Intelligent Design

Spliceosomes and Exons: The New Agents of Evolution

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Remember when evolution created all of biology one mutation at a time? That quaint idea from your high school biology class was about as likely as an alien world smashing into the Earth last Friday. But at least it had the virtue of not being circular. No such luck today as now evolution has to create itself. Call it evolvability, call it pre planned evolutionary pathways or call it just plain serendipity, it all means the same thing: Evolution must have constructed elaborate mechanisms and structures which then became crucial agents of evolution, creating all kinds of biological wonders. Simply put, evolution must have created evolution. In recent years such serendipity in the evolution narrative has skyrocketed. If it were a stock you would be a millionaire by now. And the latest IPOs are the spliceosomes and exons which, if evolution is true, must be crucial in the creation of, err, pretty much all the higher species.  Read more

5 Replies to “Spliceosomes and Exons: The New Agents of Evolution

  1. 1
    bornagain77 says:

    It is interesting to point out just how hard the alternative splicing schemes/codes were to originally decipher:

    Researchers Crack ‘Splicing Code,’ Solve a Mystery Underlying Biological Complexity – May 2010
    Excerpt: “Understanding a complex biological system is like understanding a complex electronic circuit. Our team ‘reverse-engineered’ the splicing code using large-scale experimental data generated by the group,”
    http://www.sciencedaily.com/re.....133252.htm

    Breakthrough: Second Genetic Code Revealed – May 2010
    Excerpt: The paper is a triumph of information science that sounds reminiscent of the days of the World War II codebreakers. Their methods included algebra, geometry, probability theory, vector calculus, information theory, code optimization, and other advanced methods. One thing they had no need of was evolutionary theory,,,
    http://crev.info/content/break.....e_revealed

    Remember the German ‘Enigma”?,,,,,, now finding the alternative splicing ‘scheme/code’ to be species specific is extremely problematic for Darwinism (as if Darwinism did not already have devastating problems) because random changes in the ‘scheme/code’ regulating how genes in a species are expressed would be far more devastating to an organism than just single mutations to DNA (SNPs) would be. ,,, For a illustration of what I’m talking about, Richard Dawkins gives an example of what would happen if one were to make random changes in the regulatory structure of the genetic code here:

    Venter vs. Dawkins on the Tree of Life – and Another Dawkins Whopper – March 2011
    Excerpt:,,, But first, let’s look at the reason Dawkins gives for why the code must be universal:
    “The reason is interesting. Any mutation in the genetic code itself (as opposed to mutations in the genes that it encodes) would have an instantly catastrophic effect, not just in one place but throughout the whole organism. If any word in the 64-word dictionary changed its meaning, so that it came to specify a different amino acid, just about every protein in the body would instantaneously change, probably in many places along its length. Unlike an ordinary mutation…this would spell disaster.” (2009, p. 409-10)
    OK. Keep Dawkins’ claim of universality in mind, along with his argument for why the code must be universal, and then go here (linked site listing 23 variants of the genetic code).
    Simple counting question: does “one or two” equal 23? That’s the number of known variant genetic codes compiled by the National Center for Biotechnology Information. By any measure, Dawkins is off by an order of magnitude, times a factor of two.
    http://www.evolutionnews.org/2.....44681.html

    further notes:

    “Because of Shannon channel capacity that previous (first) codon alphabet had to be at least as complex as the current codon alphabet (DNA code), otherwise transferring the information from the simpler alphabet into the current alphabet would have been mathematically impossible”
    Donald E. Johnson – Bioinformatics: The Information in Life

    Shannon Information – Channel Capacity – Perry Marshall – video
    http://www.metacafe.com/watch/5457552/

    Verse and music:

    John 1:1-4
    In the beginning was the Word, and the Word was with God, and the Word was God. He was with God in the beginning. Through him all things were made; without him nothing was made that has been made. In him was life, and that life was the light of all mankind.

    Cyndi Lauper – Early Christmas Morning (Live)
    http://www.youtube.com/watch?v=ckiofllGaSA

  2. 2
    Mung says:

    It is obvious then, isn’t it, that evolution can easily solve the search for a search problem.

  3. 3
    Starbuck says:

    traits of different species should fall into the evolutionary tree, common descent, pattern.

    True, but it depends on the rate of divergence of the traits relative to the branches in the evolutionary tree. For example, in this case
    alternative splicing levels are changing more rapidly than the divergence times between the species studied.

  4. 4
    bornagain77 says:

    OT: Sometimes Darwinists will try to say that synthetic proteins that are found to bind to ATP are proof that functional proteins are not as rare as Dr. Axe and others have found (1 in 10^64 to 1 in 10^77), but what the Darwinists conveniently fail to mention is that these synthetic proteins which bind to ATP (at a rate of 1 in 10^12) disrupt the cell. The following study is interesting for it studies the reaction of e-coli to one of these synthetic proteins that bind to ATP:

    Strange Behavior: New Study Exposes Living Cells to Synthetic Protein – Dec. 27, 2012
    Excerpt: ,,,The research results, reported in the advanced online edition of the journal ACS Chemical Biology, describe a peculiar set of adaptations exhibited by Escherichia coli bacterial cells exposed to a synthetic protein, dubbed DX. Inside the cell, DX proteins bind with molecules of ATP, the energy source required by all biological entities.
    “ATP is the energy currency of life,” Chaput says. The phosphodiester bonds of ATP contain the energy necessary to drive reactions in living systems, giving up their stored energy when these bonds are chemically cleaved. The depletion of available intracellular ATP by DX binding disrupts normal metabolic activity in the cells, preventing them from dividing, (though they continue to grow).
    After exposure to DX, the normally spherical E. coli bacteria develop into elongated filaments. Within the filamentous bacteria, dense intracellular lipid structures act to partition the cell at regular intervals along its length. These unusual structures, which the authors call endoliposomes, are an unprecedented phenomenon in such cells.
    “Somewhere along the line of this filamentation, other processes begin to happen that we haven’t fully understood at the genetic level, but we can see the results phenotypically,” Chaput says. “These dense lipid structures are forming at very regular regions along the filamented cell and it looks like it could be a defense mechanism, allowing the cell to compartmentalize itself.” This peculiar adaptation has never been observed in bacterial cells and appears unique for a single-celled organism.,,,
    In the current study, E. coli cells exposed to DX transitioned into a filamentous form, which can occur naturally when such cells are subject to conditions of stress. The cells display low metabolic activity and limited cell division, presumably owing to their ATP-starved condition.
    The study also examined the ability of E. coli to recover following DX exposure. The cells were found to enter a quiescent state known as viable but non-culturable (VBNC), meaning that they survived ATP sequestration and returned to their non-filamentous state after 48 hours, but lost their reproductive capacity. Further, this condition was difficult to reverse and seems to involve a fundamental reprogramming of the cell.
    In an additional response to DX, the filamentous cells form previously undocumented structures, which the authors refer to as endoliposomes. These dense lipid concentrations, spanning the full width of the filamented E. coli, segment the cells into distinct compartments, giving the cells a stringbean-like appearance under the microscope.
    The authors speculate that this adaptation may be an effort to maintain homeostasis in regions of the filamentous cell, which have essentially been walled off from the intrusion of ATP-depleting DX. They liken endoliposomes to the series of water-tight compartments found in submarines which are used to isolate damaged sections of the ship and speculate that DX-exposed cells are partitioning their genetic information into regions where it can be safely quarantined. Such self-compartmentalization is known to occur in some eukaryotic cells, but has not been previously observed in prokaryotes like E. coli.
    http://www.sciencedaily.com/re.....143001.htm

  5. 5
    bornagain77 says:

    Related notes:

    A Man-Made ATP-Binding Protein Evolved Independent of Nature Causes Abnormal Growth in Bacterial Cells – 2009
    Excerpt: “Recent advances in de novo protein evolution have made it possible to create synthetic proteins from unbiased libraries that fold into stable tertiary structures with predefined functions. However, it is not known whether such proteins will be functional when expressed inside living cells or how a host organism would respond to an encounter with a non-biological protein. Here, we examine the physiology and morphology of Escherichia coli cells engineered to express a synthetic ATP-binding protein evolved entirely from non-biological origins. We show that this man-made protein disrupts the normal energetic balance of the cell by altering the levels of intracellular ATP. This disruption cascades into a series of events that ultimately limit reproductive competency by inhibiting cell division.”
    http://www.plosone.org/article.....ne.0007385

    How Proteins Evolved – Cornelius Hunter – December 2010
    Excerpt: Comparing ATP binding with the incredible feats of hemoglobin, for example, is like comparing a tricycle with a jet airplane. And even the one in 10^12 shot, though it pales in comparison to the odds of constructing a more useful protein machine, is no small barrier. If that is what is required to even achieve simple ATP binding, then evolution would need to be incessantly running unsuccessful trials. The machinery to construct, use and benefit from a potential protein product would have to be in place, while failure after failure results. Evolution would make Thomas Edison appear lazy, running millions of trials after millions of trials before finding even the tiniest of function.
    http://darwins-god.blogspot.co.....olved.html

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