Tim Standish replies:
While Darwinists trumpeted noncoding DNA as prima facie evidence against design, they ignored the fact that efficiency is also accepted within the evolution paradigm as a hallmark of organisms. Efficiency is presumed to increase as natural selection eliminates less-efficient members of a population. As inefficiency increases, the burden it imposes is assumed to impact "fitness." When the impact on fitness becomes biologically significant, selection will eliminate those organisms with systems relatively less efficient than others competing for the same resources. Only efficient organisms can survive in a selective environment.
The large amount of noncoding DNA in eukaryote genomes seems very inefficient. One would think that a trend would be evident in organisms, going from less to more efficient use of DNA. Ironically, the simpler the organism, the greater its efficiency in DNA use, not the opposite (Lewin 2000). The simplest organisms have little or no noncoding DNA. Alternatively, if noncoding DNA provides grist for the evolutionary mill, one might predict that organisms with more noncoding DNA would evolve more rapidly than those with less "extra" DNA as raw material to work with. This has not been demonstrated. Bacteria with relatively compact genomes are known to adapt to environmental changes at startling rates via rapid mutation. It is true that bacteria have very short generation times, and this may contribute to their rapid adaptation. It is also true that some different mechanisms may be in place in bacteria to direct genetic change, but the reality remains that in this diverse group of organisms whose genetic behavior has been extensively studied, biochemical adaptation to changing environments does not seem to require noncoding DNA.
Relative abundance of noncoding DNA can vary significantly between closely related organisms (see Martin and Gordon 1995, and Sessions and Larson 1987 for examples of this), indicating that changes in the amount of noncoding DNA is an easy evolutionary step. If it is easy to change the quantity of noncoding DNA, the question arises, "Why are those with more than the average amount of noncoding DNA not selected against?" It could be argued that the difference in efficiency between two individuals with varying amounts of noncoding DNA would not be large enough to impact the individual's reproductive success, but this is a troubling argument that is unsupported by the data.
Making and maintaining DNA requires significant energy input on the part of cells. Not only does the cell have to provide the deoxynucleotide building blocks for extra unneeded DNA, but also enzymes to polymerize and proofread newly made DNA, gyrases to unwind the template DNA, DNA repair enzymes, and so on. Factor all that into the 75 trillion cells in an average human with six billion bases in each nucleus, and the cost becomes potentially significant, even though the cost of other cellular activities may have a much greater direct cost in terms of energy.
The problem of wasted energy would be so much greater if some "junk" DNA were translated, an apparent requirement if it is to serve as a resource for evolution of novel new proteins. Akashi and Gojobori (2002) discuss the cost of polypeptide production and ways in which proteins, particularly those most commonly expressed, are optimized to utilize amino acids with the lowest metabolic cost possible. Clearly, if selection is sensitive enough to adjust specific amino acids within proteins to lower the energy cost of their production, then it should be sensitive enough to eliminate production of any "junk" proteins. It also follows that any DNA sequences that do not provide a selective advantage, especially if they constitute a significant majority of an organism's genome, should represent a significant metabolic cost and thus be selected against.
It cannot be argued that genome size has no phenotypic impact. Sessions and Larson (1987) have shown that, at least in some closely related salamander species, genome size is negatively correlated with the rate of development. Martin and Gordon (1995) suggest that the large amount of DNA in the nucleus of obligate neotenic salamanders slows development, increases cell size and slows metabolism which they suggest improves survival in cold-water environments. Supporting the theory that increased genome size slows development, Jockusch (1997) showed that genome size is positively correlated with embryonic development time.
Another example of phenotypic change correlated with variation in nuclear DNA size is evident in populations of the flowering plant Silene latifolia. In this plant, genome size shows a significant negative correlation with calyx diameter, a trait of clear ecological importance (Meagher and Costich 1996). Vinogradov (1997) has shown that resting metabolic rate in passerine birds is negatively correlated with increased nuclear DNA when body size is held constant. It is noteworthy that these papers emphasize the supposed evolutionary significance of noncoding DNA, and contradict the assumption that it lacks function. This at least partially disqualifies the previous argument that lack of function in noncoding DNA supports the idea that it is molecular debris of the evolutionary process. Whatever the source, much DNA appears to have a significant phenotypic impact upon which selection may act, whether or not it directly codes for proteins or controls their expression.
Having unneeded DNA presents a potential danger to cells. It is not inconceivable that mutations could occur, resulting in production of noncoding RNA, some of which may interfere with production of essential - or at least beneficial - RNAs and, if they code for them, proteins. If "junk proteins" were made, their production would, at best, waste a cell's resources or, at worst, alter the activity of other proteins. Darwinists suggest that production of new proteins from old noncoding DNA is the very mechanism by which some new genes were produced. This postulated production of "junk" proteins via genes whose expression is not tightly controlled presents a potential danger to cells both by sapping the resources of the cell for a nonproductive task and also because the protein may have functions that interfere with the normal function of other essential components of the cell. Nyolase produced by Flavobacterium has been presented as an example of a new functional protein arising from a sequence (in this case assumed to be a formerly unread reading frame) which did not previously code for any protein (Ohno 1984). If functional proteins can spring forth from previously noncoding sequences, they need not all be adaptive; in fact, harm to the cell appears a far more likely outcome.
Loss of functionless DNA would seem to be a relatively easy evolutionary step. Gaining DNA may be more difficult, although data exist which are consistent with the theory that increases in the number of copies of some DNA stretches has occurred as a result of imperfect crossing over during meiosis prophase I. Alternative explanations of these repeats may be equally consistent with the data, but the important point for this argument is that DNA which is not a normal part of an organism's genome has been shown to be rapidly lost. For example, Petrov and Hartl (1998) have shown that, at least in Drosophila species, functionless DNA disappears after only a few generations. This appears to be analogous to the vision loss observed in some fish and other organisms that live in caves, or the loss of flying ability observed in birds that live on isolated islands. The conventional explanation is that without selective pressure to maintain them, these abilities are lost. In caves where there is no light, sight provides no selective advantage. Similarly, flight provides little advantage in the absence of predators and presence of abundant marine food around islands. Apparently, at least in Drosophila, extra DNA, like sight and flight, will not be maintained in the absence of selective pressure to maintain it.
The fact that DNA not normally part of a specific genome is easy to lose, combined with evidence that increases in genome size significantly impact phenotype, calls into question the idea that noncoding DNA does not impact fitness enough for natural selection to work on it. These data, combined with the logical inference that noncoding DNA may produce RNA or protein products that negatively impact fitness, all call into question the idea that noncoding DNA represents a currently functionless record of the phylogenetic history of organisms which has been passed down over many generations.
For both intelligent design theorists and Darwinists, noncoding DNA presents a problem if it is really functionless. Intelligent design assumes that a wise Designer would not add functionless rubbish to His creation. Evolutionists assume some function, exemplified in Brosius and Gould's (1992) nomenclature, if not in the present, at least as remnants of past functionality and raw material for the future. Assuming that noncoding DNA lacks function appears to violate the basic scientific assumption that what is seen in nature exhibits some purpose which can be determined through observation and experimentation. Enthusiasm for absence of function in noncoding DNA appears to have sprung more from philosophical presuppositions, than a careful analysis of data and their implications for Darwinism.
If any functionality was to be assigned to noncoding DNA, it was to be done within the context of its role in evolution, not on the basis of any immediate benefit to the organism bearing it in its nucleus.
For more information see my paper at http://www.grisda.org/origins/53007.pdf.
2010 Arthur V. Chadwick, Ph.D.