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Posted on 03/10/2006 6:12:05 AM PST by DaveLoneRanger
This story is not about Enron and Exxon, but about introns and exons. The proportions of the scandals they are causing in evolutionary theory, however, may be comparable.
Introns are spacers between genes. For several decades now, it has been a puzzle why they are there, and why a complex machine called a spliceosome takes them out and joins the active genetic parts – the exons – together. Only eukaryotes have spliceosomes, though; mitochondria have “group II introns” and some mRNAs may have them. Their presence and numbers in various groups presents a bewildering array of combinations. Figuring out a phylogenetic tree for introns has eluded evolutionary geneticists, as has understanding their origin and functions ((02/18/2005).). Why do genes come in pieces that have to be reassembled?
William Martin and Eugene Koonin said in Nature1 that “The discovery of introns had a broad effect on thoughts about early evolution.” Some theories have been falsified, and others remain in the running. Consider the scope of the problems:
A current consensus on introns would be that prokaryotes do indeed have group II introns but that they never had spliceosomes; hence, streamlining in the original sense (that is, loss of spliceosomal introns) never occurred in prokaryotes, although it did occur in some eukaryotes such as yeast or microsporidia. An expansion of that consensus would be that spliceosomes and spliceosomal introns are universal among eukaryotes, that group II introns originating from the mitochondrion are indeed the most likely precursors of eukaryotic mRNA introns and spliceosomal snRNAs, and that many—conceivably most—eukaryotic introns are as old as eukaryotes themselves. More recent are the insights that there is virtually no evolutionary grade detectable in the origin of the spliceosome, which apparently was present in its (almost) fully fledged state in the common ancestor of eukaryotic lineages studied so far, and that the suspected source of introns—mitochondria, including their anaerobic forms, hydrogenosomes and mitosomes—was also present in the common ancestor of contemporary eukaryotes (the only ones whose origin or attributes require explanation).This means that a complex molecular machine, the spliceosome (09/17/2004, 09/12/2002), appeared fully formed almost abruptly, and that the intron invasion took place over a short time and has not changed for hundreds of millions of years. They submitted a new hypothesis:
This suggests that intron origin and spread occurred within a narrow window of evolutionary time: subsequent to the origin of the mitochondrion, but before the diversification of the major eukaryotic lineages. This, in turn, indicates the existence of a turbulent phase of genome evolution in the wake of mitochondrial origin, during which group II introns invaded the host’s chromosomes, spread as transposable elements into hundreds—perhaps thousands—of positions that have been conserved to the present, and fragmented into both mRNA introns and snRNA constituents of the spliceosome.
Here we revisit the possible evolutionary significance of introns in light of mitochondrial ubiquity. We propose that the spread of group II introns and their mutational decay into spliceosomal introns created a strong selective pressure to exclude ribosomes from the vicinity of the chromosomes—thus breaking the prokaryotic paradigm of co-transcriptional translation and forcing nucleus-cytosol compartmentalization, which allowed translation to occur on properly matured mRNAs only. (Emphasis added in all quotes.)But this means that the nucleus, nucleolus and other complex structures also had to appear in a very brief period of time. It means that the engulfed organism that somehow became mitochondria had to transfer its introns rapidly into a genome lacking a nucleus. It means the nucleus had to evolve quickly to segregate the new mitochondrial genes from the nuclear genes. A lot had to happen quickly. “This bipartite cell would not be an immediate success story: it would have nothing but problems instead,” they admitted, but they believed that natural selection would favor the few that worked out a symbiotic relationship with their new invaders.
A problem of a much more severe nature arises, however, with the mutational decay of group II introns, resulting in inactivation of the maturase and/or RNA structural elements in at least some of the disseminated copies. Modern examples from prokaryotes and organelles suggest that splicing with the help of maturase and RNA structural elements provided by intact group II introns in trans could have initially rescued gene expression at such loci, although maturase action in trans is much less effective than in cis. Thus, the decay of the maturase gene in disseminated introns poses a requirement for invention of a new splicing machinery. However, as discussed below, the transition to spliceosome-dependent splicing will also impose an unforgiving demand for inventions in addition to the spliceosome.A spliceosome is not an easy thing to invent; it has five snRNAs and over 200 proteins, making it one of the most complex molecular machines in the cell. Not only that, they appeared in primitive eukaryotes and have been largely conserved since. Perhaps the miracles can be made more believable by dividing them into smaller steps:
It seems that the protospliceosome recruited the Sm-domain, possibly to replace the maturase, while retaining group II RNA domains (snRNAs) ancestrally germane to the splicing mechanism. While the later evolution of the spliceosome entailed diversification with the recruitment of additional proteins—leading to greater efficiency—the simpler, ancestral protospliceosome could, in principle, rescue expression of genes containing degenerate group II introns in a maturase-independent manner, but at the dear cost of speed.Will a lateral pass from maturase to incipient spliceosome during a long field run lead to a touchdown? If a stumbling protospliceosome could survive, in spite of vastly decreased translation rate, it might have been able to run the distance with natural selection’s encouragement, they think. Players would be falling left and right in this “extremely unhealthy situation,” they say, and “the prospects of any descendants emerging from this situation are bleak.” How could the game go on, then? “The only recognizable mechanism operating in favour of this clumsy chimaera is weakened purifying selection operating on its exceptionally small initial population.” Purifying selection means weeding out losers, not adding new champions. “Finding a solution to the new problem of slow spliceosomes in the presence of fast and abundant ribosomes required an evolutionary novelty.”
Was any of this storytelling useful? The shenanigans they pulled, couched in biochemical jargon, can be summarized by two principles in their own imaginations: (1) since the cell needed these superbly-crafted machines, it had to invent them somehow, and (2) since evolution is a fact, it had to happen somehow. Do you catch any hint of a mechanism for actually inventing a 200-protein supermachine that would actually work? Did you find any hint that any cell any time had a “protospliceosome” that only worked half-way? All this was pure fiction built on childlike faith in evolution.
Presenting a hypothesis in science is fine, but how would they ever test something like this? They offered a few tests that could discriminate between their just-so story and other just-so stories, but nothing that could explain how a spliceosome, or a nuclear membrane with its elaborate pore complexes, or nonsense-mediated decay could have been invented from scratch just because a cell needed these things.
Would that evolutionists would get off this storytelling kick and do something useful with their lives. Let’s find a cure for cancer. Let’s find better sources of energy, and think of ways to reduce risks of disease and terrorism, and use science to improve our lives and our world. Stringing together uncooperative data into a fictional account of prehistory will accomplish nothing and is wasting time and money in a world desperately in need of the productive possibilities of true science.
Huh????
Here we go again...
The splicesomes connected to the exon
the exons connected to the introns
oh them genes oh them genes
oh them species creating genes
I would love to see any evolutionist refute this in a purely scientific manner. No name calling, just refute it without calling into question its source or the agenda of the source. Can it be done?
Hmmm.
So I'm assuming that the summary of this is, "We don't understand it yet, so Godddidit."
Well, it is perfectly clear: evolution looks so good if your mind is limited..ID is obvious if your view is unlimited.
Most grad students intron during their studies, but I'll admit the above is new to me.
I saw it on the internet therefore it must be true.
LOL - now THAT I can understand.
Good post. I view evolution as a working hypothesis, not as a fact. I lump it in with “junk genes”, “dark matter” and quantum mathematics. IHMO these are useful frameworks for studying thing that we don’t understand.
Good way of saying it.......................
How true! I am a molecular biologist and worked for years on a form of breast cancer in mice. Oh, how I loved it! Going to the library to check out the latest research was like checking your mail for a letter from a loved one. Then it hit me like a rock. I was helping the principal investigator write the "relevance" section of an NIH grant and I realized that everything I was writting was a bunch of hot air. That particular form of breast cancer had nothing in common with human breast cancer. Research was fun, intellectually stimulating... whatever! There were a few dozen people around the world who were just as excited to read my papers as I was to read theirs... and that was all there was to it. It was a very exclusive club for pampered people, all paid by taxpayer money. I dropped out as soon as I could. I've lost the prestige, the easy life of a tenured research professor, and I'm proud of it! I'm not saying that research is wrong, but millions of dollars are spent in areas that will never help cure a disease or make life better for anyone.
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Huh?
For those seeking the truth (as your tag line says) you may want to add these perspectives to your mix of information gathering:
Introns of ancient origins
http://www.talkorigins.org/faqs/evolution-research.html
This is number 13 in my series of postings about current research in evolution. I'll summarize two papers from a recent issue of Science, both of which basically reported the same finding. I'm kind of pressed for time today, so this will be a bare bones summary. But, as always, I'll supply the references.
First a bit of background. In eukaryotes, (basically all organisms except bacteria) genes typically are not found as a single uninterrupted reading frame. There are sequences interspersed within the coding region of genes. They are excised after the DNA is translated into RNA. These excised DNA sequences are called introns (the coding DNA sequences are called exons).
In the two papers I will summarize, the authors present evidence of an ancient origin for introns.
According to the endosymbiotic hypothesis of eukaryote evolution, modern day chloroplasts are the descendents of ancient cyanobacteria. These cyanobacteria were engulfed by an ancient cell and a symbiotic relationship was established such that the cyanobacteria simply continued to live inside the engulfing cell. There are also free living cyanobacteria alive today. The authors of the papers document the presence of an intron in a gene of both modern day cyanobacteria and chloroplasts. In both cases this intron is the same type in all the genes looked at (it is a group I intron) and it is also in the same position. They argue that this implies the intron was present in the gene before ancient cyanobacteria split into its two present day lineages (modern cyanobacteria and chloroplasts).
In the first paper the authors document a group I intron in the same position in the leucine tRNA gene in two species of Anabena (cyanobacteria) and in the chloroplasts of several land plants (bean, liverwort, maize, rice and tobacco). In the second paper the authors (a different bunch of fellows) show a group I intron in the leucine tRNA gene in five species of cyanobacteria and many chloroplasts from very different plants.
From these data the authors (in both papers) argue that this is evidence for the intron predating the split of modern cyanobacteria and chloroplasts. If the common ancestor of these two groups (ancient cyanobacteria) had this intron in that position, it's current distribution can be explained by simple inheritance; both lineages retained it. The alternate explanation would be that the intron invaded all these lineages. Group I introns are mobile in some lineages; they can excise themselves from one stretch of DNA and insert themselves in another. However, it is highly unlikely that the same type of intron would plunk down in the same spot in all these genes. The first hypothesis (the intron was in the common ancestor) is, IMHO, much more likely.
References
Xu, et. al., Bacterial Origin of a Chloroplast Intron: Conserved Self-Splicing Group I Introns in Cyanobacteria, Science 250: 1566 - 1569
Kuhsel, et. al., An Ancient Group I Intron Shared by Eubacteria and Chloroplasts, Science 250: 1570 - 1572
*
Review of Michael Denton's Evolution: A Theory in Crisis
http://www.talkorigins.org/faqs/denton.html
Excerpt:
"...As for molecular data, Denton makes a show of cytochrome-c amino acid substitution numbers appearing to divide all life into typologically distinct classes. But this kind of division is to be expected, considering that we derived the numbers from contemporary organisms, and not from fossilized organisms. If we were able to extract DNA from enough fossils, the typological boundaries would break down. In no way is the molecular data incompatible with evolution. Denton charges that neutral amino acid replacement would not give such perfectly typological results because different organisms have different rates of mutation per generation. In response:
"There are many factors affecting mutation rates. They are not simply dependent on "number of generations". You see, it a species reproduces every twenty five years, as opposed to every two hours, you could suggest that the two hour species evolves "faster" or that it has a higher mutation rate. But that is patently a misconception. During the 25 years that the other species is not reproducing, its gametes are nonetheless (well its germ cells) subject to mutations; indeed a lot of mutations could accumulate in its 25 yrs generation time. So most emphatically, no: mutation rates are not understood to be dependent on the number of generations." ~ (Ladomery, 1995)
Given this, evolutionary processes would be expected to yield the molecular data shown. Moreover, there are sequences of DNA (called "introns") that are excised from RNA copies before translation, and these introns, despite never being subject to selective effects, give the same general pattern as cytochrome-c amino acid sequences - namely the degree of similarity that evolutionists have come to expect. The fact that this pattern is maintained for a sequence of nucleotides that can mutate freely without consequence indicates that the organisms containing them have shared ancestry (because before they split off, their intron nucleotide sequences could not possibly diverge!). The fact that introns reveal the same "distance" between classes as functional sequences rather than giving wildly different distances may well be damaging to typology, unless we presume the archetype contains archetypal non-functional sequences. In any case, without a typological process proposed to support the typological interpretation of the molecular evidence, the evolutionary mechanism wins over and the molecular evidence is shown to reveal an evolutionary pattern. ..." [snip]
*
Christian Forums
http://www.christianforums.com/t110746
4th April 2004, 07:18 AM Essay by caravelair
Evolution was much easier to attack in Darwins time, especially since the mechanism of inheritance was not yet known. Since then, evolution by mutation and natural selection has been directly observed both in the lab and the field, and corroborated by genetic studies. As a result, even creationists have been forced to accept that evolution does occur, at least on a small scale. So now, in order to deny macroevolution or common descent, the creationist must argue that the evolution we observe today is not the type of modification that would add up to large-scale morphological change. Perhaps the most commonly used argument today is that mutations do not add information to the genome, and that this is required for common descent via mutation and selection. The aim of this paper is to address this general argument, and show that it is not valid.
Since the information argument is considered by creationists to be quite important, and is quite commonly used, it therefore deserves special attention. Phillip E. Johnson is a professor of law, and author of well-known creationist books such as Darwin On Trial. In an interview with the Christian magazine Touchstone, Johnson commented on the argument in question:
You have said there is no natural explanation for the rise of genetic information. How important is that question in the debate?"
PJ: The Wedge of Truth is all about those issues. The scientific key is, "No natural processes create genetic information." As soon as we get that out, theres only one way the debate can go because Darwinists arent going to come up with a mechanism Once you get that in the debate, then we will be poised for a metaphysical and intellectual reversal that is every bit as profound as the one with Copernicus. (5).
Clearly, the argument is one worth addressing. Either it says something very important, or it is misleading those who think it does.
Before addressing the argument, it is important to understand exactly what it implies. It would not refute common descent, because the case for common descent is independent of any specific mechanism. That is, the evidence in support of common descent does not assume the validity of mutation and natural selection as a mechanism for that change (15). Furthermore, the inability to gain information would not prevent all types of macroevolutionary change. For example, it is unclear that the information content of other mammals genomes is any less than that of our own. So even if we assume mutations cannot add information to the genome, mutation and natural selection would not be prevented from successfully explaining macroevolutionary changes such as that from early apes to modern humans. So what would the argument tell us, if it were indeed correct? Information theorist David J.C. MacKay says Evolution has been happening on earth for about the last 109 years. Undeniably, information has been acquired during this process. (7: p269). This is something that is generally agreed upon. So what the argument would show, if it were correct, is that mutation and selection could never sufficiently account for the descent of all modern species from a common ancestor.
It should be noted at this point, that it is not at all necessary to consider information to examine the change of genomic properties in question. What were really talking about here is how the complexity of the genome can change. In an article published in Science called The Origins of Genome Complexity,
The ~100 fully sequenced eubacterial and archaeal genomes contain between 350 and 6000 genes, packed into 0.6 to 7.6 megabases (Mb) all well-characterized genomes of animals and plants contain more than 13,000 genes in at least 100Mb Accompanying the increase in gene number in multicellular species is an expansion in the size and number of intragenic spacers (introns) and a dramatic proliferation of mobile genetic elements. (3: p1401).
No one is claiming this list to be exhaustive of the differences in genomes, but it is interesting to note that these types of changes do indeed occur.
There are a few ways that gene number can be increased, including Molecular mechanisms such as illegitimate recombination and LINE element mediated 3' transduction underlying exon shuffling (6). Another mechanism is duplication mutation. It is estimated that 15,000 of the 40,000 genes in the human genome were acquired in this way (12). In this type of mutation, we get a second copy of some functional gene. Although this new gene will initially be the same as the gene it was copied from, Preservation of both members of a duplicate pair can be promoted when one member of the pair acquires a beneficial mutation at the expense of an original essential function retained by the other (neofunctionalization). (3: p1401). So, subsequent mutation of the new gene can result in a novel gene, while preserving the increased total number of genes. For example, from the pancreatic ribonuclease gene (RNASE1) in a leaf-eating monkey, a duplication and subsequent mutation resulted in a second gene (RNASE1B), which functions differently than its parent gene (11). Other examples abound in the primary literature, as an online search of the PubMed database will show.
Introns are non-coding sections of DNA that occur within a gene. Introns are found between exons, which code for functional domains of the protein corresponding to the gene. The size of an intron can be increased by an insertion mutation. Introns are non-coding, so changing an intron in this way may not affect the protein produced by the gene at all. There is not much certainty about how new introns are introduced, but among other theories, there is evidence for the insertion of new introns in certain genes. For example, there is evidence for the insertion of an intron into the sex-determining gene, SRY, of dasyurid marsupials. The scientists who determined this say [their] data demonstrate that introns may be inserted as spliced units within a developmentally crucial gene without disrupting its function. (10: p1653). The total number of introns in the genome can also be increased by duplication of genes with introns.
It is also interesting to note that a multicellular form of the green alga, Chlorella vulgaris, has evolved in the lab from the usual unicellular form (2).
So we have seen specific examples of the type of change that occurred during the evolution of modern species from our prokaryotic ancestors. We will now examine whether information theory has any implications for this problem.
By this point, an important question should be coming to mind. What is information, exactly? The intuitive meaning is obvious, but to talk about changes in information content, we need a formal, quantifiable definition. This question deserves special attention, because the validity of the information argument is dependant on how we define evolution. Unfortunately, our question has no simple answer. The information content of something depends on how information is defined, and there is no one right way to do that. A definition may be useful in answering one question, but meaningless to another. In his book Information Theory, Inference, and Learning Algorithms, MacKay poses the question of why some organisms reproduce sexually, rather than asexually. By MacKays model, asexually reproducing populations can gain 1 bit of information per generation, while the number of bits that a sexually reproducing population can accumulate is up to the square root of the size of the genome (7: p269). However, creationists are unlikely to define information the way MacKay did in his example.
Unfortunately, most creationists use the term information without explicitly stating what information is. This is often the main strength of the information argument for creationists. Without a formal definition of information, we cant really say what type of change in the genome would represent increased information and in turn, it is then difficult to provide an example of such a change by mutation. One should be weary of any argument involving information content where the term is not explicitly defined.
Even without a strict definition of information, something can be said about the information argument. There is no shortage of creationist claims that certain mutations represent a loss of information. This exposes a problem with the information argument, because for any mutation, the opposite mutation is also possible, and in many cases, equally likely. So if a mutation can result in a loss of information, then surely the opposite mutation would mean a gain of information; if information can be lost, it can certainly be gained as well.
Dr. Lee Spetner has been more cooperative than other creationists in defining information. In an online exchange with Dr. Edward E. Max, Spetner says I thought it rather obvious that a mutation that destroys the functionality of a gene (such as a repressor gene) is a loss of information. I also thought it rather obvious that a mutation that reduces the specificity of an enzyme is also a loss of information. (13). This gives us an idea of what is considered to be a gain of information. If the loss of gene functionality is a loss of information, surely gaining a new functional gene would be a gain of information. An example of this has already been provided, but there are others that are of interest. For example, a frame shift mutation in a Japanese bacterium gave it the ability to digest nylon waste (16). Since the bacteria did not previously have this ability, this is a new biological function, and thus represents an increase in information. Spetner agrees, but contends that the mutation was not a random occurrence (14). Creationist organization Answers in Genesis claims that because the gene is on a plasmid, it has likely always existed, and was just transferred to the bacteria from another strain (1). However, nylon is an artificial compound that did not exist until it was invented in the 30s, and bacteria with the gene require nylon to survive. The gene, therefore, could not have existed before the 30s. This example is especially interesting in that the nylon digesting ability has given these bacteria an entirely new ecological niche to inhabit. One in which they have no competition but each other!
A well-known, good example of increased protein specificity is the evolution of a mutant version of a protein called Apolipoprotein AI (Apo-AI) in a small Italian community. The new version of the protein, Apo-AIM (the M is for Milano) is associated with reduced risk of arteriosclerosis, heart attack, and stroke.
Apo-AI is a lipid-binding protein and is the major component of High Density Lipoprotein (HDL) particles, which play an important role in removing cholesterol from cells. Subsequent detailed research of the Apo-AIM mutation has demonstrated that it has improved biological function that directly contributes to lowering the incidence of cardiovascular disease in the individuals carrying it. (8).
It works by actively stimulating cholesterol removal from cells (8). It also prevents some of the inflammatory damage of arteriosclerosis because of its antioxidant ability (8). Incidentally, the antioxidant ability is a new biological function, not possessed by the original Apo-AI protein (8). It has been shown that Apo-AIM is 1) of a more complex tertiary structure 2) more stable and 3) activates cholesterol efflux more effectively than Apo-AI. Furthermore, Apo-AIM has an antioxidant activity not present in Apo-AI that is sequence and substrate specific. (8). The mutation therefore represents increased specificity, and consequently is an increase in information by Spetners standards.
Footnotes:
(1) Answers in Genesis. That depends on what your definition of information is. Answers in Genesis. [Online]. Available: http://www.answersingenesis.org/home...e7-24-2000.asp, Jan. 12, 2004.
(2) Boraas, Martin E. and Boxhorn, Joseph E. and Seale, Dianne B. 1998. Phagotrophy by a flagellate selects for colonial prey: A possible origin of multicellularity. Evolutionary Ecology. 12 (2): 153-164. Also available online: http://www.kluweronline.com/oasis.htm/171545, Jan. 12, 2004.
(3) Conery, John S. and Lynch, Michael. 2003. The Origins of Genome Complexity. Science. 302: 1401-04.
(4) Isaak, Mark. Ed. Index to Creationist Claims. The Talk.Origins Archive. 2003. [Online]. Available: http://www.talkorigins.org/indexcc/CA/CA111.html, Jan. 12, 2004.
(5) Interview with Phillip E. Johnson. Touchstone Magazine. 2002. Available online:
http://www.touchstonemag.com/docs/is.../15-5pg40.html
(6) Long, M. 2001. Evolution of Novel Genes. Current Opinion in Genetics & Development. Dec. 11(6): 673-80. Reproduced in PubMed. [Online]. Available: http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract, Jan. 12, 2004.
(7) MacKay, David J.C. Information Theory, Inference, and Learning Algorithms. Cambridge University Press, 2003. Also available online: http://www.cs.toronto.edu/~mackay/itprnn/book.pdf.
(8) Musgrave, Ian, and Pirie-Shepherd, Steven, and Theobald, Douglas. 2003. Apolipoprotein AI Mutations and Information. The Talk.Origins Archive. [Online]. Available: http://www.talkorigins.org/faqs/info...poprotein.html, Jan. 12, 2004.
(9) National Center for Science Education. Voices for Evolution National Center for Science Education. [Online]. Available: http://www.ncseweb.org/article.asp?category=2, Jan. 12, 2004.
(10) Nei, Masatoshi. Ed. De novo insertion of an intron into the mammalian sex determining gene, SRY. Proceedings of the National Academy of Sciences of the USA. 1998 February 17; 95 (4): 16531657. [Online]. Available: http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract, Jan. 12, 2004.
(11) Rosenberg, Helene F. and Zhang, Jianzhi and Zhang, Ya-ping. Adaptive evolution of a duplicated pancreatic ribonuclease gene in a leaf-eating monkey. Nature. 30 no. 4: 411-415. [Online]. Available: http://www.nature.com/cgi-taf/DynaPa...abs/ng852.html, Jan. 12, 2004.
(12) Ross-Flannigan, Nancy. Ed. How gene duplication helps in adapting to changing environments. University of Michigan News and Information Services. [Online]. Available: http://www.umich.edu/~newsinfo/Relea.../r022802b.html, Jan. 12, 2004.
(13) Spetner, Lee. Lee Spetner/Edward Max Dialogue. The True.Origins Archive. [Online]. 2002. Available: http://www.trueorigins.org/spetner2.asp, Jan. 12, 2004.
(14) Spetner, Lee. The Nylon Bug. [Online]. 2002. Available: http://members.tripod.com/aslodge/id89.htm, Jan. 12, 2004.
(15) Theobald, Douglas, PhD. 29+ Evidences for Macroevolution: The Scientific Case for Common Descent. The Talk.Origins Archive. [Online] http://www.talkorigins.org/faqs/comdesc/, Jan. 12, 2004.
(16) Thomas, Dave. Evolution and Information. New Mexicans for Science and Reason. [Online]. Available http://www.nmsr.org/nylon.htm, Jan. 12, 2004.
4th April 2004, 11:55 AM Comment by Aggie
This is one of the best explanations of this I've seen here. You should consider sending it to Talk.Origins--my one suggestion if you do is that you not use Talk.Origins as a source, since they would probably prefer that their articles refer to the primary material.
Someone should keep track of this essay so we can bump it each time creationists use their "no new information" argument.
[snip]
Spamming evangelistic tracts I see.
Appreciated them.
If future humans were to discover a working, functional microprocessor chip imbedded in the rock of some distant world, would they assume that some intelligent being designed and manufactured the chip, or that it was the result of random processes of nature acting upon silicon over billions of years? What would Occam's Razor dictate in such a case?
A single living cell is far more complex than any microprocessor chip.
Natural selection of species in a functioning biosphere is one thing, but abiogenesis is something else entirely. The idea that a functioning, living cell of any kind -- much less a human cell - could have just sort of accidentally happened is ludicrous.
Speciation may or may not be the result of natural processes, but the cell is not. Life is an artifact.
I can't find the article I read recently to that talked about how virus's are the missing link here.
Basically, a new very large class of virus's have been found whose genes predate the three other cell types. So these virus's are being touted as being the missing link between organic and inorganic chemistry and their behavior makes for a better fit to the first fusion of the mitochondria and the cell.
"nylon is an artificial compound that did not exist until it was invented in the 30s, and bacteria with the gene require nylon to survive."
Picky eaters, maybe we can train them to eat all manner of waste and I can quit lugging the garbage can out to the street every week.
No, more like Evolutionists, as usual, don't wish to understand what God has told us, so they pretend that God didn't do it.
Maybe initially. But if they then observed a continual progression of older, slightly simpler chips also embedded in the rocks. And observed that chips merge together with other chips and create different chips that are a combination of features of each chip. And observed that recombinant chips that are more complex and more successful will then have a greater chance of creating more chips. And observed a means for how these chips would pass their improvements on to the new chips they created. And observed that of all the different chips doing a myriad of very different calculations and running very different computers, they all shared a very large base of identical circuitry. And observed that if all the similar chips are grouped together, a tree like structure is created showing convergence as they go back in time.
At that point they would logically assume these chips have been slowly building from one or a small number of simple base chips.
(Apologies for the awful punctuation/gramar).
Before they could make such an assumption, they would have to explain the source of the potatoes.
But first they would have to explain how the simplest chip precursor (a single integrated circuit, say) somehow magically developed by random chance, then magically developed the ability to split in two, recombine, and grow new circuits by random chance, and how all these randomly-produced circuits became magically able to work together in systems, developing their own energy sources and specialized functions, all by sheer luck.
It's hard enough creating chips that work by design. To assume that something as complex as a VLSILC could appear by the random action of radiation, wind, and liquid upon silicon is fantastic.
That's "fantastic" as in "fantasy".
Dr. Valadkhan has been doing some fascinating and ground-breaking work on finding the minimal spliceosome. In breaking down the spliceosome to its functional parts she has succeeded in making a 2 RNA spliceosome. I'll see if I can post some of her research later if I have time.
http://www.rnaresearch.org/valadkhan.htm
See, now that's what I'm talkin' about! When they start out with a premise that is wrong to begin with, it's all wrong, and it just gets deeper and deeper, generating distance from the facts.
They still show "ape to human" devolopement through evolution in "scientific texts" that have long since been proven incorrect. Example: Neanerthal Man=Man
Nebraska Man=A pig tooth
Piltdown Man=Jawbone of an ape
connected to the
braindcase of a man
Ramapithicus=Ape
Still shown as examples of evolution. How can this be with the approval of the "scientific community??? Maybe science it is not Hmmmmm? Maybe religion more like. (Yoda)Sorry!
To assume that something as complex as a VLSILC could appear by the random action of radiation, wind, and liquid upon silicon is fantastic.Indeed. Who is suggesting this is analogous to evolutionary theory? Those arguing against it, whether by ignorance or design. One of the legion of strawmen.
Twas brillig in the mimsywabe.....
Not so...
...some is solder!
No, you've broken the analogy. The Theory of Evolution doesn't address how the first life forms came to being, just how it's obvious that today's life formed from simpler earlier organisms. (Something that ID denies).
A better way to say it is: "God did it. Let us try to understand what it is and how it works."
Thanks for the ping!
I never said anything about evolution by natural selection being false. It is apparent from the best evidence that species change over time via natural selection. Speciation via natural selection is not so well grounded in the evidence, but I won't say it couldn't have happened that way.
What I am saying is that the materialist hypothesis that lies at the basis of scientific thought is itself non-scientific: that an objective universe of matter, energy, space, and time (MEST) exists, and that this Universe constitutes the whole of reality. As a (hopefully) sane man, I accept the existence of the MEST universe on faith; however, I do not accept the undemonstrable (and thus unscientific) claim that the MEST universe is All There Is.
In like manner I do not accept the undemonstrable and unscientific idea of abiogenesis.
Instead, I believe (and the evidence suggests) that the MEST Universe in all its complexity and beauty is an artifact; in fact, by every standard of esthetics, it fits the definition of Art. And if the cosmos is a collection of artworks, there must logically be an Artist, outside of and superior to His work.
There is such an Artist, Whom men call God; and Life -- with the human person at its pinnacle -- is His magnum opus.
Goodness. Where are the obligatory bon mots and slanderous "Luddite bumps" from the Usual Suspects?!
Archive
Ah yes, the "bump without responding to the poster" tactic...
I asked to be put on your ping list.
If you don't want me I'll see if the other
guys will take me.
If you would be so kind as to show me why it is wrong (highlight flaws, deceptions, misconceptions, fraud, misattribution, etc.) then I'll listen. Otherwise, please do not waste my time.
The idea of "complexity," like the ideas of "intelligence" and "design," is alien to those who attribute the presence of organized matter to unguided, unpurposeful forces.
Please accept my apology. There's no need to jump to conclusions; with all the information and posts and pings and reading, I frequently have dozens of windows up on my computer's task bar at any given time, thus it is sometimes easy to miss one request. I will freep-mail you shortly, and again, my apologies for the oversight.
I didn't say you did. I did say that divergence of species from common ancestors was based on observation and not magic as you implied.
What I am saying is that the materialist hypothesis that lies at the basis of scientific thought is itself non-scientific: that an objective universe of matter, energy, space, and time (MEST) exists, and that this Universe constitutes the whole of reality.
But that's a misstatement of it. Science is what science is, and that's a way to define what we know and what we don't know. It doesn't say that the latter group is not true, just that we don't know it.
So, what science says is that assumptions without evidence are to be ignored. Your belief is fine, but it's not science and the "evidence" you suggest has been reviewed objectively and found to be quite lacking.
So, do you hold that the spliceosome is irreduceably complex?
No problem
it would take a lot more than that
for me to switch sides :>)
Hey, shuffle it a few zillion more times and I'm sure you'll produce a duck!
No, it isn't. See my post 28.
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