Where Science and Faith Converge

Yet Another Use for “Junk” DNA

By - June 30, 2000

A team of scientists from Case Western Reserve (CWRU) School of Medicine in Cleveland, Ohio, has developed convincing circumstantial evidence for yet another function for so-called “junk” DNA.1-2 Critical to this discovery was the sequence data recently made available by the Human Genome Project.

Researchers have used the term “junk” DNA to refer to the non-coding DNA found in the genomes (an organism’s DNA content) that presumably has no function. Many scientists have long held that “junk” DNA results from random biochemical events.  According to these scientists, “junk” DNA has persisted in the genomes of organisms (including humans) from generation to generation due solely to its physical attachment to the coding of functional DNA.3

Some scientists have regarded “junk” DNA as evidence against Intelligent Design.  “Junk” DNA is viewed as an example of an imperfection in nature. This argument against Design has become more prevalent, amid the current fanfare associated with the Human Genome Project.

A number of important functions have been identified for so-called “junk” DNA in the last five years.4 Even with these findings, one class of “junk” DNA remains problematic from a Design standpoint. That class is called LINE (long interspersed nuclear element) DNA.

The recent work by the CWRU scientists effectively addresses this concern by identifying a functional role for LINEs in X chromosome inactivation.5 X chromosome inactivation occurs in healthy females as a way to compensate for duplicate genes found on the X chromosomes.6 (Recall that females have two X chromosomes, whereas males have an X and Y chromosome). The inactivation of one set of X chromosomal genes ensures proper level of gene expression for individuals with more than one X chromosome.

Scientists are beginning to understand the molecular mechanism of X chromosome inactivation.7 Inactivation begins at the inactivation center, which contains the Xist gene, and then spreads along the X chromosome. The Xist gene on the inactive X chromosome expresses messenger RNA. Messenger RNA is a molecule that is similar in structure to DNA. Messenger RNA contains a copy of the information found in DNA that is used to direct the synthesis of proteins. Messenger RNA does this by migrating from the nucleus (which houses the DNA) to ribosomes found in the cytoplasm. It is at the ribosomes that messenger RNA directs protein synthesis. The Xist RNA never leaves the nucleus. Rather, it binds to and coats the entire length of the inactive X chromosome, with the heaviest coating occurring at the X-inactivation center. In contrast, the Xist gene is “turned-off” on the active X chromosome.8

The work of the CWRU team strongly implicates LINEs as the binding site for Xist RNA. Data from the Human Genome Project shows that the X chromosome contains a significant enrichment of LINE sequences compared to other chromosomes. The greatest concentration of LINEs is at the inactivation center. Moreover, sites that escape X chromosome inactivation lack LINE sequences. The recognition by the CWRU team that LINE DNA functions in X chromosome inactivation adds to the growing evidence that the genome is the product of a Designer.

Another finding by the CWRU researchers that is surprising and further supports the notion that LINE DNA is the product of Design is what appears to be the “sudden” appearances of LINE DNA in placental mammals. Based on their analysis (assuming an evolutionary perspective), the CWRU scientists were forced to recognize that at the time that placental mammals “separated” from marsupial mammals, LINE DNA appeared in placental mammals. This LINE DNA has persisted largely unchanged. This result makes little sense from an evolutionary perspective because one would expect the LINE DNA to accumulate gradually in the genome over long periods of time. The sudden appearance of LINE DNA that essentially persists unchanged and has a clear function is expected for a Design scenario.

The only characteristic of LINE DNA that could be used to argue against Design is its similarity to retroviral DNA. A retrovirus is an RNA virus that is able to incorporate its DNA into the DNA of the infected host organism.  Once the retroviral DNA becomes incorporated into the host DNA it can become inactivated through mutational events. It is believed that LINE DNA is inactive retroviral DNA that can self-propagate through the genome once incorporated. However, in 1989, a worker classifying LINE DNA in humans offered up an interesting role for LINEs that addresses this concern.9 This researcher suggested that the similarity of retroviral DNA and LINE DNA may represent an anti-retroviral mechanism, noting that LINE DNA becomes expressed at high levels when retroviral infection occurs. This being the case, the RNA produced from the LINE DNA will interfere with the retrovirus life cycle, inhibiting its spread beyond the infected cell. That is, the structural similarity between retroviruses and LINE DNA argues not for common ancestry and descent with modification at a molecular level but rather for purpose and function.

There is still much to learn about genome structure. However, the more we learn about genomes, the more we recognize the diverse functional importance of “junk” DNA. At the same time, we uncover more evidence for Design.


  1. Jeffrey A. Bailey et al., “Molecular Evidence for a Relationship Between LINE-1 Elements and X Chromosome Inactivation: The Lyon Repeat Hypothesis,” Proceedings of the National Academy of Sciences USA 97 (2000): 6634-39.
  2. Mary F. Lyon, “LINE-1 Elements and X Chromosome Inactivation: A Function for ‘Junk’ DNA?” Proceedings of the National Academy of Sciences USA 97 (2000): 6248-49.
  3. Wen-Hsiung Li, Molecular Evolution (Sunderland, MA: Sinauer Associates, Inc. Publishers, 1997), 395-99.
  4. Fazale R. Rana, “Junk DNA Not So Junky,” Connections 2, no. 1 (2000): 2.
  5. Bailey, et al., 6634-39.
  6. Edith Heard, Philippe Clerc, and Philip Avner, “XChromosome Inactivation in Mammals,” Annual Review of Genetics 31 (1997): 571-610.
  7. Lyon, 6248-49.
  8. Alan G. Atherly, Jack R. Girton, and John F. McDonald, The Science of Genetics (Fort   Worth, TX: Saunders College Publishing, 2000), 597-608.
  9. Jerzy Jurka, “Subfamily Structure and Evolution of the Human L1 Family of Repetitive   Sequences,” Journal of Molecular Evolution 29 (1989): 496-503.

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