Every "critique" of the evolutionary model that Ray has provided in this introduction has been answered anywhere from recently, to well over a hundred years ago. The problem seems to be that Ray doesn't understand them, and in many cases doesn't even understand the critiques themselves.
This is correct. Although it is important to note that around half of our genome is comprised of repeat sequences, as explained in the 'Initial sequencing and analysis of the human genome' (2001):
In the human, coding sequences comprise less than 5% of the genome (see below), whereas repeat sequences account for at least 50% and probably much more. Broadly, the repeats fall into five classes: (1) transposon-derived repeats, often referred to as interspersed repeats; (2) inactive (partially) retroposed copies of cellular genes (including protein-coding genes and small structural RNAs), usually referred to as processed pseudogenes; (3) simple sequence repeats, consisting of direct repetitions of relatively short k-mers such as (A)n, (CA)n or (CGG)n; (4) segmental duplications, consisting of blocks of around 10±300 kb that have been copied from one region of the genome into another region; and (5) blocks of tandemly repeated sequences, such as at centromeres, telomeres, the short arms of acrocentric chromosomes and ribosomal gene clusters. (These regions are intentionally under-represented in the draft genome sequence and are not discussed here.)
Repeats are often described as ‘junk’ and dismissed as uninteresting. However, they actually represent an extraordinary trove of information about biological processes. The repeats constitute a rich palaeontological record, holding crucial clues about evolutionary events and forces. As passive markers, they provide assays for studying processes of mutation and selection. It is possible to recognize cohorts of repeats ‘born’ at the same time and to follow their fates in different regions of the genome or in different species. As active agents, repeats have reshaped the genome by causing ectopic rearrangements, creating entirely new genes, modifying and reshuffling existing genes, and modulating overall GC content. They also shed light on chromosome structure and dynamics, and provide tools for medical genetic and population genetic studies.The human is the first repeat-rich genome to be sequenced, and so we investigated what information could be gleaned from this majority component of the human genome. Although some of the general observations about repeats were suggested by previous studies, the draft genome sequence provides the first comprehensive view, allowing some questions to be resolved and new mysteries to emerge.
Aside from the immense volume of information that your
The misrepresentation of evolutionary change as "purely random" and "sheer chance" is one Ray uses over and over throughout this introduction. Mutation is random, but it only contributes the necessary variation for nonrandom processes, such as natural selection to act on. The use of analogies that ignore this reality, such as this one, is another thing Ray repeatedly relies on. The following portion of my response to a similar assertion and analogy Ray made in his section
That analogy is fundamentally inapplicable to living organisms for a few simple reasons; neither airplanes nor watches nor paintings (nor books) reproduce, witch rules out the possibility that their configurations are the result of decent with modification. Living organisms, on the other hand, do reproduce. They also pass on a large amount of the information that makes their configuration what it is to their offspring. The third critical trait of living things is that there is a consistent increase in variability caused by mutation from each generation to the next. And finally, living organisms exist in populations for finite amounts of time, and must stave off their demise while competing for limited resources. All of these principles together have an interesting result. As new variation is introduced by mutation, modifications to proteins, such as the way the catalyze reactions and configure to form anatomical structures, that allow for more efficient performance of tasks in the organisms’ environment, the organisms become either more or less able to both survive and compete for resources (thrive) in their environment. The measure of this efficiency is called fitness. Configurations that increase fitness make the organism more able—and thus more likely—to make significant contributions to their populations’ gene pools. This increases the frequencies of the alleles with those configurations, with time. Likewise, the frequencies of alleles with configurations that decrease fitness decrease, with time. This process is called natural selection. Since the differences between species are observed to be structural and functional modifications that increase fitness in the organisms’ environments, this is powerful evidence that these differences were the result of decent with modification caused by mutation and natural selection.
Physical chemist Charles Thaxton writes:
DNAcode is quite simple in its basic structure (although enormously complex in its functioning). By now most people are familiar with the double helix structure of the DNAmolecule. It is like a long ladder, twisted into a spiral. Sugar and phosphate molecules form the sides of the ladder. Four bases make up its “rungs.” These are adenine, thymine, guanine, and cytosine. These bases act as the “letters” of a genetic alphabet. They combine in various sequences to form words, sentences, and paragraphs. These base sequences are all the instructions needed to guide the functioning of the cell.
DNAcode is a genetic “language” that communicates information to the cell … The DNAmolecule is exquisitely complex, and extremely precise: the “letters” must be in a very exact sequence. If they are out of order, it is like a typing error in a message. The instructions that it gives the cell are garbled. This is what a mutation is.
… Since life is at its core a chemical code, the origin of life is the origin of a code. A code is a very special kind of order. It represents “specified complexity.”8
To ponder how
When you have for the first time in front of you this 3.1-billion-letter instruction book that conveys all kinds of information and all kinds of mystery about humankind, you can’t survey that going through page after page without a sense of awe. I can’t help but look at those pages and have a vague sense that this is giving me a glimpse of God’s mind.9
... DNA is an incredibly detailed language, revealing vast amounts of information encoded in each and every living cell—design which could not have arisen by purely naturalistic means. In every other area of our world, we recognize that information requires intelligence and design requires a designer. With our present-day knowledge of DNA, this presents a formidable challenge to Darwinian evolution.
Firstly, mutations are not necessarily detrimental—they can also either be neutral or beneficial. And when this is taken into consideration, along with natural selection, it is clear how an increase in information is a result. The following portion of my response to Ray's section on vestiges explains this principle and provides an example of a beneficial mutation:
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 human tripartite motif-containing 5 alpha (TRIM5α) antiviral protein 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
- A gene’s domains are rearranged (Moore et al., 2008).
- 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).
- A frameshift mutation forms a new gene by causing the resulting polypeptide chain to be comprised of entirely different amino acids (Okamura, 2006).
- 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).
Secondly, it is incorrect to imply that codes cannot form naturally. As explained by Dr. Kuhn (1978) and colleges in their research on the origins of the genetic code:
By a number of rare chance events, each suppressing other events of equal a priori probability, a single code results out of an immense number of possible codes of the same a priori probability.
Hall BG. Changes in the substrate specificities of an enzyme during directed evolution of new functions. Biochemistry. 1981 Jul 7;20(14):4042–4049 <http://www.ncbi.nlm.nih.gov/pubmed/6793063>.
Hall, B. G. & Zuzel, T. (1980) Evolution of a new enzymatic function by recombination within a gene. Proceedings of the National Academy of Science USA 77(6): 3529-33 <http://www.pnas.org/content/77/6/3529.full.pdf+html>.
Hayashi Y, Aita T, Toyota H, Husimi Y, Urabe I, Yomo T. Experimental rugged fitness landscape in protein sequence space. PLoS ONE. 2006;1:e96 <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1762315/>.
International Human Genome Sequencing Consortium. Initial sequencing and analysis of the human genome. Nature. 2001;409:860–921 <http://www.nature.com/nature/journal/v409/n6822/full/409860a0.html>.
Kaiser, S. M., Malik, H. S., and Emerman, M. (2007) Restriction of an Extinct Retrovirus by the Human TRIM5a Antiviral Protein. Science 316: 1756-1758 <http://www.sciencemag.org/cgi/content/abstract/316/5832/1756>.
Kuhn H, Kuhn C. Evolution of a Genetic Code Simulated With the Computer. Origins of Life. 1978;9:137–150. <http://www.springerlink.com/content/v61004u7v7873k78/>.
Moore AD, Bjorklund AK, Ekman D, Bornberg-Bauer E, Elofsson A. Arrangements in the modular evolution of proteins. Trends Biochem Sci. 2008;33:444–51. doi: 10.1016/j.tibs.2008.05.008 <http://www.ncbi.nlm.nih.gov/pubmed/18656364>.
Okamura K., Feuk L., Marquès-Bonet T., Navarro A., Scherer S. W. Frequent appearance of novel protein-coding sequences by frameshift translation. Genomics. 2006;88:690–697 <http://tinyurl.com/lds4jg>.
Schmidt EE, Davies CJ. “The origins of polypeptide domains.” Bioessays. 2007;29(3):262–70 <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1994825/?tool=pubmed>.
Schneider, Thomas D. Evolution of biological information. 2000. Nucleic Acids Research vol 28 no 14 pp. 2794-2799 <http://nar.oxfordjournals.org/cgi/content/abstract/28/14/2794>.
7. “Genome Facts,” Nova Online <www.pbs.org/wgbh/nova/genome/facts.html>.
8. Charles B. Thaxton, Ph.D., “DNA, Design and the Origin of Life,” November 13–16, 1986 <www.origins.org/articles/thaxton_dnadesign.html#ref15>.
9. Steven Swinford, “I’ve found God, says man who cracked the genome,” June 11, 2006 <www.timesonline.co.uk/tol/news/uk/article673663.ece>.