which most creationists seem to put at about 2,500 –4,500 years ago. Let us go with the older date, 4,500 years ago.

John Paul:
First either something is literal or it is an interpretation. Literal interpretation would be an
oxymoron.

Fine by me. You’d best explain that to your YEC friends, you say that the bible is literally true yet feel the need to ‘interpret’ it whenever what is written seems troublesome.

Secondly literal Genesis Creationists offer their best-educated “guess” as to the timeframe of the Flood. This timeframe is in no way “etched in stone.” For example John
Morris, in his book Young Earth puts the age of the Earth between 6,000 & 12,000 years
based upon a literal Genesis. I have seen at least one other go as high as 15,000 years.

All I am saying is that we have to take into consideration that a faulty assumption may be being made in Scott’s calculations.

Nit-picky stuff, and that is why I went with the older date for the flood (of those that I seen mentioned on the net) of 4,500 years ago. I could have gone with 2,500 years ago, which I have also seen. Obviously, there is a large margin of error. My calculations are not intended nor should they have been seen as to be all-encompassing statements of irreproachable fact.

Scott Page:
Chimps have a generation time of around 10-15 years, so this means that a maximum of about 450 generations have come and gone since the flood waters subsided.
John Paul:
That would assume your timeframe is correct and that chimps generation time hasn’t increased over the time since the Flood.

Again, I am using the more generous timeframe. You really shouldn’t be arguing that. I also used the youngest possible generation time in my calculation, again, being generous to the YEC timeframe.

Scott Page:
If we assume that the rate of evolution has been stochastically consistent over time, then we should expect an average of 42,600 nucleotide changes to become fixed in the chimp population, or about 21,300 in each lineage (chimp v. bonobo) in the allotted time – PER GENERATION.

John Paul:
That assumption wouldn’t be realistic. Why? Because right after the Flood all the niches would be wide open, meaning the rate of evolution would have been much higher at that time.

Your response is, in fact, unrealistic. After the flood, there would have been NO niches at all. An earth totally inundated with brackish muddy water does not simply recede to reveal lush tropical forests, jungles, etc. all intact and ready to be inhabited by whatever species gets there first – after descending in hyperspeed from their original stock, of course. In addition, I mentioned that we can assume a stochastic process – that is, a more or less random one that ‘averages out’ over time. [/quote]

Scott Page:
Clearly, only a fraction of these changes would be of the beneficial variety, but we should consider that many deleterious mutations, especially the very deleterious ones, will have been removed via selection (I will ignore that for the sake of simplicity). Creationists accepts ReMine's claim that non-beneficial changes actually require longer to reach fixation, and we will ignore that as well. Pro-ReMine creationists unquestioningly accept Haldane's model, which puts a 'speed limit' on evolution of the fixation of 1 beneficial mutation per 300 generations, the chimp-bonobo descent from an original kind requires a fixation of some 21300 mutations per generation, or about 6.4 MILLION times faster than allowed by Haldane's model (if I did the math right).

John Paul:
But would Haldane’s model even apply to a population (or populations) of organisms that already has the genetic information available for the variation necessary for survival?[/quote]

That is what my analysis is about. It is the creationist position that what appear to be related species descended from an original Kind – an ancestral stock. It is also the YEC position that therefore this original kind had – as you indicate – all of the genetic material needed to adapt. All that is required is some environmental cue to activate/deactivate certain genes and POOF! New species (ignoring for the time being the fact that chimp and bonobo environments are virtually identical). If your postulate is correct, then they should be even more ‘identical’, with only a few minor nucleotide changes in specific loci to account for the behavioural and morphological differences between them.
Yet my analysis uses data from regions that should not be affected at all by such things. That in itself should give pause to those advocating the ‘already had the genes’ position. For if that were so, we should expect much less variation, especially given the YEC timeframe.

Scott Page:
Section added for the Baptist Board:

The notion behind NREH is that the “information is already there” in the genome, and some environmental change induces some suite of mutations that activates or deactivates genes already in the genome, producing multiple species form the original Kind.

John Paul:
That is only part of it. If you had read his book you would have known that.

Why is it that some people think they can accurately comment on a book that they haven’t read?

I am not commenting on the book, and never said that I was. I am commenting on his online statements and on the posts made by people like you. I often wonder why it is that some people think that they can accurately comment on a field of science in which they have no education, training or research experience, but I am usually chastised as being elitist when I do that.

Scott Page:
Let us take the chimp-bonobo example. The fact that they seem to differ by so many substitutions is in itself sufficient to severely damage if not outright falsify what appears the be Spetner’s central tenet, for if these extant creatures descended from some original ‘chimp kind’, in the YEC timeline of a generous 4,500 years ago (post-flood), then there is no possible way that the observed changes could have occurred. Even if we much too generously assume that half of the observed difference is due to polymorphism, we still havce some 6 million differences per lineage to account for. 6 million changes in 4,500 years= 13,333 per year, or 133,330 per generation to be accounted for (as opposed to 1 every 300 generations under the Haldane model). This works out to roughly 2 million times faster than allowed in Haldane’s model, which creationists seem to embrace. Keep in mind thatnon-beneficial mutations take LONGER to reach fixation in a population than do beneficial ones, so I am being very generous here. (looks like I made a math error in my earlier analysis – either way, it doesn’t help the creationist position much!). So, young earth creationists have a choice – regardless of whether or not they accept the NREH/directed mutation scenario, they either have to:

1. reject the use of Haldane’s model as an argument against evolution
or

2. abandon their hope of trying to use genetics/science to claim that YECism is scientifically tenable.

John Paul:
First it must be shown that Haldane’s model applies to the NREH. It could but as it stands it applies to random mutations culled and directed by natural selection.

Actually, the fixation of any allele/mutation falls under the Haldane model umbrella. I used the constraints employed by Haldane to, again, be generous to the YEC position, as most creationists agree that, under most circumstances, beneficial alleles reach fixation faster than neutral ones. I am assuming that the non-polymorphic differences are fixed in each species and are thus subject to the Haldane ‘speed limit.’

Secondly you have to provide evidence that the assumptions you made are correct.

All of my assumptions have been generous to the YEC timeframe/position. If you want to argue that, we can take into account actual scientific data that makes the YEC timeframe look ridiculous. As far as my assumptions with regard to the nucleotide differences between chimps and bonobos, I employed the same techniques that were used to glean the original estimates of the human chimp difference. Indeed – those original estimates were derived using much less DNA sequence data than I employed. The estimates of human-chimp difference have been borne out over an over with additional loci being sequenced and compared. I see little reason to assume that my estimates will have some gigantic margin of error that would render my assumption invalid.

Finally without knowing the differences in the pair of chimps aboard the Ark, any calculations from them could hardly be accurate.

If the YEC position is correct, there should have been, for purposes of this sort of analysis, no difference. It seems that you are suggesting or hinting at the possibility of somehow segregating all of the changes form the male and female original chimp kind and that these segregated changes will only be seen in either the bonobo or the common chimp. Of course, I have not mentioned that there are, in fact, several subspecies of chimp as well.
Of course, again, you make a good argument against using ReMine’s claims at all, since we do not know what the ancestral ape-like ancestor of humans was.

Dissasortive mating can greatly increase the opportunity for new genetic combinations to arise, and thereby increase the overall level of genetic variation upon which selection can operate. Templeton, A.R., and B. Read. 1983. The eliminating of inbreeding depression in a captive herd of Speke’s Gazelle (pp. 241-61) in Schonewald-Cox, C.M., Chambers, S., MacBryde, B., and W.L. Thomas, eds. Genetics and Conservation. Benjamin/ Cummings Publishing Co., London, Amsterdam.

That’s great. Which of those papers deals with the disassortive mating between only two individuals?

If chimps and bobnobos could interbreed at the time of the Flood, would that help the YEC case? I think it would.

There would not have been chimps and bonobos, as they would have arisen form the same original kind.

Until you take all things into consideration I can’t see that your argument has any merit. It could, but it doesn’t as it is.

I don’t think your ‘analysis’ of my analysis has any merit at all, as I show above.

 

[Administrator2]

DAVE COX

I don't mean to butt in to your discussion, but I have a couple of questions for John Paul.

You have stated:

The EF is satisfied that DNA of living organisms can be inferred to have at one time, been designed. The EF cannot tell us what happened to that &gt; design after eons of replication, mixing and environmental pressures.

That CSI can arise from CSI is NOT the debate.

Here are my questions:

If a small amount of CSI is acted upon by "eons of replication, mixing and environmental pressures", could the end result be a significant increase in CSI? It would still be a product of design, as the original CSI was designed.

Must any portion of the original CSI remain intact after "eons of replication, mixing and environmental pressures", or can it be transformed into different information?

Is there a lower limit on the amount of CSI necessary to give rise to CSI?

Must the CSI be in the same form, or can CSI of one kind give rise to CSI of another kind. For example, must the CSI in DNA always be expressed in DNA? Can that CSI give rise to a postulated "hyper DNA" or some other form of information carrying mechanism?

 

[Administrator2]

SCOTT PAGE

HELEN
To Scott Page: the function of DNA certainly is dictated by the sequencing, but that was not my point. My point was that the concept of irreducible complexity does not lie in the sequence of any portion of the DNA. On strictly mathematical grounds, any sequence is as probable or improbable and any other sequence, so that is not the relevancy.

And yet it seems to be a claim – implicit if not explicit – that a particular sequence of DNA should exhibit CSI if it encodes a specific protein. It seems to me that the specificity is determined after the fact. That is, the anti-Darwinian does not/cannot tell if a particular segment of DNA is supposed to be the product of ‘design’ or of ‘natural’ causes UNLESS they already know that it encodes something, i.e., that it does something. If this is so, and your opening statement seems to me to imply this, then the concept of a mathematical ‘explanatory filter’ is just a big hoax. There is no explanatory power at all if the ‘filter’ needs to know the outcome beforehand.

What my point was is that the function of the DNA requires the cellular mechanism to ‘understand’ and deal with it in an appropriate way. And this, in many cases, such as shape of the resulting cell, is NOT to be found in the DNA, by the way.

I am most interested to read more about the shape of a cell not being influenced by its genetic complement. Please direct me to where I can read about this.

However, here is what you wrote that I was responding to:

Helen:
”Barbarian, the concept of IC lies NOT in the sequencing, but in the function.”

The ‘sequencing’ dictates the function. That was MY point.

It truly does take a cell to make a cell, and there is a distinct concept of irreducible complexity there. The very fact that geneticists are looking to find the least amount of genetic material necessary for cellular life and reproduction means they are implicitly working with the concept of IC. There is a point at which the genetic material cannot lose any more ‘parts’ without losing its ability to program the workings of the cell. However, it must also be remembered in the meantime that the genetic material without the cell is useless – it cannot function.

It takes an extant cell to make an extant cell, true. It takes an extant mycoplasma to make a modern mycoplasma, true. Lets look at bicycles. What is the simplest bicycle, and what does it require to function? Well, it needs wheels with tires on it. It needs pedals. It needs a chain to transfer energy from the pedals to one of the wheels. It needs handlebars. It needs a seat. Right? Not right. Some bicycles have pedals attached directly to the wheels, omitting the ‘requirement’ for a chain and gear assembly. Some bicycles do not have tires on their wheels. Some bicycles in fact only have one wheel and thus no chain and gear assembly (not technically a bicycle, but operates on the same principle). So, these geneticists that are looking for the minimal genetic complement required for cellular life. What kind of cellular life? The kind we see today. Even if we are generous and grant that they are implicitly working with/on IC, what exactly does that mean in this debate? Does that mean that this ‘simplest’ cellular life must have been the product of some intelligent agent (wink wink), or would it mean something else?

It is all well and good to say that system X requires parts 1-10 to function, therefore, as it is, system X is IC. It is quite another to say that system X is the handiwork of my preferred Intelligent Agent, which is obviously where this is going.

And the cell requires the membrane, for instance, to be a cohesive unit capable of functioning. The cell itself, then, is an example of irreducible complexity. This is the point I was attempting to make. And this is why Pat’s ‘challenge’ to show that one stretch of DNA is the product of intelligent design while another is not is a challenge based on a lack of comprehension of what is going on.

I totally disagree. You are simply trying to make it ‘easier’ for the ‘EF’ to find what you think you need it to find. An extant cell may or not be IC, but how – exactly – would the EF conclude this? And if it did, so what? IC in and of itself is not ‘proof’ of intelligent or supernatural intervention. It is not ‘proof’ that natural mechanisms could not have produced it. Indeed, my old and valid criticism of this concept is that there is an ignorance of the history involved. Without this knowledge, it seems to me, attempting to explain the extant by this criterion and extrapolate conclusions is foolhardy at best.

It is entirely logical that, since the very workings of a cell are premised on its DNA complement, then that is where the EF and similar attempts at identifying ‘ID’ should be focused. Back to the bikes – what you seem to be saying is that given the choice between looking at two bikes or looking at the instruction manual for the bikes and trying to decide which one is harder to assemble, one should simply ignore the manuals and opt for looking at the bikes. The end product does not always indicate the complexity of its manafacture.

It requires the rest of the cell to see what that bit of DNA does

Hyperbole.

– its stochastic complexity ‘rating’ means nothing. What it does – its SPECIFIED complexity, means everything, and until we can see what the specification is, we cannot make any determination regarding possible ID with the information now available to us.

In other words, we have to know the end of the story before we attempt to understand the first chapter….

And all of this, by the way, has nothing to do with mutations or even natural selection. It has to do with the actual process of living and replicating which is the business of any cell, mutated or unmutated, naturally or artificially or non-selected. Sumac’s material was therefore of no import where this discussion is concerned.

It was insofar as John Paul’s reference to Spetner’s NREH. That much should have been obvious.

 

[Administrator2]

HELEN

Although this should by rights go under 'the human brain', or some such
topic, since IC is right on top, maybe this might spark a few thoughts:
“In light of what we know about evolution, it seems most likely that
our extraordinary
cognitive capacity was somehow acquired as a unit, rather than in a
gradual process of
modular accretion, for it is plainly wrong to regard naturral selection
as a long-term
fine-tuning of specific characteristics, however much we like the
resulting stories.
And it’s important to remember that even today we are still testing the
limits of this
generalized capacity that makes so much possible. .. .. .. ..”
__________

Letters, Page 12, Scientific American April 2002. Ian Tattersall,
Reply to letter by
Dudley Miles, concerning Tattersall’s article “How We Came to Be Human”
in
Scientific American, Dec 2001, pages 56-63.

===========

I also thought the following was interesting from Franklin Harold's The Way of the Cell which I completed the other day:


"A bacterial cell consists of more than three hundred million molecules (not counting water), several thousand different kinds of molecules, and requires some 2000 genes for its specification. There is nothing random about this assemblage, which reproduces itself with constant composition and form generation after generation." (pp 10-11)

"Indeed, even a machine is not explained by mechanical principles alone, for its construction is guided by the designer's purposes which constrain the blind operation of physical laws. In the case of living organisms, it is their hierarchical organization and their origin in the interplay of random variation and natural selection that should give pause to any radical reductionist. And it is noteworthy that our unquestioned success in unraveling the molecular mechanics of life have thus far yielded little insight into the genesis of coherent forms and functions on the scale of cells and organisms." (13-14)

"The idea that biological organization is fully determined by molecular structures is popular, seductive, potent and true up to a point -- yet fundamentally wrong. Many scientists cling hopefully to Lederberg's dictum of thirty years ago: "The point of faith is this: make the macromolecules at the right time and in the right amount, and the organization will take care of itself." But this faith is too simple to suit modern knowledge. It disregards the fact that the cell as a whole is require to create the proper environment for self-assembly to proceed. Furthermore, both prokaryotic and eukarytoic cells make sure to control self-assembly, so that it takes place only as part of a larger purpose." (56)

"How much is chance, and how much design is one of the many deep questions we do not quite know how to ask." (71)

"Is this pattern of purposeful chemistry [metabolism in the cell] laid out in the genome? Not in any identifiable form, and no one could have inferred its existence from a knowledge of the gene sequences or even of the gene products." (75)

"As matters stand, the nucleotide sequence of a gene is not sufficient to let us predict the three-dimensional structure of an enzyme, let alone its kinetic characteristics; the coordinated operation of a metabolic module is quite out of sight. Whether the metabolic economy can be 'in principle' reduced to the molecular level is irrelevant to the question that demands an answer now. How does a coordinated, purposeful economic society emerge from the interactions among its multitudinous molecular citizens? (76)

"Even those for whom life is simply the expression of the instructions encoded in the genes acknowledge that it takes cellular machinery to implement those instructions...Growth and division refer not simply to the accretion of biomolecules, but to the replication of an integrated pattern of functions and structures." (99)

"What pulls together the cacophany of molecules and ion channels and regulated pathways into a coherent whole: a cylinder with rounded caps [E.coli], quickly and every time? If a cell is an orchestra and DNA the score, who or what conducts?...Here we reach an edge, and are left comtemplating the disquieting notion of an orchestra without a conductor." (113)

All quotes above from The Way of the Cell, Franklin Harold (2001, Oxford University Press)

Something that intrigued me about Harold's book is that he insists on naturalistic materialism, stating from the start that an understanding of evolution is essential, and that all phenomena will eventually be understood in terms of natural and material explanations. And yet the material he presents in his book often stands in stark juxtaposition to that, as though he is spending the time challenging himself. It's a fascinating read both on a biological level and a psychological level.

 

[Administrator2]

GALATIAN

I got this in the mail today.

Another one of Michael Behe's claims, the principal claim that
he
makes, is that the cell is filled with these complex biochemical
machines
with multiple parts, and we know, he says, that they could not have
evolved,
and the reason we know that is because those parts by themselves have
absolutely no function. It's an interesting statement. It's also a
testable
statement. And it turns out to be false. Let's take his favorite
example,
everybody's favorite actually -- the bacterial flagella -- which is
this
wonderful little rotary engine that has about 40 different parts in
it, 40
different proteins. He says that's irreducibly complex, the parts
aren't
good for anything.

Well, it turns out that in 1999, scientists were investigating a
group of
about 10 proteins -- it's called the Type-III secretory system --
that pumps
proteins out of a bacterium into one of the cells in our body. It's a
nasty
little thing. It's like a syringe. The bacterium that causes bubonic
plague,
Yersinia pestis, has one of these guys.
"Well, the people investigating the structure, when they got the DNA
sequences of the proteins, suddenly discovered, My God, these 10
proteins
are almost exactly the same as 10 proteins in the bacterial flagellum
of all
things.

So, in other words, despite Behe's claims that the parts are useless
by
themselves, here's a little assembly of about 10 parts that is
perfectly
useful to the bacterium in terms of producing this secretory
apparatus. So
that means that the central claim, which is all the parts have to be
together before you get function is wrong. And it turns out that
there are
other examples as well.

http://minyos.its.rmit.edu.au/~e21092/flagella.htm

 

[Administrator2]

HELEN

The author of the email Galatian received has mis-stated the case regarding Behe. Behe never claimed that the individual proteins did not serve other functions in the cell. That is simply not in his material.

Behe’s point is that something like the flagellum cannot operate without a minimal number of ‘protein parts’ and that some partial combination of these proteins means nothing to the cell – they would be destroyed as the cell continually takes apart old or useless proteins and recycles their amino acids into new proteins. So the partial whatever would not be allowed to hang around waiting for new parts to serendipitously arrive and attach and allow the entire organelle to begin a function, doing something the cell had never done before!

So this business of testing a statement that Behe never made (to the best of my knowledge, having read his book and other materials of his) is a complete straw man. The argument means nothing. One must deal with what Behe actually said!

And, by the way, the flagella requires only three basic parts, regardless of how many proteins are involved in each… It is those parts which must all be together and functioning to have an operating flagella. ”Because the bacterial flagellum is necessarily composed of at least three parts – a paddle, a rotor, and a motor – it is irreducibly complex.” (Behe, Darwin’s Black Box, p. 72)

 

[Administrator2]

JOHN PAUL

Behe’s book, Darwin’s Black Box was a challenge to the biochemical community to get their ideas published in peer-reviewed journals. Explanations, speculations and conjecture are not to be confused with empirical evidence. The website the galatian linked to does not offer anything beyond speculation and conjecture, neither did the “mail” he quoted. Unless either one makes it into a peer-reviewed journal Behe’s challenge would stand unmet.

"Well, the people investigating the structure, when they got the DNA
sequences of the proteins, suddenly discovered, My God, these 10
proteins are almost exactly the same as 10 proteins in the bacterial flagellum
of all things.

John Paul:
All that means is that similar DNA sequences can produce different things depending on the configuration. Seeing that we haven’t deciphered any genome I don’t see why this would be cause for any conclusion jumping.

So, in other words, despite Behe's claims that the parts are useless
by themselves, here's a little assembly of about 10 parts that is
perfectly useful to the bacterium in terms of producing this secretory
apparatus.

John Paul:
“By themselves” is different than groups of ten. When I am with 9 friends I am not by myself. What happens once the secretory apparatus no longer functions as such because of mutation accumulation? Part of Behe’s argument also deals with minimal function. How did those ten parts come together in the first place? Was each step functional in any way?

So that means that the central claim, which is all the parts have to be
together before you get function is wrong. And it turns out that
there are other examples as well.

John Paul:
Maybe if the people who are trying to refute Behe actually read the book and his responses to the critics they wouldn’t misrepresent what he is saying. In your example we had ten parts working together. Would it work or have any function at all if 1 part was removed?

Even Behe’s mousetrap analogy has withstood scrutiny as all alleged rebuttals of that analogy include intelligent intervention.