Because you posted a comment on a Behe thread, so I thought you might want to learn something about the flaws in his work. Silly me.
What a waste of bits.
Well in your case, yeah, apparently so.
But, since you did ... That link above didn't work. How lazy of you.
Oh, get a grip. Mr. Lindsay has apparently moved his pages to his own website now from their previous home. You can now find that review at: Review: "Darwin's Black Box, The Biochemical Challenge to Evolution" by Michael J. Behe .
Now, also, you omitted all references to the blood clotting stuff.
...because Behe has already been hammered on that point thorougly enough that he has pretty much stopped using it as an "example". He has been concentrating on the flagellum mostly, thus the focus of my response.
For pete's sake, lets get comprehensive here! In detail, discuss why gradual evolution of blood clotting with 10 protein feedback loops all working at once is actually quite feasible evolutionarily speaking.
Well, okay, since you insist... Check out The Evolution of Vertebrate Blood Clotting, or The evolution of vertebrate blood coagulation as viewed from a comparison of puffer fish and sea squirt genomes. Excerpt from the latter paper:
It is thought that 50–100 million years separate the appearances of urochordates (which include the sea squirt) and vertebrates. During that time the machinery for thrombin-catalyzed fibrin formation had to be concocted by gene duplication and the shuffling about of key modular domains. The relative times of duplicative events can be estimated by various means, the most obvious being the presence or absence of a gene in earlier diverging organisms, although it must be kept in mind that lineages may lose genes. Another way to gauge events is from the relative positions of various gene products on phylogenetic trees, earlier branching implying earlier appearance. In this regard, (pro)thrombin invariably appears lower on the phylogenetic trees than do the other vitamin K-dependent factors (Fig. 2).Also, Evolution of enzyme cascades from embryonic development to blood coagulation:The order of events can also be inferred by considering the most parsimonious route to assembling the various clusters of peripheral domains. Nine of the proteases under discussion can be accounted for by six domain-swapping events (Fig. 5). Indeed, the presence of a multiple-kringle protease in the sea squirt genome provides a reasonable model for a step-by-step parallel evolution of the clotting and lysis systems. It should be noted that a serine protease with only one kringle has been found in the ascidian Herdmania momus (36). Although numerous scenarios have been offered in the past about how modular exchange was involved in generating these schemes (refs. 4, 12, and 37–41, inter alia), the new genomic data now provide a realistic set of starting materials.
Recent delineation of the serine protease cascade controlling dorsal-ventral patterning during Drosophila embryogenesis allows this cascade to be compared with those controlling clotting and complement in vertebrates and invertebrates. The identification of discrete markers of serine protease evolution has made it possible to reconstruct the probable chronology of enzyme evolution and to gain new insights into functional linkages among the cascades. Here, it is proposed that a single ancestral developmental/immunity cascade gave rise to the protostome and deuterostome developmental, clotting and complement cascades. Extensive similarities suggest that these cascades were built by adding enzymes from the bottom of the cascade up and from similar macromolecular building blocks.That was the abstract. An excerpt from the text:
The downstream protease of the vertebrate clotting cascade (Fig. 1d), thrombin, belongs to the same lineage as complement factors C1r and C1s. The upstream and middle proteases of the clotting cascade (factors VII, IX and X) belong to the most modern lineage, that of horseshoe crab clotting factor C. Therefore, the lineage of thrombin is parental to that of the upstream and middle proteases of the clotting cascade (Table 1) and distinguishes it from the other vitamin-K-dependent clotting proteases (factors VII, IX and X, and protein C). This conclusion agrees with sequence and species comparisons implying that thrombin was the ancestral blood-clotting protein [11]. It also suggests that vertebrate blood clotting emerged as a by-product of innate immunity, because the entire functional core of vertebrate clotting shares ancestry with complement proteases.And if that's not enough, you could check these out:
Banyai, L., Varadi, A. and Patthy, L. (1983). “Common evolutionary origin of the fibrin-binding structures of fibronectin and tissue-type plasminogen activator.” FEBS Letters, 163(1): 37-41.And so on...
Bazan, J. F. (1990). “Structural design and molecular evolution of a cytokine receptor superfamily.” Proceedings of the National Academy of Sciences of the United States of America, 87(18): 6934-6938.
Blake, C. C. F., Harlos, K. and Holland, S. K. (1987). “Exon and Domain Evolution in the Proenzymes of Blood Coagulation and Fibrinolysis.” Cold Spring Harbor Symposia on Quantitative Biology: The Evolution of Catalytic Function, LII: 925-932.
Fornace AJ Jr, Cummings DE, Comeau CM, Kant JA, Crabtree GR. “The Structure of the human gamma-fibrinogen gene. Alternate mRNA splicing near the 3' end of the gene produces gamma A and gamma B forms of gamma-fibrinogen.” J Biol Chem. 1984 Oct 25;259(20):12826-30.
Crabtree, G. R., Comeau, C. M., Fowlkes, D. M., Fornace, A. J., Jr., Malley, J. D. and Kant, J. A. (1985). “Evolution and structure of the fibrinogen genes: Random insertion of introns or selective loss?” Journal of Molecular Biology, 185(1): 1-20.
Di Cera, E., Dang, Q. D. and Ayala, Y. M. (1997). “Molecular mechanisms of thrombin function.” Cell Mol Life Sci, 53(9): 701-730.
Doolittle, R. F. (1985). “More homologies among the vertebrate plasma proteins.” Biosci Rep, 5(10-11): 877-884.
Doolittle, R. F. (1990). “The Structure and Evolution of Vertebrate Fibrinogen A Comparison of the Lamprey and Mammalian Proteins,” in ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY: FIBRINOGEN, THROMBOSIS, COAGULATION, AND FIBRINOLYSIS. C. Y. Liu and Chien, S. New York, Plenum Press. 281.
Doolittle, R. F. (1992). “A detailed consideration of a principal domain of vertebrate fibrinogen and its relatives.” Protein Science, 1(12): 1563-1577.
Doolittle, R. F. (1992). “Early Evolution of the Vertebrate Fibrinogen Molecule.” Biophysical Journal, 61(2 PART 2): A410.
Doolittle, R. F. (1992). “Stein and Moore Award address. Reconstructing history with amino acid sequences.” Protein Science, 1(2): 191-200.
Doolittle, R. F. (1993). “The Evolution of Vertebrate Blood Coagulation - a Case of Yin and Yang.” Thrombosis and Haemostasis, V70(N1): 24-28.
Doolittle, R. F. and Feng, D. F. (1987). “Reconstructing the Evolution of Vertebrate Blood Coagulation from a Consideration of the Amino Acid Sequences of Clotting Proteins.” Cold Spring Harbor Symposia on Quantitative Biology: The Evolution of Catalytic Function, LII: 869-874.
Doolittle, R. F., G., Spraggon and J., Everse S. (1997). “Evolution of vertebrate fibrin formation and the process of its dissolution.” Ciba Found Symp, 212: 4-17; discussion 17-23.
Doolittle, R. F. and Riley, M. (1990). “The amino-terminal sequence of lobster fibrinogen reveals common ancestry with vitellogenins.” Biochemical and Biophysical Research Communications, 167(1): 16-19.
Edgington, T. S., Curtiss, L. K. and Plow, E. F. (1985). “A linkage between the hemostatic and immune systems embodied in the fibrinolytic release of lymphocyte suppressive peptides.” Journal of Immunology, 134(1): 471-477.
Ghidalia, W., Vendrely, R., Montmory, C., Coirault, Y., Samama, M., Lucet, B., Bellay, A. M. and Vergoz, D. (1989). “Overall study of the in vitro plasma clotting system in an invertebrate, Liocarcinus puber (Crustacea Decapoda): Considerations on the structure of the Crustacea plasma fibrinogen in relation to evolution.” Journal of Invertebrate Pathology, 53(2): 197-205.
Hervio, L. S., Coombs, G. S., Bergstrom, R. C., Trivedi, K., Corey, D. R. and Madison, E. L. (2000). “Negative selectivity and the evolution of protease cascades: the specificity of plasmin for peptide and protein substrates.” Chemistry & Biology, V7(N6): 443-452.
Hewett-Emmett, D., Czelusniak, J. and Goodman, M. (1981). “The evolutionary relationship of the enzymes involved in blood coagulation and hemostasis.” Annals of the New York Academy of Sciences, 370(20): 511-527.
Holland, S. K., Harlos, K. and Blake, C. C. F. (1987). “Deriving the generic structure of the fibronectin type II domain from the prothrombin Kringle 1 crystal structure.” EMBO (European Molecular Biology Organization) Journal, 6(7): 1875-1880.
Jordan, R. E. (1983). “Antithrombin in vertebrate species: conservation of the heparin-dependent anticoagulant mechanism.” Archives of Biochemistry and Biophysics, 227(2): 587-595.
Kant, J. A., Fornace, A. J., Jr., Saxe, D., Simon, M. J., McBride, O. W. and Crabtree, G. R. (1985). “Evolution and organization of the fibrinogen locus on chromosome 4: Gene duplication accompanied by transposition and inversion.” Proceedings of the National Academy of Sciences of the United States of America, 82(8): 2344-2348.
Kornblihtt, A. R., Pesce, C. G., Alonso, C. R., Cramer, P., Srebrow, A., Werbajh, S. and Muro, A. F. (1996). “The fibronectin gene as a model for splicing and transcription studies.” FASEB Journal, 10(2): 248-257.
Laki, K. (1972). “Our ancient heritage in blood clotting and some of its consequences.” Annals of the New York Academy of Sciences, 202(4): 297-307.
Neurath, H. (1984). “Evolution of proteolytic enzymes.” Science, 224(4647): 350-357.
Neurath, H. (1986). “The Versatility of Proteolytic Enzymes.” Journal of Cellular Biochemistry, 32(1): 35-50.
Oldberg, A. and Ruoslahti, E. (1986). “Evolution of the fibronectin gene: Exon structure of cell attachment domain.” Journal of Biological Chemistry, 261(5): 2113-2116.
Opal, S. M. (2000). “Phylogenetic and functional relationships between coagulation and the innate immune response.” Critical Care Medicine, V28(N9 SUPPS): S77-S80.
Pan, Y. and Doolittle, R. F. (1991). “Distribution of Introns in Lamprey Fibrinogen Genes.” Journal of Cellular Biochemistry Supplement(15 PART D): 75.
Pan, Y. and Doolittle, R. F. (1992). “cDNA sequence of a second fibrinogen alpha chain in lamprey: an archetypal version alignable with full-length beta and gamma chains.” Proceedings of the National Academy of Sciences of the United States of America, 89(6): 2066-2070.
Patthy, L. (1985). “Evolution of the Proteases of Blood Coagulation and Fibrinolysis by Assembly from Modules.” Cell, 41(3): 657-664.
Patthy, L. (1990). “Evolution of blood coagulation and fibrinolysis.” Blood Coagulation and Fibrinolysis, 1(2): 153-166.
Patthy, L. (1990). “Evolutionary Assembly of Blood Coagulation Proteins.” Seminars in Thrombosis and Hemostasis, 16(3): 245-259.
Patthy, L. (1999). “Genome evolution and the evolution of exon-shuffling—a review.” Gene, 238(1): 103-114.
Roberts, Lewis R., Nichols, Lanita A. and Holland, Lene J. (1995). “CDNA and amino-acid sequences and organization of the gene encoding the B-beta subunit of fibrinogen from Xenopus laevis.” Gene (Amsterdam), 160(2): 223-228.
Sosnoski, D. M., Emanuel, B. S., Hawkins, A. L., Van Tuinen, P., Ledbetter, D. H., Nussbaum, R. L., Kaos, F. T., Schwartz, E., Phillips, D. and et al. (1988). “Chromosomal localization of the genes for the vitronectin and fibronectin receptors .alpha. subunits and for platelet glycoproteins IIb and IIIa.” Journal of Clinical Investigation, 81(6): 1993-1998.
Wang, Y. Z., Patterson, J., Gray, J. E., Yu, C., Cottrell, B. A., Shimizu, A., Graham, D., Riley, M. and Doolittle, R. F. (1989). “Complete sequence of the lamprey fibrinogen .alpha. chain.” Biochemistry, 28(25): 9801-9806.
Xu, X. and Doolittle, R. F. (1990). “Presence of a vertebrate fibrinogen-like sequence in an echinoderm.” Proceedings of the National Academy of Sciences of the United States of America, 87(6): 2097-2101.
Zhang, Y. L., Hervio, L., Strandberg, L. and Madison, E. L. (1999). “Distinct contributions of residue 192 to the specificity of coagulation and fibrinolytic serine proteases.” Journal of Biological Chemistry, V274(N11): 7153-7156.
Zimmermann, E. (1983). “[The evolution of the coagulation system from primitive defense mechanisms].” Behring Institute Mitteilungen, 82(73): 1-12.
The 2.0-Å crystal structure of tachylectin 5A provides evidence for the common origin of the innate immunity and the blood coagulation systems
Davidson CJ, Tuddenham EG, McVey JH. 450 million years of hemostasis J Thromb Haemost. 2003 Jul;1(7):1487-94.
And even dogs ... you would agree folks that deliberately avoid dogs (or worse, refuse to own dogs; they can only handle cats) ... you'd agree dog owners vote for W. disproportionately. Right? I mean, look at how cute Barney is! (And remember what happened to Buddy?) Where are your links about how dogs can help the GOP? Or, is it this: Ayn Rand hated kids and dogs, and only kept cats ..... and its Ayn's Answers that will save the day? Would you say most scientist types love cats? I'm just asking mr. I....
You're going to feel pretty silly when you sober up in the morning.
And one other thing; what is your opinion regarding the fact that the overwhelming number of admissions to sex change hospitals feature hordes of men desperate to get rid of their equipment? Very, very few women will get caught alive or dead in a sex change clinic; why is that?
It's because the "default" sexuality for mammals during fetal development is female. It's only by action of genes on the "Y" chromosome that ontogeny is diverted down the developmental paths towards male physical and neurological development. Thus, it's "easier" for a genetic abnormality on the Y chromosome, or interference with development (e.g., fetal alcohol syndrome) to result in a genetic "XY" male which is not fully "imprinted" as a male, than it is for a genetic "XX" female to somehow acquire traits carried on the the "Y" chromosome (which "XX" individuals don't even *have*).
I mean, chances are good you have an opinion on this. Do you think that some men could have an autoimmune response to their own testosterone and that's what drives this madness?
No, see above.
And one last thing: have you read Shelly's 'Frankenstein'?
Yes, although it was pretty tedious in spots.
I expected you to fix the link. You did. I found the review to be unimpressive. I expected you to be comprehensive regarding the blood clotting stuff, and you were. Some of that stuff is interesting; but all of it is speculation.
I didn't expect you to provide links to my marriage stuff and how it relates to the GOP and why that is a good thing to spend time on ... and you didn't. For whatever reason, the health of the GOP, its bedrock support by marrieds ... to you, not worthy of consideration.
I didn't expect you to spend time on Ayn Rand and how she hated kids and dogs ... and you didn't.
I didn't expect you to respond to the sex change stuff, and surprise!, you exceeded my expectations!
So, to be clear, the primary cause of men lining up at the sex change clinics is abnormal fetal development due to genetic dis-switching on the Y chromosone in the womb? I'm interested in those links Mr. I. Where are they? And how unusual of you not to include them.
(This of course means you likely can provide links which discuss that homosexual males is an artifact of similar genetic misswitiching, correct? Evolution certainly wouldn't create 'gay men', correct?)
Btw, my impression about sex change clinics and the men who visit them has been greatly influenced by this observation: most fathers of those men appear not to care one bit about this act by their sons.
I never see articles, information which indicate support or opposition by the fathers of these sons for this kind of cutting edge decision making.
Now this observation is consistent w/ my observation that most men eager for the scalpel were also badly betrayed or more commonly, ignored, by the biological fathers; and, naturally, these men uniformly reject God. But I gather you would argue otherwise.
I am really curious now, more so, about my questions about marriage and kids and the GOP that you didn't answer.
So I have concluded that most gay men, and most men who travel to the sex change clinic share in common the desire to adopt the only identity that socially/psychologically they understand .... mom's. Although a tiny fraction do indeed suffer from bona fide detectable genetic disasters, most men, gay, transv, mass murderers, whatever .... genetically they are fully identifable as men and function biologically just fine.
A poor fathering 'imprint' is my primary understanding for all this gay nonsense. I can find plenty of links about that if you are interested; but maybe your links about how genetic all this nonsense is would be more compelling?
I do have a few issues though.
In post 104 you assert that a person doesn’t have to be atheist to support evolution. On this point, I agree – but the converse is true as well. A person who does not support the classic formulation of evolution ("random mutation + natural selection > species") - is not necessarily a religionist. Crick for instance was a panspermia supporter – and the arguments for cosmic ancestry are often indistinguishable from the arguments for Intelligent Design.
Frequently, on this forum, the defense of the theory of evolution overlooks the internal conflicts about the theory itself. IOW, among those who agree that evolution has happened, there are differences as to the mechanisms. Frequently the difference breaks between biologists-chemists-paleontologists on the one side - and physicists-mathematicians-astrobiologists on the other.
Or to put it in a different framework: if the age of the universe is understood by the correspondents to be old from our space/time coordinates (13.7 by) and the existence of a fossil record as a quantizing of the continuum is accepted – then the argument reduces to the interpretation of the evidence.
Darwin didn’t have the benefit of modern science when he proposed “random mutation + natural selection > species". Nowadays there are other interpretations on the table including “punctuated equilibrium”, “autonomous biological self organizing complexity”, "cosmic ancestry" and other formulations of Intelligent Design.
When I look at all of this – I truly don’t understand all the contention towards Intelligent Design supporters. ID doesn’t name a Designer and doesn’t deny either the age of the universe or the fossil record.
It is wrongful to argue with ID supporters as if they were Young Earth Creationists. We ought to look at the issues instead.
At bottom, all the newer formulations question how complexity arose in biological systems. Sadly, ID has introduced an unnecessary new type of complexity to ask those questions ---- but, most importantly, the underlying question is valid no matter who is doing the asking.
I strongly urge the combatants on these threads to lay down their verbal arms and take up the issue of complexity and biological systems to see if we can find some common ground to answer the basic question: what do the children in publicly funded K-12 schools need to know about the various interpretations of the evidence:
Here’s a start, to define the terminology:
Complexity is ...[the abstract notion of complexity has been captured in many different ways. Most, if not all of these, are related to each other and they fall into two classes of definitions]:
2) ...the (minimal) amount of time it takes to create the system.
Least Description
Definition: The minimum number of bits into which a string can be compressed without losing information. This is defined with respect to a fixed, but universal decompression scheme, given by a universal Turing machine.
Wikipedia: Cellular Automata (aka Self-Organizing Complexity)
A cellular automaton (plural: cellular automata) is a discrete model studied in computability theory and mathematics. It consists of an infinite, regular grid of cells, each in one of a finite number of states. The grid can be in any finite number of dimensions. Time is also discrete, and the state of a cell at time t is a function of the state of a finite number of cells called the neighborhood at time t-1. These neighbors are a selection of cells relative to some specified, and does not change (Though the cell itself may be in its neighborhood, it is not usually considered a neighbor). Every cell has the same rule for updating, based on the values in this neighbourhood. Each time the rules are applied to the whole grid a new generation is produced.
In this paper, we skirt the issue of structural and functional complexity by examining genomic complexity. It is tempting to believe that genomic complexity is mirrored in functional complexity and vice versa. Such an hypothesis, however, hinges upon both the aforementioned ambiguous definition of complexity and the obvious difficulty of matching genes with function. Several developments allow us to bring a new perspective to this old problem. On the one hand, genomic complexity can be defined in a consistent information-theoretic manner [the "physical" complexity (4)], which appears to encompass intuitive notions of complexity used in the analysis of genomic structure and organization (5). On the other hand, it has been shown that evolution can be observed in an artificial medium (6, 7), providing a unique glimpse at universal aspects of the evolutionary process in a computational world. In this system, the symbolic sequences subject to evolution are computer programs that have the ability to self-replicate via the execution of their own code. In this respect, they are computational analogs of catalytically active RNA sequences that serve as the templates of their own reproduction. In populations of such sequences that adapt to their world (inside of a computer's memory), noisy self-replication coupled with finite resources and an information-rich environment leads to a growth in sequence length as the digital organisms incorporate more and more information about their environment into their genome. Evolution in an information-poor landscape, on the contrary, leads to selection for replication only, and a shrinking genome size as in the experiments of Spiegelman and colleagues (8). These populations allow us to observe the growth of physical complexity explicitly, and also to distinguish distinct evolutionary pressures acting on the genome and analyze them in a mathematical framework.
If an organism's complexity is a reflection of the physical complexity of its genome (as we assume here), the latter is of prime importance in evolutionary theory. Physical complexity, roughly speaking, reflects the number of base pairs in a sequence that are functional. As is well known, equating genomic complexity with genome length in base pairs gives rise to a conundrum (known as the C-value paradox) because large variations in genomic complexity (in particular in eukaryotes) seem to bear little relation to the differences in organismic complexity (9). The C-value paradox is partly resolved by recognizing that not all of DNA is functional: that there is a neutral fraction that can vary from species to species. If we were able to monitor the non-neutral fraction, it is likely that a significant increase in this fraction could be observed throughout at least the early course of evolution. For the later period, in particular the later Phanerozoic Era, it is unlikely that the growth in complexity of genomes is due solely to innovations in which genes with novel functions arise de novo. Indeed, most of the enzyme activity classes in mammals, for example, are already present in prokaryotes (10). Rather, gene duplication events leading to repetitive DNA and subsequent diversification (11) as well as the evolution of gene regulation patterns appears to be a more likely scenario for this stage. Still, we believe that the Maxwell Demon mechanism described below is at work during all phases of evolution and provides the driving force toward ever increasing complexity in the natural world.
Given a system whose function we want to specify, for which the environmental (input) variables have a complexity of C(e), and the actions of the system have a complexity of C(a), then the complexity of specification of the function of the system is:
Wikipedia: Irreducible Complexity
The term "irreducible complexity" is defined by Behe as:
In his recent book The Fifth Miracle, Paul Davies suggests that any laws capable of explaining the origin of life must be radically different from scientific laws known to date. The problem, as he sees it, with currently known scientific laws, like the laws of chemistry and physics, is that they are not up to explaining the key feature of life that needs to be explained. That feature is specified complexity. Life is both complex and specified. The basic intuition here is straightforward. A single letter of the alphabet is specified without being complex (i.e., it conforms to an independently given pattern but is simple). A long sequence of random letters is complex without being specified (i.e., it requires a complicated instruction-set to characterize but conforms to no independently given pattern). A Shakespearean sonnet is both complex and specified...
How does the scientific community explain specified complexity? Usually via an evolutionary algorithm. By an evolutionary algorithm I mean any algorithm that generates contingency via some chance process and then sifts the so-generated contingency via some law-like process. The Darwinian mutation-selection mechanism, neural nets, and genetic algorithms all fall within this broad definition of evolutionary algorithms. Now the problem with invoking evolutionary algorithms to explain specified complexity at the origin of life is absence of any identifiable evolutionary algorithm that might account for it. Once life has started and self-replication has begun, the Darwinian mechanism is usually invoked to explain the specified complexity of living things.
But what is the relevant evolutionary algorithm that drives chemical evolution? No convincing answer has been given to date. To be sure, one can hope that an evolutionary algorithm that generates specified complexity at the origin of life exists and remains to be discovered. Manfred Eigen, for instance, writes, "Our task is to find an algorithm, a natural law that leads to the origin of information," where by "information" I understand him to mean specified complexity. But if some evolutionary algorithm can be found to account for the origin of life, it would not be a radically new law in Davies's sense. Rather, it would be a special case of a known process.
Principia Cybernetica: Metatransition (a kind of punctuated equilibrium)
Consider a system S of any kind. Suppose that there is a way to make some number of copies from it, possibly with variations. Suppose that these systems are united into a new system S' which has the systems of the S type as its subsystems, and includes also an additional mechanism which controls the behavior and production of the S-subsystems. Then we call S' a metasystem with respect to S, and the creation of S' a metasystem transition. As a result of consecutive metasystem transitions a multilevel structure of control arises, which allows complicated forms of behavior.