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Author
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Topic: Response to Howard Van Till
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brauer
Member
Member # 398
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posted 04. October 2002 12:34
Hi Paul,
I agree with you that the "why" questions are the most interesting and most fruitful to pursue.
They suffer from an intrinsic vagueness, however, in that there are different subjective meanings of the question.
One example of this is hierarchical "why" explanations, such as you pointed out in the context of your laptop cooling system. Why does your laptop have a cooling fan and vents? Because heat needs to be dissipated, because the logic can't work at high temperatures, because the cpu generates heat, because the electrons lose energy in a particular way, etc., etc., down to an explanation of subatomic physics. Each question might not have equal interest and/or value, and each answer may be meaningless depending on the assumptions of the questioner.
In non-engineering fields, the ambiguity of the "why" questions is even more striking. Consider: "Why do humans suffer from malaria?" How you go about answering the question depends upon your unique stance and viewpoint. You could say it's because:
- Anopheles is a host of both humans and Plasmodium
- there is not enough selection against virulence to diminish the effects of malaria
- the developed nations haven't spent enough money on tropical diseases
- a sloppy designer didn't account for that side-effect of introducing mosquitoes into the biosphere
- Adam's fall
- etc.
All of these answers are correct in their proper context. The question as stated, though interesting and relevant, does not distinguish between the different domains from where an answer can come.
That's why scientific "why" questions have to be specific. Otherwise the strict requirement for inter-observer verifibility (or "viewpoint neutrality") is violated.
ID can ask all of the "why" questions it likes. But they need to be made specific. This, I think, was RB's point when he wrote:
quote:
Which is why science does not ask such vague WHY questions, but more specific why questions, usually noted by the word HOW.
Note: science does not ask such vague WHY questions, but more specific why questions, usually noted by the word HOW.
Getting back to my current obsession about ID. This is the reason "design-centered" ID is doomed: it is simply never specific enough to qualify as science.
[ 04. October 2002, 12:35: Message edited by: brauer ]
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Paul A. Nelson
Member
Member # 26
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posted 04. October 2002 13:39
Of course "why" questions need specificity. Consider the V2 rockets Maynard Smith was examining:
Q. Why is the rocket's gyroscope connected to the fuel supply?
A. Because Hitler hated the Jews and led Germany into war and madness.
Incidentally, here's the next paragraph in Maynard Smith's provocative article:
quote:
Of course, when thinking about the V2 rocket I was thinking about a product of human design, whereas, a few years later, when I was thinking about the shapes of mammalian teeth, I was asking why mammals were better at chewing, and so left more descendants. But this difference had no effect on the way I thought about the two problems. Indeed, I have become increasingly convinced that there is no way of telling the difference between an evolved organism and an artifact designed by an intelligent being. Thus imagine the first spacemen to land on Mars are met by an object which appears to have sense organs (eyes, ears) and organs of locomotion (legs, wings). How will they know whether it is an evolved organism, or a robot designed by an evolved organism? Only, I think, by finding out where it came from, and perhaps not even then. (John Maynard Smith, "Genes, Memes, & Minds," New York Review of Books 30 Nov 1995, p. 46)
Matt wrote:
quote:
This is the reason "design-centered" ID is doomed: it is simply never specific enough to qualify as science.
Time will tell.
[ 04. October 2002, 13:41: Message edited by: Paul A. Nelson ]
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Daniel Edington
Member
Member # 421
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posted 04. October 2002 17:45
Paul,
"function -- DNA -- RNA -- protein -- function -"
and just where is the feedback mechanism to go from the function at the end to the function you arbitrarily placed at the beginning?
My point is that a far more valid calculation of the probability of the formation of the bacterial flagellum would be to compute the probability of the formation of the genetic sequence that codes fo this assembly. The reverse, having the protein form first is meaningless, a protein without the genetic code would not be passed on to offspring. It seems like common sense to me.
"DNA on its own is an inert molecule."
No, I don't think so. Even on its own DNA has chemical activity and is far from inert.
Dan
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RB
Member
Member # 263
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posted 05. October 2002 12:58
The problem with why questions is that even with specificity, they can be answered at multiple levels. The famous of example, Why did the frog jump?
All levels of answers are very interesting, but only some can be addressed empirically.
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Daniel Edington
Member
Member # 421
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posted 15. October 2002 15:05
In his response to Howard Van Till, Dembski fails to answer one question that I feel is particularly important.
"Well, then, suppose that the flagellum really was assembled for the first time by the form conferring action of an unembodied intelligent designer independently of genomic instructions, as Dembski’s approach implies. Since instructions for the development of flagella are now part of the E. coli genome, are we to believe that the designer added those instructions to the genome as a separate act? Are there two independent form-conferring acts here—one for the first flagellum and another for the genomic instructions to produce all subsequent flagella?"
to which Dembski replied:
“(2) Van Till claims that my probabilistic analysis of the bacterial flagellum is "radically out of touch with contemporary genetics and developmental biology." I'm not sure what developmental biology has to do with it (bacteria don't have embryos that develop into adults). As for genetics, he would have preferred to see the probabilistic analysis of the flagellum center on the genes that code for its proteins rather than the proteins that go into its assembly. But the genes follow the proteins which follow the function, and not vice versa, so my analysis is the correct one. Even so, since genes map to proteins, the probabilities assigned to the flagellum's proteins and assemblage can easily enough be backtracked to the genes themselves (this is standard probability theory, in which probabilities on the space mapped into backtrack to probabilities on the space mapped out of).”
I however was somewhat less than satisfied with this answer. I am not so sure that Dembski’s “analysis is the correct one”
A simplified version of this question is: What does it take to go from a bacteria without a flagellum to one with a flagellum and how would be the best way to calculate the probability of such an event?
Another question: Is Dembski implying that the flagellum was intelligently designed first and the intelligent design of the genomic instructions to produce all subsequent flagella followed from that?
What is to prevent us from splicing the appropriate gene sequence into a bacteria without a flagellum and producing a new bacteria, one with a flagellum?
I don't know about anyone else but I think this issue is important enough to spend some time on.
Dan
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jasonyoung
Member
Member # 432
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posted 15. October 2002 17:02
"A simplified version of this question is: What does it take to go from a bacteria without a flagellum to one with a flagellum and how would be the best way to calculate the probability of such an event?"
Stated directly for the sake of brevity: Any evolutionary model that fails to supply us with a detailed reconstruction and analysis of specific causal pathways is altogether useless for calculating probabilities.
-Jason
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Daniel Edington
Member
Member # 421
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posted 15. October 2002 19:03
Jasonyoung,
Yes, an interesting thought. In a much more general sense we can state that any origins model that fails to supply us with a detailed reconstruction and analysis of specific causal pathways is altogether useless for calculating probabilities.
However, that doesn't really answer the question.
Dan
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rafe gutman
Member
Member # 134
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posted 16. October 2002 01:32
quote:
dembski:
As for genetics, he would have preferred to see the probabilistic analysis of the flagellum center on the genes that code for its proteins rather than the proteins that go into its assembly. But the genes follow the proteins which follow the function, and not vice versa, so my analysis is the correct one. Even so, since genes map to proteins, the probabilities assigned to the flagellum's proteins and assemblage can easily enough be backtracked to the genes themselves
(emphasis mine)
if genes follow proteins, how can you backtrack from genes to proteins? how do genes follow proteins? am i missing something here?
[ 16. October 2002, 01:34: Message edited by: rafe gutman ]
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djmullen
unregistered
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posted 16. October 2002 06:12
[Message Deleted]
Talk about people's motives elsewhere. Talk about their ideas here.
[ 18. October 2002, 23:24: Message edited by: Moderator ]
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djmullen
unregistered
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posted 18. October 2002 09:15
[Message Deleted]
Please do not talk about other people's character. Talk about their ideas.
[ 18. October 2002, 23:26: Message edited by: Moderator ]
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Paul A. Nelson
Member
Member # 26
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posted 18. October 2002 10:32
David Mullenix wrote:
quote:
Translated: when Wells "blocked" (that is, when he apparently really scrambled the cells), the chemical gradients were all screwed up and the cells didn't develop into anything remotely resembling a tadpole. But if he moved bits of cells around AFTER they had begun to differentiate into a head and were no longer dependant on the chemical gradient, then they continued their development as if they hadn't been moved and he wound up with a two-headed tadpole. This had EVERYTHING to do with the DNA and specifically, it had to do with which sections of DNA were activated by the chemical gradients.
Some questions:
1. What is the chemical gradient in question?
2. What DNA sequences were being activated by the gradient?
3. You argue that Wells's membership in the Unification Church affected his biological research at UC-Berkeley. Please explain, in detail, the cause-and-effect relationship here. Presumably, you know better than John Gerhart, David Wake, and Wells's other supervisors at Berkeley, about problems in his work there.
Note to Moderator: If Mr. Mullenix does not provide specific evidence for (3), I suggest that his post be deleted as violating Brainstorm rules.
[ 18. October 2002, 11:08: Message edited by: Paul A. Nelson ]
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djmullen
unregistered
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posted 18. October 2002 14:53
1: The chemicals are small proteins and they are apparently quite numerous. They bind to specific short sequences of DNA, thus turning them on or off. On page 87, one of them is mentioned as binding to the DNA sequence TTATTG.
2: The DNA sequences affected are in areas called regulatory regions that tend to be near the sections of DNA being turned on and off. One of the sequences, as mentioned above, is TTATTG.
Do you doubt Dr. Coen or my condensation of the information provided in his book? You can probably get it from your local library and it is well worth the effort to read. Amazon doesn't seem to have it. I believe I ordered mine through Borders.
[ 18. October 2002, 23:28: Message edited by: Moderator ]
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charlie d.
Member
Member # 159
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posted 18. October 2002 15:31
quote:
Some questions:
1. What is the chemical gradient in question?
2. What DNA sequences were being activated by the gradient?
3. You argue that Wells's membership in the Unification Church affected his biological research at UC-Berkeley. Please explain, in detail, the cause-and-effect relationship here. Presumably, you know better than John Gerhart, David Wake, and Wells's other supervisors at Berkeley, about problems in his work there.
I have no clue what Wells specifically did during his postdoc research, but as far as I know there are several recognized morphogenetic gradients in vertebrates, involved at different stages and at different sites during development. The hottest family, judging from recent papers, is that of bone morphogenetic protein (BMP) factors, which determine both dorsoventral and anteroposterior axis formation in - apparently - all vertebrates. BMPs are known to activate specific receptors that signal through proteins call Smads, which act directly as transcription factors by, interestingly, interacting with Hox factors to regulate the expression of a number of genes involved in development. A quick Pubmed search would likely reveal a number of potential and established targtes (I am trying to avoid Pubmed-bombing here - besides I don't have time right now).
Again, I am not saying this is what was Wells' coauthors were aiming for in their studies, just that this is the kind of model by which chemical gradients regulate gene expression during vertebrate development.
In general, this protein vs gene diatribe is really a chicken vs egg issue (pardon the pun). Of course genes are regulated by proteins, and they direct the production of yet more proteins that may influence more genes and so on. Any morphogenetic gradient is in itself established through the activity of proteins, encoded by genes, regulated by proteins that also come from genes ... you get the picture.
One can alter development equally by altering proteins (for instance disrupting, or artificially creating, morphogenetic gradients), or by altering genes (such as hox knock-outs/duplications, trangenics etc). The fact remains, though, that if you place a mouflon differentiated cell nucleus inside a sheep's egg, with all its sheep gradient proteins, you still get a baby mouflon, and not a sheep. That must mean something about the role of genes in directing embryonic development, right?
[message edited: concern for the motivation of Dr. Wells work may be appropriate in other places, but certainly not here.]
[ 18. October 2002, 23:34: Message edited by: Moderator ]
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Paul A. Nelson
Member
Member # 26
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posted 18. October 2002 21:25
To David Mullenix:
You accuse Jonathan Wells of making "amateurish" mistakes in interpreting his experiments at Berkeley, and argue that this happened because of his religious beliefs. I asked you to support these claims by evidence.
In reply, you cited a book by Coen. You may assume that I know about developmental regulatory elements. What I want to know is how -- from your knowledge of Xenopus embryology -- you have identified Wells's mistakes of interpretation. My questions (1) and (2) above ask for the relevant details in frogs.
As for evidence supporting your claim about the negative influence of Wells's religious beliefs on his work at Berkeley, you've provided none. Instead, you claim -– again, without evidence -– that religious beliefs make it impossible for one to investigate scientifically anything that may conflict with those beliefs.
That's nonsense. Charles Darwin set out on the voyage of the Beagle as a creationist; he returned to London unsure of his views; he later became persuaded of descent with modification by natural causes. “The view which most naturalists entertain,” he wrote in the Origin, “and which I formerly entertained –- namely, that each species has been independently created –- is erroneous.” The history of science is replete with religious believers coming to doubt their religiously-involved views about the world.
Motives and propositions are not the same thing. This is why logic textbooks include discussions of the genetic fallacy, a fallacy your posts display in abundance. If religious beliefs self-evidently discredited scientists, then much of Western science would have to be tossed out.
[edited by moderator]
[ 19. October 2002, 11:05: Message edited by: Paul A. Nelson ]
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charlie d.
Member
Member # 159
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posted 18. October 2002 23:47
I have been re-reading Wells' quote carefully, and I think I get the point he was trying to make. As often the case with Wells, he seems to be walking a very fine line between telling the plain truth and actually bending it for rhetorical purposes.
As far as I can tell, this is the story: Wells has studied very early Xenopus development, between the fertilization stage and the first few cell divisions, when the general pattern of the future embryo (such as anteroposterior and dorsoventral polarity, etc) is determined. At these very early stages, in pretty much all organisms I know of (from worms to vertebrates), the embryo is usually said to be under control of the maternal genome: essentially all proteins and mRNA in the zygote derive from the egg, i.e. from the mother during oogenesis, and they supply the early embryo with everything it needs early on. It is only later that the embryonic genome "kicks in" (in part, as discussed above, under the influence of maternally derived factors originally present in the egg). The stage at which this happens depends in large part on the size of the egg: big, fat eggs like Xenopus', with lots of maternal proteins and mRNAs, don't start to transcribe the zygote's genome until relatively late (10-12 cell divisions, when the embryo has already thousands of cells), while small, mammalian zygotes become transcriptionally active much earlier, like after 2 cell divisions, or 4 cells).
So, very strictly speaking Wells is right, in Xenopus the early stages of embryo development are not controlled by the embryo genome. However, he is being misleading (or badly misinterprets the data, if the error is unintentional) when he says that "DNA does not program the development of the embryo".
First, because even the early embryo is under genetic control (albeit the mother's), and second because, past the very early stages of development, it is indeed the embryos genome that determines the developmental process (quite obviously).
PS: I just noticed most previous posts on this subjects have been mod'ed. Oh well, it won't be the first time I look completely out of sync with the ongoing conversation. ![[Wink]](wink.gif)
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