Evidence for the Evolutionary Model

Vestigial Organs—Leftovers Again? …yes; until it sinks in, Ray

 

(p.30-31)                     The pdf of the entire book, with Ray's 50 page introduction, can be found here.

For many years, “vestigial organs” have been considered proof that man has evolved from more primitive forms. With no known purpose, these organs were assumed to have outlived their usefulness and to be “leftovers” from our less advanced ancestors.

See: Vestigial Evidence for Common Ancestry

 

      However, if an organ were no longer needed, it could at best be considered devolution.

      It is a mistake to regard evolutionary change as necessarily transitioning from simplicity to complexity. Not only can changes to an organism, or a structure there in, alter or rearrange it without changing its complexity, but either one can have non essential portions removed from it. Both of these alterations can be either neutral or even beneficial and naturally selected for. Evolution is merely changes to gene frequency in populations over time, as per their ability to either increase or decrease the organisms’ likelihood of making significant contributions to their populations’ gene pools. Even a decrease in complexity can be an example of evolutionary change.

 

This is consistent with the Law of Entropy—that all things deteriorate over time.

      It is disingenuous to use the second law of thermodynamics in this context. And yes, Ray is using the second law, here; the zeroth law pertains to determination of whether or not systems are in thermal equilibrium with one another, the first law pertains to the conservation of energy, and the third law pertains to the entropy of a system as its temperature approaches absolute zero. So what does the second law state? It states that the net entropy of an isolated system increase with time. Within that isolated system, there can be numerous subsystems interacting with one another. As heat flows from one subsystem to another, the entropy of one decreases as the entropy of the other increases. Crystallization and refrigeration are good examples of such a local entropy decreases. Thus, if we set our system as the universe or the solar system, there is no violation.

       If one is to claim that evolutionary change violates the law of thermodynamics, one would have to not only specifically show how single cellular life growing in complexity over billions of years to result in humans is in violation, but would also have to do so in a way that wouldn't simultaneously indicate that a single cell growing in complexity over nine months to result in a human child is in violation; after all, we can directly observe that taking place.

 

What evolution requires, however, is not the loss but the addition of information, where an organism increases in complexity. “Vestigial organs” therefore do not serve as evidence for evolution.

      As time progresses, the increase in genetic variability caused by mutation doesn’t generally increase useful information, by itself. When that variability is acted on by natural selection, however, there are two main results; the frequency of configurations that make it more likely for the given organism to make a sizable contribution to its population’s gene pool (beneficial) increase with time, and the frequency of detrimental configurations decrease with time. The net result is an increase in useful information (Schneider, 2000). Let us use direct observation of the effects of mutation on the alpha isoforms of human tripartite motif-containing antiviral protein 5 (TRIM5α) genes as an example. The current configuration includes arginine (R) as the 332 amino acid, within the B30.2/SPRY domain. This makes human TRIM5α efficient at restricting the extinct type-1 Pan Troglodytes endogenous retroviruses (PtERV1). Since virions of this retrovirus no longer exist in the environment to do humans any harm, this ability is neither beneficial nor detrimental—it is neutral. When a single nucleotide mutation is enacted that changes the 332 amino acid to glutamine (Q), the efficiency of PtERV1 restriction gives way to an increased efficiency of restricting type-1 human immunodeficiency virus (HIV1) (Kaiser, Malik, & Emerman, 2007). Since HIV1 virions do still exist in the environment, and do humans quite a bit of harm, the R332Q mutation causes an increase of beneficial ability, at the loss of neutral ability. This would cause an increase in the frequency of the configuration in the gene pool, with time. The net change would be an increase in useful information—a benefit.

      Proteins do more than just catalyze reactions in an organism—they bind and interact with many other proteins and chemicals, as well as provide much of the organism’s structure. Mutations in genes that code for these proteins change the way the proteins interact, the way they arrange into structures, and the way they catalyze reactions. As in the example above, a mutation can change the efficiency of an enzyme in binding to its substrates and its rate of catalyzation (Hall, 1981); but it can also cause the enzyme to bind with additional substrates or to different ones all together (Hall & Zuzel, 1980). Regardless of a given protein’s roll in the organism, mutation can either change or replace the way it interacts, reacts, or arranges.

      When the replaced function is necessary, and when there is only one copy of the gene that codes for the protein, mutations are often detrimental. But when the gene is a duplicate, resulting from a duplication of chromosomal DNA, mutations are often neutral, as the original function is retained in the other copy. Further mutations to duplicate genes acted on by natural selection can then cause them to form into entirely new ones, allowing organisms and their genomes to grow in size and complexity by purely natural means. There are several processes by which this occurs:

  1. A gene’s domains are rearranged (Moore et al., 2008).
  2. A new domain is formed when point mutations or insertions within an intron cause the acquisition of a splice donor and splice acceptor, witch forms a novel alternatively splicable exon (Schmidt & Davies, 2008).
  3. A frameshift mutation forms a new gene by causing the resulting polypeptide chain to be comprised of entirely different amino acids (Okamura, 2006).
  4. Mutations in random genetic sequences can convert them into genes, as observed when the D2 domain of coliphage fd's minor coat protein g3p (crucial for infectivity) was replaced with a random sequence of 139 amino acids and subjected to random mutagenesis. A 240-fold increase in fitness was observed after only 7 generations, eventually reaching a maximum of a 17,000-fold increase (Hayashi et al., 2006).

 

      In addition, it isn’t scientifically possible to prove that something has no use, because its use can always be discovered as more information becomes available. And that’s exactly what has happened. It was claimed at the Scopes trial that there were “no less than 180 vestigial structures in the human body, sufficient to make of a man a veritable walking museum of antiquities.”48 As science has advanced, the list has shrunk to virtually zero today. Scientists have discovered that each of these organs does indeed have a purpose; for example, the appendix is part of the human immune system, and the “tailbone” supports muscles that are necessary for daily bodily functions.

      As explained in the beginning of this response, vestiges need not be functionless; they can retain preexisting secondary functions or co-op new ones. The list has only shrunk to virtually zero” if one uses an incorrect definition of a vestige, like Ray does.

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My References

Hall, B. G. "Changes in the substrate specificities of an enzyme during directed evolution of new functions." Biochemistry 20.14 (1981): 4042-049. <http://www.ncbi.nlm.nih.gov/pubmed/6793063>.

Hall, B. G., and T. Zuzel. "Evolution of a new enzymatic function by recombination within a gene." Proceedings of the National Academy of Science USA 77.6 (1980): 3529-33 <http://www.pnas.org/content/77/6/3529.full.pdf+html>.

Hayashi, Y., T. Aita, H. Toyota, Y. Husimi, I. Urabe, and T. Yomo. "Experimental rugged fitness landscape in protein sequence space." PLoS One 1.E96 (2006). <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1762315/>.

Kaiser, S. M., H. S. Malik, and M. Emerman. "Restriction of an extinct retrovirus by the human TRIM5alpha antiviral protein." Science 316.5832 (2007): 1756-758. <http://www.sciencemag.org/cgi/content/abstract/316/5832/1756>.

Moore, A. D., A. K. Bjorklund, D. Ekman, E. Bornberg-Bauer, and A. Elofsson. "Arrangements in the modular evolution of proteins." Trends in Biochemical Sciences 33.9 (2008): 444-51. <http://www.ncbi.nlm.nih.gov/pubmed/18656364>.

 

Okamura, K., L. Feuk, T. Marquès-Bonet, A. Navarro, and S. W. Scherer. "Frequent appearance of novel protein-coding sequences by frameshift translation." Genomics 88.6 (2006): 690-97. <http://tinyurl.com/lds4jg>.

Schmidt, E. E., and C. J. Davies. "The origins of polypeptide domains." Bioessays 29.3 (2007): 262-70. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1994825/?tool=pubmed>.

Schneider, T. D. "Evolution of biological information." Nucleic Acids Research 28.14 (2000): 2794-799. <http://nar.oxfordjournals.org/cgi/content/abstract/28/14/2794>.

Thomson, S., and J. Staley. "Entropy and the Second Law of Thermodynamics." National Small-Scale Chemistry Center. Web. 29 Sept. 2009. <http://www.smallscalechemistry.colostate.edu/PowerfulPictures/EntropyAndTheSecondLaw.pdf>.

 

Ray’s Reference

31. Horatio Hackett Newman, quoted in The World’s Most Famous Court Trial: The Tennessee Evolution Case (Dayton, TN: Bryan College, 1925, reprinted 1990), p. 268.