Freethought & Rationalism Archive

DNAunion · 03-16-2002, 09:26 AM

DNAunion: Okay, so here's the thing. I have recently been rereading several of my texts on the cell cycle and was left thinking, "Wow, how fantastically complex!".

Let me explicitly state some things.

a)I realize that I am looking at a system as it currently exists - one that has been evolving for billions of years. So yes, its current state may be very much unlike its original state.

b) I am not claiming that eukaryotic cell division is irreducibly complex (unlike many others, I don't go around haphazzardly asserting or stating X is IC - that is something that needs to be determined by checking the system against Behe's criteria). But I do claim that it is amazingly complex.

c) I am not stating or arguing that evolution could not have produced the system. I am saying that I don't personally know exactly how evolution would have produced it, step-by-step. If someone knows the answer, then tell me. If not, let's investigate it.

To investigate this topic, I propose a two-step process, each involving the answering of a question.

1) What parts of eukaryotic cell division - as it currently occurs - can be eliminated without eliminating the function of cell division?

Answering that question will help us strip away the "superfluous add-ons" to arrive at the simplest state of the system - its core - as it currently exists.

Only once that has been done.

2) Is there a convincing and detailed evolutionary explanation for how that basic system could have arisen?

theyeti · 03-16-2002, 10:14 AM

Quote:

Originally posted by DNAunion:
[QB]
1) What parts of eukaryotic cell division - as it currently occurs - can be eliminated without eliminating the function of cell division?

Answering that question will help us strip away the "superfluous add-ons" to arrive at the simplest state of the system - its core - as it currently exists.[/qb

That's a good question, but unfortunately I'm not too knowledable about eukaryotic cell division. Here's a PubMed search on <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=&DB=PubMed" target="_blank">eukaryotic cell division evolution</a> that turned up four pages of hits. Here are a couple of articles that I came across randomly with various searches:

<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=108085 50&dopt=Abstract" target="_blank">Evolutionary origin of eukaryotic cells.</a>

<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=115433 44&dopt=Abstract" target="_blank">Thinking of biology: toward a theory of cellularity--speculations on the nature of the living cell</a>. Somewhere in there is the info you're looking for. Oh, and this one is mostly unrealted but I thought it was cool anyway:

<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=116986 51&dopt=Abstract" target="_blank">Evolutionary route to diploidy and sex.</a>

Quote:

By using a bit-string model of evolution, we find a successful route to diploidy and sex in simple organisms. Allowing the sexually reproducing diploid individuals to also perform mitosis, as they do in a haploid-diploid cycle, leads to the complete takeover of the population by sexual diploids. This mechanism is so robust that even the accidental conversion and pairing of only two diploids give rise to a sexual population.

I'm not sure that the best approach it to look for "superfluous" bits involved (though probably good for starters). For instance, there are parts of the spliceosome that can't be stripped away and still have it function. But there is strong evidence that the spliceosome evolved from group II introns that didn't need any protein parts -- just the catalytic RNA. Presumably, the proteins were just helpful at first until the RNA evolved dependacy on them. This is one of the more common objections to Behe's IC criteria.

Quote:

Only once that has been done.

2) Is there a convincing and detailed evolutionary explanation for how that basic system could have arisen?

I think that this is probably the best approach. One should start with a hypothesized ancestor and try to work out evolutionary pathways from there, and try to check those potential pathways against phylogenetics and known phenomena of cell biology. Keeping in mind that things like the mitotic spindle may have evolved from preexisting tubulin. I'd be willing to bet that someone has done this, but I don't know where. I think that "evolvability" is a more useful concept than IC. I should also mention that we don't know everything about how eukaryotic cell division works, and therefore a complete hypothesis as to its origins shouldn't be expected until sometime in the future.

theyeti

Richiyaado · 03-16-2002, 10:20 AM

Hello All,

Many IDists constantly berate evolutionary 'just-so' stories, and give them no credence. But the other day, I read an article where the writer suggested we refer to them as 'how-possibly' stories, as they may lead us down fruitful avenues of research.

But, as I understand Behe and IC, doesn't he categorically and conclusively say that IC biochemical systems are, by definition, incapable of having arisen by any evolutionary pathway?

If that's the case and one accepts Behe's definition of IC, wouldn't an investigation of eukaryotic cell division, or any biochemical system, just be a huge waste of time at this point?

DNAunion · 03-16-2002, 11:00 AM

Quote:

Richiyaado:
But, as I understand Behe and IC, doesn't he categorically and conclusively say that IC biochemical systems are, by definition, incapable of having arisen by any evolutionary pathway?

DNAunion: No, Behe does not claim that.

By the way, I was hoping to avoid discussions of what IC is or is not and to look at the biology without involving ID.

Richiyaado · 03-16-2002, 11:10 AM

Hello All,

To DNAunion: Then what does Behe mean when he says this?

Quote:

An irreducibly complex system cannot be produced directly by slight, successive modification of a precursor system, since any precursor to an irreducibly complex system is by definition nonfunctional.

Isn't he categorically denying that any evolutionary pathway is impossible? If not, what is he denying?

mturner · 03-16-2002, 01:12 PM

Quote:

Originally posted by Richiyaado:
<strong>Hello All,

To DNAunion: Then what does Behe mean when he says this?

Isn't he categorically denying that any evolutionary pathway is impossible? If not, what is he denying?</strong>

**
Sounds like he's just dissing phyletic gradualism, to me.

mturner

DNAunion · 03-16-2002, 01:20 PM

Quote:

Richiyaado:

To DNAunion: Then what does Behe mean when he says this?

!!!!!!!!!!!!!!!!!! An irreducibly complex system cannot be produced directly by slight, successive modification of a precursor system, since any precursor to an irreducibly complex system is by definition nonfunctional.
!!!!!!!!!!!!!!!!!!

Isn't he categorically denying that any evolutionary pathway is impossible?

DNAunion: No, he isn't.

He is referring to what one of his critics ended up calling something like "serial direct Darwinian evolution".

On page 40 of his book (right after he says what you quoted) Behe says:

Quote:

"Even if a system is irreducibly complex (and thus cannot have been produced DIRECTLY), however, one can not definitively rule out the possibility of an INDIRECT, CIRCUITOUS route."

[ March 16, 2002: Message edited by: DNAunion ]</p>

DNAunion · 03-16-2002, 01:27 PM

DNAunion: I found an abstract for an article entitled “Evolution of the Cell Cycle”. Perhaps we could begin by discussing it.

Quote:

”Eukaryotic cells evolved from bacterial ancestors whose … genome was replicated from a single origin and whose means of segregating sister chromatids depended on fixing their identity at replication. Evolution of … [a] cytoskeleton, initially as means of consuming other bacteria, eventually enabled evolution of the mitotic spindle and a new means of segregating sister chromatids whose replication could be initiated from multiple origins. In this primitive eukaryotic cell, S and M phases might have been triggered by activation of a single cyclin-dependent kinase whose destruction along with that of other proteins would have triggered anaphase. Mitotic non-disjunction would have greatly facilitated genomic expansion, now possible due to multiple origins, and thereby accelerated the tempo of evolution when permitted by environmental conditions.” (K Nasmyth, Evolution of the Cell Cycle, Philos Trans R Soc Lond B Biol Sci 1995 Sep 29;349(1329):271-81)

DNAunion: Several questions came to mind.

1) “Evolution of … [a] cytoskeleton, initially as means of consuming other bacteria…”.

How was the cytoskeleton used to consume other bacteria?

2) “Mitotic non-disjunction would have greatly facilitated genomic expansion… and thereby accelerated the tempo of evolution…”.

Non-disjunction would have resulted in one of the two daughter cells receiving an additional copy of one or more chromosomes (aneuploidy or euploidy, respectively), duplicating only preexisting genetic information. In humans, having an additional copy of a chromosome is deleterious (trisomy 21, for example) and having an additional complete haploid set of chromosomes (polyploidy, euploidy) is also. But polyploid plants are quite common. Anyone know about the affects of aneuploidy and euploidy in lower eukaryotes, such as yeasts?

3) “In this primitive eukaryotic cell, S and M phases might have been triggered by activation of a single cyclin-dependent kinase whose destruction along with that of other proteins would have triggered anaphase.”

Aren’t there multiple Cdk’s that are highly conserved between organisms as distantly related as humans and yeasts? Anyone know of any findings the author might be basing his hunch on?

Speaking of highly conserved components of the eukaryotic cell cycle, here are some extracts from abstracts. All of these conserved components (as well as the conserved process itself) suggests to me that there is a core eukaryotic cell cycle system that could be gotten down to.

Cdc2, Cdc3, gamma-tubulin, pericentrin

Quote:

”Constituent sequences of mitotic spindle-centriole-kinetosome proteins (gamma-tubulin,pericentrin, and the cyclin-dependent kinases Cdc2 and Cdc3, members of the centrin family) are conserved across taxa, occurring in animal and protist centrioles, plant MTOCs, and fungal spindle pole bodies.” (Chapman MJ, Dolan MF, Margulis L, Centrioles and kinetosomes: form, function, and evolution, Q Rev Biol 2000 Dec;75(4):409-29)

nudC gene

Quote:

”Essential genes which are required for normal nuclear migration and play a role in developmental processes have been isolated from model genetic organisms. One such gene is nudC (nuclear distribution C), which is required for positioning nuclei in the cytoplasm of the filamentous fungus Aspergillus nidulans and for normal colony growth. This gene is highly conserved, structurally and functionally, throughout evolution and the human homolog, HnudC, has been cloned. … In induced cultures, many mitotic cells demonstrated defects in spindle architecture during mitosis. The most common defect observed was multiple mitotic spindle poles rather than the expected bipolar structure. These data demonstrate the fundamental importance of HnudC in eukaryotic cell proliferation and a functional role for HnudC in
spindle formation at mitosis. “ (Zhang MY, Huang NN, Clawson GA, Osmani SA, Pan W, Xin P,
Razzaque MS, Miller BA, Involvement of the fungal nuclear migration gene nudC human homolog in
cell proliferation and mitotic spindle formation, Exp Cell Res 2002 Feb 1;273(1):73-84)

SKP1 gene (and CBF3 protein?)

Quote:

“The budding yeast SKP1 gene, identified as a dosage suppressor of a known kinetochore protein mutant, encodes an intrinsic 22.3 kDa subunit of CBF3, a multiprotein complex that binds centromere DNA in vitro. Temperature-sensitive mutations in SKP1 define two distinct phenotypic classes. skp1-4 mutants arrest predominantly as large budded cells with a G2 DNA content and short mitotic spindle, consistent with a role in kinetochore function. skp1-3 mutants, however, arrest predominantly as multiply budded cells with a G1 DNA content, suggesting an additional role during the G1/S phase. Identification of Skp1p homologs from C. elegans, A. thaliana, and H. sapiens indicates that SKP1 is evolutionarily highly conserved. Skp1p therefore represents an intrinsic kinetochore protein conserved throughout eukaryotic evolution and may be directly involved in linking kinetochore function with the cell cycle-regulatory machinery.” (Connelly C, Hieter P, Budding yeast SKP1 encodes an evolutionarily conserved kinetochore protein required for cell cycle progression, Cell 1996 Jul 26;86(2):275-85)

General Kinetochore components

Quote:

”Accurate chromosome segregation during mitosis requires the correct assembly of kinetochores—complexes of centromeric DNA and proteins that link chromosomes to spindle microtubules. Studies on the kinetochore of the budding yeast Saccharomyces cerevisiae have revealed functionally novel components of the kinetochore and its regulatory complexes, some of which are highly conserved in humans.” (Kitagawa K, Hieter P., Evolutionary conservation between budding yeast and human kinetochores, Nat
Rev Mol Cell Biol 2001 Sep;2(9):678-87)

mast gene

Quote:

”Through mutational analysis in Drosopjila we have identified the gene multiple asters (mast), which encodes a new 165 kDa protein. mast mutant neuroblasts are highly polyploid and show severe mitotic abnormalities including the formation of mono- and multi-polar spindles organized by an irregular number of microtubule-organizing centres of abnormal size and shape. The mast gene product is evolutionarily conserved since homologues were identified from yeast to man, revealing a novel protein family. Antibodies against Mast and analysis of tissue culture cells expressing an enhanced green fluorescent protein-Mast fusion protein show that during mitosis, this protein localizes to centrosomes, the mitotic spindle, centromeres and spindle midzone. Microtubule-binding assays indicate that Mast is a microtubule-associated protein displaying strong affinity for polymerized microtubules. The defects observed in the mutant alleles and the intracellular localization of the protein suggest that Mast plays an essential role in centrosome separation and organization of the bipolar mitotic spindle.” (Lemos CL, Sampaio P, Maiato H, Costa M, Omel'yanchuk LV, Liberal V, Sunkel CE, Mast, a conserved microtubule-associated protein required for bipolar mitotic spindle organization, EMBO J 2000 Jul 17;19(14):3668-82)

Cytostellin

Quote:

”Cytostellin, a 240 kDa protein, has been purified from mammalian cells by immunoaffinity chromatography using monoclonal antibody H5. Immunofluorescence microscopy shows diffuse and punctate cytostellin immunoreactivity in interphase nuclei. Nuclease digestion and salt extraction are not required to expose the epitope. The onset of prophase is marked by the appearance of multiple intensely mmunofluorescent cytostellin-containing 'bodies' within the nucleus. Nuclear disassembly is heralded by the movement of cytostellin bodies from the nucleus to multiple positions throughout the cell. Cytostellin bodies in metaphase, anaphase and telophase cells are widely dispersed, including some in cell processes far removed from the mitotic spindle apparatus. However, a distinct subset of larger, more intensely staining bodies surrounds the mitotic spindle apparatus. Cytostellin bodies remain in the cytoplasm of the daughter cells and disappear after the appearance of nascent nuclei. Cytostellin is immunologically distinct from other nuclear and cytoplasmic proteins, and it has been detected by immunoblot analysis in all species tested from yeast to humans. Based upon these findings, we postulate that cytostellin has a cell cycle-dependent function which is conserved in higher and lower eukaryotic cells.” (Warren SL, Landolfi AS, Curtis C, Morrow JS, Cytostellin: a novel, highly conserved protein that undergoes continuous redistribution during the cell cycle, J Cell Sci 1992 Oct;103 ( Pt 2):381-8)

mAb 6C6 antigen

Quote:

”We have used monoclonal antibodies raised against isolated native calf thymus centrosomes to probe the structure and composition of the pericentriolar material. To distinguish prospective antibodies as specific to conserved elements of this material, we screened clones by their identification of microtubule organizing centers (MTOCs) in different animal and plant cells. Among the clonal antibodies that reacted with MTOCs in both plant and mammalian cells, we describe one (mAb 6C6) that was found to immunostain centrosomes in a variety of bovine and human cells. In cycling cells this signal persisted through the entire cell cycle. Microscopy showed that the mAb 6C6 antigen was a component of the pericentriolar material and this was confirmed by biochemical analysis of centrosomes. Using immunoblot analysis of protein fractions derived from purified components of centrosomes, we have characterized the mAb 6C6 antigen as a 180 kDa polypeptide. We conclude that we have identified a protein component
permanently associated with the pericentriolar material. Surprisingly, monoclonal antibody 6C6 also stained other mitotic organelles in mammalian cells, in a cell-cycle-dependent manner. During prometaphase and metaphase the antibody stained both centrosomes and kinetochores. At the onset of anaphase the kinetochore-specific staining dissociated from chromosomes and was subsequently redistributed onto a newly characterized organelle, the telophase disc while the centrosomal stain remained intact. It is not known if the 180 kDa centrosomal protein itself redistributes during mitosis, or if the pattern observed represents other antigens with shared epitopes. The pericentriolar material is thought to be
composed of conserved elements, which appeared very early during the evolution of eukaryotes. Our results strongly suggest that mAb 6C6 identifies one of these elements.” (Chevrier V, Komesli S, Schmit AC, Vantard M, Lambert AM, Job D, A monoclonal antibody, raised against mammalian centrosomes and screened by recognition of plant microtubule organizing centers, identifies a pericentriolar component in different cell types, : J Cell Sci 1992 Apr;101 ( Pt 4):823-35)

zyg-8 and Doublecortin?

Quote:

“Proper spindle positioning is essential for spatial control of cell division. Here, we show that zyg-8 plays a key role in spindle positioning during asymmetric division of one-cell stage C. elegans embryos by promoting microtubule assembly during anaphase. ZYG-8 harbors a kinase domain and a domain related to Doublecortin, a microtubule-associated protein (MAP) affected in patients with neuronal migration disorders. Sequencing of zyg-8 mutant alleles demonstrates that both domains are essential for function. ZYG-8 binds to microtubules in vitro, colocalizes with microtubules in vivo, and promotes stabilization of microtubules to drug or cold depolymerization in COS-7 cells. Our findings demonstrate that ZYG-8 is a MAP crucial for proper spindle positioning in C. elegans, and indicate that the function of the Doublecortin domain in modulating microtubule dynamics is conserved across metazoan evolution.” (Gonczy P, Bellanger JM, Kirkham M, Pozniakowski A, Baumer K, Phillips JB, Hyman AA, zyg-8, a gene required for spindle positioning in C. elegans, encodes a doublecortin-related kinase that promotes microtubule assembly, Dev Cell 2001 Sep;1(3):363-75)

Stu2 and KIP3?

Quote:

”During anaphase, mitotic spindles elongate up to five times their metaphase length. This process, known as anaphase B, is essential for correct segregation of chromosomes. Here, we examine the control of spindle length during anaphase in the budding yeast Saccharomyces cerevisiae. We show that microtubule stabilization during anaphase requires the microtubule-associated protein Stu2. We further show that the activity of Stu2 is opposed by the activity of the kinesin-related protein Kip3. Reexamination of the kinesin homology tree suggests that KIP3 is the S. cerevisiae orthologue of the microtubule-destabilizing subfamily of kinesins (Kin I). We conclude that a balance of activity between evolutionally conserved microtubule-stabilizing and microtubule-destabilizing factors is essential for correct spindle elongation during anaphase B.”(Severin F, Habermann B, Huffaker T, Hyman T, Stu2 promotes mitotic spindle elongation in anaphase, J Cell Biol 2001 Apr 16;153(2):435-42)

INCENP protein (and HP1?)

Quote:

The inner centromere protein (INCENP) has a modular organization, with domains required for
chromosomal and cytoskeletal functions concentrated near the amino and carboxyl termini, respectively. In this study we have identified an autonomous centromere- and midbody-targeting module in the amino-terminal 68 amino acids of INCENP. Within this module, we have identified two evolutionarily conserved amino acid sequence motifs: a 13-amino acid motif that is required for targeting to centromeres and transfer
to the spindle, and an 11-amino acid motif that is required for transfer to the spindle by molecules that have targeted previously to the centromere. To begin to understand the mechanisms of INCENP function in mitosis, we have performed a yeast two-hybrid screen for interacting proteins. These and subsequent in vitro binding experiments identify a physical interaction between INCENP and heterochromatin protein
HP1(Hsalpha). Surprisingly, this interaction does not appear to be involved in targeting INCENP to the centromeric heterochromatin, but may instead have a role in its transfer from the chromosomes to the anaphase spindle.” (Ainsztein AM, Kandels-Lewis SE, Mackay AM, Earnshaw WC, INCENP centromere and spindle targeting: identification of essential conserved motifs and involvement of heterochromatin protein HP1, J Cell Biol 1998 Dec 28;143(7):1763-74)

Mal3/EB-1

Quote:

”Through a screen designed to isolate novel fission yeast genes required for chromosome segregation, we have identified mal3+. The mal3-1 mutation decreased the transmission fidelity of a nonessential minichromosome and altered sensitivity to microtubule-destabilizing drugs. Sequence analysis revealed that the 35-kD Mal3 is a member of an evolutionary conserved protein family. Its human counterpart EB-1 was identified in an interaction screen with the tumour suppressor protein APC. EB-1 was able to substitute for the complete loss of the mal3+ gene product suggesting that the two proteins
might have similar functions. Cells containing a mal3 null allele were viable but showed a variety of phenotypes, including impaired control of cell shape. A fusion protein of Mal3 with the Aequorea victoria green fluorescent protein led to in vivo visualization of both cytoplasmic and mitotic microtubule structures indicating association of Mal3 with microtubules. The absence of Mal3 protein led to abnormally short, often faint cytoplasmic microtubules as seen by indirect antitubulin immunofluorescence. While loss of the
mal3+ gene product had no gross effect on mitotic spindle morphology, overexpression of mal3+
compromised spindle formation and function and led to severe growth inhibition and abnormal cell
morphology. We propose that Mal3 plays a role in regulating the integrity of microtubules possibly by influencing their stability.” (Beinhauer JD, Hagan IM, Hegemann JH, Fleig U, Mal3, the fission yeast homologue of the human APC-interacting protein EB-1 is required for microtubule integrity and the maintenance of cell form, J Cell Biol 1997 Nov 3;139(3):717-28)

[ March 16, 2002: Message edited by: DNAunion ]</p>

Richiyaado · 03-16-2002, 01:43 PM

Hi mturner!

Hmm... I'm not so sure. It seems to me he's saying rather decidedly that any successive step-wise process is necessarily ruled out (including EAM, I'd guess).

And if that's the case, doesn't that moot any need for further research into a given biomechanical structure or biochemical system that's IC?

Plus, since Behe is saying that at the level of molecular biology, we're faced with a 'black box', the implication seems to be that once the determination of IC is made, further investigation would be futile.

Richiyaado · 03-16-2002, 02:23 PM

Hi DNAunion,

In my source for the Behe quote I cited, I didn't find the additional quote. Whatever the case, I don't understand the distinction he's making. In fact, it seems to me that he wants to have his cake and eat it, too.

On the one hand, he says "An IC system cannot be produced directly by slight, successive modification of a precursor system...", but "Even if a system is irreducibly complex, however, one can not definitively rule out the possibility of an indirect, circuitous route."

Is he saying that an IC structure or system arising via an indirect, circuitous route wouldn't involve slight, successive modification? Or what?

03-16-2002, 09:26 AM	#1
DNAunion Veteran Member Join Date: Jan 2001 Location: USA Posts: 1,072	Eukaryotic cell division DNAunion: Okay, so here's the thing. I have recently been rereading several of my texts on the cell cycle and was left thinking, "Wow, how fantastically complex!". Let me explicitly state some things. a)I realize that I am looking at a system as it currently exists - one that has been evolving for billions of years. So yes, its current state may be very much unlike its original state. b) I am not claiming that eukaryotic cell division is irreducibly complex (unlike many others, I don't go around haphazzardly asserting or stating X is IC - that is something that needs to be determined by checking the system against Behe's criteria). But I do claim that it is amazingly complex. c) I am not stating or arguing that evolution could not have produced the system. I am saying that I don't personally know exactly how evolution would have produced it, step-by-step. If someone knows the answer, then tell me. If not, let's investigate it. To investigate this topic, I propose a two-step process, each involving the answering of a question. 1) What parts of eukaryotic cell division - as it currently occurs - can be eliminated without eliminating the function of cell division? Answering that question will help us strip away the "superfluous add-ons" to arrive at the simplest state of the system - its core - as it currently exists. Only once that has been done. 2) Is there a convincing and detailed evolutionary explanation for how that basic system could have arisen?

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03-16-2002, 10:20 AM	#3
Richiyaado Regular Member Join Date: May 2001 Location: New Orleans Posts: 172	Hello All, Many IDists constantly berate evolutionary 'just-so' stories, and give them no credence. But the other day, I read an article where the writer suggested we refer to them as 'how-possibly' stories, as they may lead us down fruitful avenues of research. But, as I understand Behe and IC, doesn't he categorically and conclusively say that IC biochemical systems are, by definition, incapable of having arisen by any evolutionary pathway? If that's the case and one accepts Behe's definition of IC, wouldn't an investigation of eukaryotic cell division, or any biochemical system, just be a huge waste of time at this point?

03-16-2002, 01:43 PM	#9
Richiyaado Regular Member Join Date: May 2001 Location: New Orleans Posts: 172	Hi mturner! Hmm... I'm not so sure. It seems to me he's saying rather decidedly that any successive step-wise process is necessarily ruled out (including EAM, I'd guess). And if that's the case, doesn't that moot any need for further research into a given biomechanical structure or biochemical system that's IC? Plus, since Behe is saying that at the level of molecular biology, we're faced with a 'black box', the implication seems to be that once the determination of IC is made, further investigation would be futile.

03-16-2002, 02:23 PM	#10
Richiyaado Regular Member Join Date: May 2001 Location: New Orleans Posts: 172	Hi DNAunion, In my source for the Behe quote I cited, I didn't find the additional quote. Whatever the case, I don't understand the distinction he's making. In fact, it seems to me that he wants to have his cake and eat it, too. On the one hand, he says "An IC system cannot be produced directly by slight, successive modification of a precursor system...", but "Even if a system is irreducibly complex, however, one can not definitively rule out the possibility of an indirect, circuitous route." Is he saying that an IC structure or system arising via an indirect, circuitous route wouldn't involve slight, successive modification? Or what?

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