There are so, so many independent lines of evidence that support evolution. If I had to pick one, though, that is really compelling and easy and quick to explain, it may be non-homologous end joining.

Sometimes DNA breaks. I mean both strands snap, a complete break. This injury could be the result of a stray proton, or a gamma ray, or something else. It is often due to radiation.

In many cases, the cell can repair the DNA effectively, using a nearby chromosome as a template. When a template is not available, the cell panics. Plan B is enacted. Plan B is called non-homologous end joining, or NHEJ for short. The process is quite complex. The end result is that the broken ends are often trimmed, and the two parts are joined back together.

Now, there are a few different versions of NHEJ. Especially with a couple of these in particular, such as theta-mediated end joining, the result is messy.[1] Parts of the DNA, like the part that got blown away by the proton particle, and some of the ends that got trimmed in the repair process, are missing. What’s more, the whole process is error prone, and we often see mutations at the repair site. And in some cases spare parts get pulled in as the cell grabs whatever is around to use in its fight to stay alive.

As Yuichiro Miyaoka and colleagues remark, “NHEJ is an error-prone mechanism in which broken ends of DNA are joined together, often resulting in a heterogeneous pool of insertions and deletions.”[2] Likewise, as Howard Chang and colleagues write, “This flexibility permits NHEJ to function on a wide range of DNA-end configurations, with the resulting repaired DNA junctions often containing mutations.”[3]

And again, as Graeme Finlay explains, “The stitched-up break might be held together by extraneous segments of DNA, usually copied from a site nearby on the same chromosome, but sometimes copied from anywhere else in the genome. The repair site may have lost some of the original base sequence, either when the injury happened or during the trimming of the loose ends by exonucleases. And a few bases may have been inserted that were not copied from any DNA template.”[4]

Finally, I’ll quote Michael Lieber, one of the foremost experts in this area. He comments, “NHEJ does not return the local DNA to its original sequence, thus accounting for the wide range of end results. Part of this heterogeneity arises from the diversity of the DNA ends, but much of it arises from the many alternative ways in which the nuclease, polymerases, and ligase can act during NHEJ.[5]

So, we can often tell there was a repair. There is a scar. And, the scars are not all alike. They are often recognizable from each other. As Graeme Finlay asserts,  “Any one double-stranded DNA break spliced together by NHEJ generates a unique mutational fingerprint that would provide a perfect marker of monoclonality in the descendants of the damaged cell.”[6]

And this is the key to how NHEJ proves evolution. We have found lots of these scars in the chimpanzee genome. “Scientists have scrolled through genome databases to search for segments of DNA that bear the fingerprints of DNA repair patches. The key indications are that a piece of DNA has been copied from one site into another, concomitantly with losses and gains of bases at the recipient site.”[7]

Then, when we look at the human genome, we see many cases of the same scar in the same place as in the chimp genome. We see this over and over again.[8]

How does this happen? The locations where stray photons break DNA strands should be random. Photons don’t aim at certain locations. And so it seems inconceivable that all these repairs would happen in chimps and humans in the exact same places, over and over and over again.

The explanation is quite clear: These breaks, and repairs, happened in the common ancestor of chimps and humans, and we inherited them, as did chimps. Chimps and humans share a common ancestor. Evolution is true. I haven’t seen an argument from direct creationists refuting this evidence. I don’t think there is any reasonable refutation.

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[1] Kasey Rodgers and Mitch McVey, “Error-prone repair of DNA double strand breaks,” J Cell Physiol. 2016 January; 231(1): 15–24. doi:10.1002/jcp.25053.

[2] Yuichiro Miyaoka et al, “Systematic quantification of HDR and NHEJ reveals effects of locus, nuclease, and cell type on genome-editing,” Scientific Reports, Published: 31 March 2016

[3] Howard H.Y. Chang et al, “Non-homologous DNA end joining and alternative pathways to double-strand break repair,” Nature Reviews: Molecular Cell Biology, 2017 Aug;18(8):495-506. doi: 10.1038/nrm.2017.48. Epub 2017 May 17.

[4] Graeme Findlay, Human Evolution (Cambridge: Cambridge University Press, 2013), 139.

[5] Michael R Lieber, “The mechanism of human nonhomologous DNA end joining,” The Journal of Biological Chemistry January 4, 2008, 283(1).

[6] Graeme Findlay, Human Evolution (Cambridge: Cambridge University Press, 2013), 139.

[7] Graeme Findlay, Human Evolution (Cambridge: Cambridge University Press, 2013), 139.

[8] Graeme Findlay, Human Evolution (Cambridge: Cambridge University Press, 2013), 140.

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