“Junk” DNA: An Outdated Concept, Part 6 (of 6)

“Junk” DNA: An Outdated Concept, Part 6 (of 6)

by Patricia Babin

I started this article series by retelling an evolutionist’s claim that the existence of Alu elements in the human genome is proof of evolution. His hypothesis could be stated as follows:

Supporting statements:

  1. Nonfunctional DNA sequences that have the same location in many species prove that their DNA was “inherited” through the process of evolution.
  2. Alu elements are nonfunctional DNA sequences that have the same location in many species.


  1. Alu elements prove that their DNA was “inherited” through the process of evolution.

As demonstrated throughout this series, Alu elements are not nonfunctional DNA sequences; thus, their presence in the human genome cannot be used legitimately as a proof of evolution. There will still be those who have not kept up with the scientific literature and who still attempt to use this argument for evolution. Hopefully, this series will equip readers to challenge such attempts.

In concluding this series, I’d like to point out that, in addition to their abundant function, there are other reasons for viewing Alu elements as designed.

Which Function Now?
Unlike humans, a cell cannot be confused. It will be able to determine which function a particular Alu element possesses based on the content of the DNA surrounding the Alu element. This illustrates another level of functionality in Alu elements—the ability to function unambiguously in a context-dependent fashion.

Certainly, the cell has mechanisms for determining how each Alu element functions, but it’s not something readily understood from a human perspective. This particular cellular activity exhibits extraordinary design—as much or more as in the Alu element itself.

Consider this: Could genetic engineers design a synthetic DNA segment of only 300 nucleotides in length with such abundant functionality? Could they then place it strategically at a million locations in a complex genome and have it execute the appropriate function based on the context of the surrounding DNA? Obviously, we are not yet capable of doing anything on that scale. And, if someday we are, you can be assured that such engineering will require the best minds, lots of time, and lots of money. In other words, it will be evident how extraordinarily designed that DNA segment is. It will be Nobel-Prize worthy.

The existence of that kind of element in our genomes points to an incredible level design.

What about Our Furry Friends?
Are primates the only species in need of something like an Alu element? Apparently not.  Scientists have been aware of an “Alu-like” element in the genomes of other mammalian species for some time. As more is learned about these elements, the more “Alu-like” they appear.

Take, for example, the mouse Alu equivalent—the B1 element. The sequence of B1 is so similar to Alu that evolutionary scientists have concluded both elements derived from the same molecule (the signal recognition particle) at different times in evolutionary history. In simple terms, B1 corresponds to half of an Alu element.

Evolutionists have concluded that Alu elements in primates and B1 elements in mice arose after the two lineages separated from one another. Therefore, each of them evolved their sequence separately, using the signal recognition particle as the starting point. But after that the similarity gets more difficult to explain from an evolutionary perspective.

Soon after the mouse genome was first published, the scientists realized their data analysis indicated that the best predictor of B1 elements location in the mouse genome was the Alu elements location in the comparable region of the human genome.1 This realization begged the question, Why would these disparate organisms—humans and mice—have very similar sequences placed in the same locations in their respective genomes?

From an evolutionary perspective, this doesn’t make sense. But consider that scientists have also recently discovered overlapping functionality in B1 and Alu elements.2 This doesn’t help the evolutionary case, but it certainly helps the design case. Evolutionists conjecture that repetitive elements like Alu and B1 are placed randomly in the genome and then evolve new function based on where they are placed. But, from the design perspective, if we need Alu elements in certain locations, mice (with whom we share a lot of common biology) will need a similar sequence in the same location.

Evolution can’t readily explain how the sequences came to be in the same places because the Alu elements and B1 elements arose supposedly after the lines diverged.3 But from a design perspective, it seems the Designer placed a similar element in the same location because it was needed for function.

Shortly after the publication of the first part in this series, I received an e-mail from a reader who asked whether I really thought it was possible to prove function for virtually all of the Alu elements in the human genome. Hopefully, by this time, readers are convinced that I’ve built a strong fact based case for just that.  Further, evidence for function in the other categories of so-called “junk” DNA is also growing. Are there any sequences in our genome that are functionless? Yes. I believe there are, but they are far fewer than scientists used to believe.

Mutations and other processes that occur in our cells create sequences that no longer have a function. But, the hypothesis that large numbers of useless sequences are present in our genomes because of evolutionary inheritance is in the process of  being disproven. Instead, the data demonstrates wide-ranging function for these sequences. There is so much function in Alu elements that they certainly appear to be designed, incredibly well designed.

Part 1 | Part 2 | Part 3 | Part 4 | Part 5 | Part 6
  1. Robert H. Waterston et al., “Initial Sequencing and Comparative Analysis of the Mouse Genome,” Nature 420 (2002): 520–62.
  2. Paz Polak and Eytan Domany, “Alu Elements Contain Many Binding Sites for Transcription Factors and May Play a Role in Regulation of Developmental Processes,” BMC Genomics 7 (2006): 133–47.
  3. Ibid.