DNA is a remarkable molecule—its double helix design displays a certain beauty and, in biochemical terms, its structure and function are no less pleasing to behold. As I discuss in my book The Cell’s Design, DNA is structurally optimized to carry out its chief function: storage of information used by the cell’s machinery to generate life’s building blocks and direct the cell’s operation. (For an example of the optimized structure-function relationships found in DNA, see “DNA Soaks Up Sun’s Rays.”)
Yet there is more to DNA’s purpose than information storage. Recently, biologist Claudiu Bandea of the US Centers for Disease Control and Prevention argued that DNA sequences assume noninformational roles that biologists have often overlooked.1These noninformational functions help account for the existence of abundant junk DNA in the genomes of humans and other organisms.
First, Bandea shows that DNA plays a skeletal role by helping to establish and maintain the size of the cell’s nucleus. This function is called the nucleoskeletal hypothesis. According to this idea, the amount of DNA in a cell dictates the nuclear volume. The size of the nucleus is not arbitrary, however, but must be maintained within tight limits. The cell will die if the ratio of the nuclear volume relative to overall cell volume deviates too much. Presumably, the nucleoskeletal role of DNA can account for the vast amount of junk DNA within genomes and helps explain the C-value paradox. Larger cells require a larger nucleus and, consequently, a greater amount of junk DNA in their genomes to maintain an adequate nuclear volume. (For more, see “TNRTB Classic: Junk DNA and the Nucleoskeletal Hypothesis.”)
Bandea also asserts that junk DNA may serve as a mutational buffer. He notes that the human genome (and the genomes of other organisms) consists of a significant fraction of mobile DNA pieces called transposons. These pieces of DNA move around the genome and, presumably, insert at random into different locations. (Some transposons also possess the capacity to duplicate in the process.) If insertions occur in coding or regulatory regions of the genome, mutations result.
Retroviruses pose a similar problem. When viruses invade a cell, retroviral DNA inserts into the host’s genome. Again, these insertion events can be disruptive if they occur within functional sequences.
But Bandea posits that high levels of junk DNA can make genomes more resistant to the deleterious effects of insertion events. If insertion events are random, then the offending DNA is much more likely to insert itself into “junk DNA” regions instead of coding and regulatory sequences—thus, protecting information-harboring regions of the genome. To say it another way, junk DNA sequences could serve as buffers against mutations that arise from transposon and retroviral DNA insertion events.
Solving the C-Value Paradox
If junk DNA functions as a mutational buffer, then it could also help account for the C-value paradox (which observes “that genome size does not correlate with organismal complexity”).2 It could be that the varying genome sizes are not arbitrary, but instead correlate with the amount of protective DNA. Genomes with higher transposon activity could require a greater buffering capacity and, consequently, more junk DNA.
When it comes to understanding genomes (human or otherwise), the evolutionary paradigm has continuously restricted the view of many people in the scientific community by compelling them to classify, noncoding DNA as the leftover vestiges of evolution. But, as Bandea’s research shows, a narrow focus on DNA’s informational role has interfered with the acknowledgment of junk DNA’s important noninformational functions. Such discoveries help open up the possibility for nonevolutionary interpretations of genome content, including the notion that these tiny pieces of DNA stem from an intelligent Mind.