Identical twins are known to share many features with each other. Having been born from one sperm and one egg that split once fertilized, identical twins go as far as having matching DNA. One of the rare things that each twin doesn’t share with the other, however, is their fingerprints. Human fingerprints are completely unique from person to person which makes them such an important identification tool. At the same time, this begs the question of how twins can have identical DNA structures but do not have the same fingerprints. A recent study conducted by Denis Headon, a geneticist at the University of Edinburgh, aims to explain why this is the case.
Like with some animals, humans develop their fingerprints early on. By the 13th week of gestation, the first indentations in the fingertips, known as primary ridges, start to form. There are three types of primary ridges: whorls, loops, and arches. Whorls are symmetrical and circular in shape, loops are longer, curved patterns, and arches are triangular ridges. An individual’s genes determine what combination of the primary ridges will their fingertips have but scientists have found that biochemical mechanisms can alter the ridges even if encoded a certain way in a person’s genes. This explains why identical twins who share the same DNA still have different fingerprints.
Headon and his colleagues were successful in identifying three families of signaling molecules that affect a person’s fingerprints outside of their genetics. They did so by sequencing the RNA from the nuclei of human embryonic fingertip cells. This led to the discovery of three families of proteins that pass on instructions between cells in the fingertips: WNT, BMP, and EDAR. WNT and BMP work in opposite ways. WNT stimulates cell growth which leads to more raised bumps on the skin whereas BMP suppresses cell growth which creates grooves. EDAR works independently and helps determine the size and spacing of the ridges.
All three of these proteins play an important role together in the creation of each person’s unique fingertip but experts wanted to see the abilities of each protein individually. Since mice have ridge patterns too, the experts blocked one protein to see what would happen. When the WNT pathway was blocked, there were no ridges on the mice. Knocking out the BMP pathway made the ridges wider. Lastly, in the case of there being no EDAR, the mice involved formed a polka dot pattern rather than stripes. This showed scientists that all three molecules must work together for the formation of ridges on human fingertips.
On top of the ridges, the actual fingerprints are subjective to the anatomy of the finger and the timing of the ridges. The scientists found that the primary ridges occur in three distinct locations: the center of the fetal finger’s soft raised pad, the end of the finger under the nail, and the crease at the joint where the finger bends. From there, the ridges grow outward. Headon describes this as, “waves […] each ridge serving to define the position of the next one out.” The finger’s anatomy now helps direct the finger’s cell growth. Pads that are large and symmetrical produce a whorl. Even larger and asymmetrical pads produce loops. If ridges fail to form or form late, it will result in an arch.
Circling back to the topic of identical twins, it is now evident through this study why despite having identical genetics, each twin processes their own unique fingerprint. This study not only answers this but also additionally lets scientists learn that the three molecular families—WNT, BMP, and EDAR— are also responsible for the growth of hair follicles elsewhere in the body. The reason why hair follicles are not present on the fingertips is because the formation of follicles halts pretty early on in the developmental process.
